Unit2

WEEK 2.1

The excitable cells of the nervous system

Excitable cell: A cell that uses the resting membrane potential to generate an electrochemical impulse called an action potential. For example, Neurons, muscle cells and some endocrine cells.

Non-excitable cell: Do not generate action potentials

How are action potentials generated?: depolarization events within the cell

Depolarization: The process by which ions move in and out of the cell so that the inside of the cell becomes more positive relative to the resting membrane potential.

Hyperpolarization: K+ leaves the cell through chemically- or voltage-gated channels, making the inside more negative than resting potential

What are voltage-gated vs. chemically-gated ion channels?:

Voltage-gated: Open with a change in membrane voltage.

Chemically-gated: Open when a specific chemical (ligand) binds.

What is the threshold for triggering an action potential (AP)?: -55 mV. Depolarizations must reach this level to start an AP.

Steps on Action potential:

Stimulus: Triggers depolarization making the inside of the cell more positive but Action potential is only triggered if it reaches -55mV.

Depolarization: Voltage-gated Na+ channels open, Na+ comes in, the cell becomes more positive. ( voltage-gated K+ channels are closed)

Repolarization: Voltage-gated K+ channels open, K+ leaves, the cell becomes more negative. ( voltage-gated Na+ channels are closed)

Hyperpolarization: Cell overcorrects and makes the cell more negative than the resting membrane potential. AKA Relative refractory period.

Resting state: Resting membrane potential has been restored.

Why are Na⁺ and K⁺ channels called "voltage-gated"?: Because their opening is triggered by a change in membrane voltage.

Why don't Na⁺ and K⁺ channels open at the same time?: Na⁺ channels open first at threshold, then inactivate as K⁺ channels open later during more positive voltage.

Absolute refractory period: The time during depolarization and repolarization when no new AP can be initiated (Na+ channels are closed)

Relative refractory period: Cell overcorrects and makes the cell more negative than the resting membrane potential.

Propagation of an action potential

Neurons: Excitable cells that communicate through action potentials.

Structure of a neuron:

Soma: Body of the cell, where the nucleus and most organelles are located

Dendrites: Projections of the soma and the site of communication with other neurons. They direct the AP towards the soma.

Axon: Projection of the body that directs AP away from the soma

Axon terminals: Ends of the axon that transmit information to the next cell through the release of neurotransmitters.

Myelin Sheath: Insulating layers that form around the axon. Made of proteins and fatty acids. Its presence ensures that the AP is transmitted fast along the axon.

Schwann cell: Type of cell that surrounds the axon. It produces myelin and ensures that the neuron stays alive.

Nodes of Ranvier: myelin-sheath gaps that are rich in ion channels. Participate in the fast propagation of an AP.

In which direction does an action potential travel in a neuron?: From dendrites → to soma → to axon → to axon terminals.

What happens when neurotransmitters are released from the presynaptic neuron?: They bind to ion channels on the postsynaptic cell, causing depolarization.

What influences the speed of signal propagation in a neuron?: Whether the axon is myelinated or unmyelinated. (faster through the myelinated because of saltatory conduction).

What ensures the unidirectionality of action potential propagation?: The refractory periods of the action potential.

Neurons and glial cells

What are the two main divisions of the nervous system?: The central nervous system (CNS) and the peripheral nervous system (PNS).

What structures make up the central nervous system (CNS)?: The brain and spinal cord.

What structures make up the peripheral nervous system (PNS)?: Nerves that extend from the central nervous system to muscles and organs like heart, liver, stomach.

What are the two divisions of the PNS?:

Somamotor: Skeletal muscles for voluntary movement

Autonomic: Organs that are automatically controlled by the brain and not under voluntary control.

What are the two MAIN cell types that make up the brain?: Neurons and glial cells

What is the function of glial cells?: To provide the environment necessary for neurons to function properly.

What glial cell type is involved in axon myelination?: The Schwann cell

Types of neurons:

Bipolar: One axon, one dendrite. Found in the retina of the eye

Unipolar: Straight connection between axon and dendrite. Located in the peripheral nerves outside of the CNS. Sensory in nature, transmit signals to and from the spinal cord.

Multipolar: Many branching dendrites and one axon. Most common in the CNS. They connect the CNS with the effector organs

Types of neuroglia:

Ependymal cells: Produce cerebrospinal fluid and line the brain’s ventricle and spinal cord. Their cuboidal shape and cilia and microvilli are used to absorb and circulate CSF. Distribute hormones/signaling molecules and regulate ion and glucose movement for osmotic control.

Oligodendrocytes: Myelin-forming cells. One oligodendrocyte can myelinate several axons and are incapable of replication upon injury.

Satellite cells: Ensheath the soma of neuron bodies in ganglions. Believed to act similar to astrocytes in the CNS. They provide nutrients and structural support to neurons of the PNS, by bundling the axons close together and keeping them from touching each other.

Astrocytes: Most abundant cell in the brain, Star shaped cell that provides physical and nutritional support for neurons. Functions include:

- clean-up brain debris

- transport nutrients to neurons

- hold neurons in place

- digest dead neurons

- regulate content of extracellular space

- promote synaptic connections

- are involved in response to brain injury and inflammation

Microglia: Engulf and remove foreign or damaged materials, cells or organisms. They are sparsely distributed and dynamic, as they move to actively survey the brain for active foreign invaders. Also involved in the removal of previously formed synapses that are no longer useful.

Schwann cells: Glial cells of PNS. Surround the neurons, keeping them alive and covering axons in myelin sheaths. Play a key role in development, maintenance, function and regeneration of the peripheral nerves.

Multiple Sclerosis: The immune system attacks the myelin sheaths of neurons.

What happens to action potential conduction in MS?: It becomes disrupted or blocked due to myelin sheath damage.

What are possible consequences if a damaged neuron is connected to a muscle?: The muscle may not contract, leading to paralysis.

Is MS a disease of the CNS or PNS?: CNS

What happens to axons when myelin is destroyed in MS?: Axons become exposed and vulnerable to immune system attacks.

The brain

How many cerebral hemispheres does the brain have?: Two

Left: Sends signals to activate muscles on the right side of the body, while sensory information from the right side of the body travels to the left hemisphere and vice versa.

Right:

What are the bumps on the brain called?: Gyri (singular: gyrus)

What are the dips or valleys between the gyri called?: Sulci (singular: sulcus).

Why are gyri and sulci important?: They increase brain surface area and serve as landmarks for dividing the brain into lobes.

What do hemisphere divide into?: Lobes, each lobe has different functions.

Midbrain: Bridges the lower brainstem with the diencephalon. It controls eye movements, and it exerts control over auditory and visual motor flexes.

Pons: Act as a relay station for transferring information between the cerebellum and cerebral cortex. It also coordinates and controls breathing

Medulla: Primary control over involuntary functions such as breathing, blood pressure and swallowing. It is also here that fibers from the corticospinal tract, cross over to the opposite of the body .

Lobes of the brain:

Frontal Lobe:

Primary motor cortex: Processes input from skeletal muscles

Premotor cortex: Works with the prefrontal cortex to integrate movement information with other sensory inputs to generate perception/interpretation of stimuli

Prefrontal cortex

Parietal Lobe:

Primary Somatosensory cortex: Receives input from the major senses: skin, musculoskeletal system, taste buds.

Association Areas: Integrate sensory information to create meaningful perceptions.

Temporal Lobe:

Primary Auditory Cortex: Receive and process signals from the auditory nerve and integrate them with other sensory inputs

Auditory Association Areas: ‘’

Also involved with olfaction and in mediating short term memory storage and call.

Occipital Lobe: Lobe responsible for vision

Primary visual cortex: Receives input directly from the optic nerve

Visual Association areas: Process information and integrate it with other sensory inputs

Cerebellum: Responsible for coordinated movement. Processes sensory information and coordinates execution of movement in the body. It is the structure with the largest number of neurons in the brain. It receives input from somatic receptors, receptors for equilibrium, balance and motor neurons from the higher centers of the brain

Brain Stem: Controls heart rate and respiration. It incorporates 9 cranial nerves

Corpus Callosum:A dense bundle of nerve fibers connecting the two cerebral hemispheres. It Integrates sensory and motor information from both sides of the body and coordinates whole-body movement.

Diencephalon:

Thalamus: Receives sensory input as it travels from the spinal cord, and integrates sensory information before sending it to the cortex

Hypothalamus: Controls a variety of endocrine functions (body temperature, thirst, food intake,) mainly through the release of hormones.

Pituitary gland (Hypophyse): Regulates endocrine organs

Anterior Pituitary: Derived from epithelial tissue of the pharynx

Posterior Pituitary: Derived from neural tissue of the hypothalamus

WEEK 2.2

Synaptic Transmission

What do neurons use to communicate with each other?: Synapses

What is a synapse?: A site where neurons exchange information and pass impulses to another cell.

What are the two types of synapses?:

Electrical synapse: Site of cell-cell communication where neurons directly exchange ions through channels that span the two communicating cells. This exchange of ions can lead to an AP developing in the next cell.

Chemical synapse: Site of cell-cell communication where excitable cells release chemicals called neurotransmitters to communicate. The two neurons are separated by a small space where neurotransmitters are released. Components:

Presynaptic neuron: Transmits the information towards the synaptic cleft via its axon and axon terminals, to the dendrites of the next neuron.

Synaptic cleft: Small space between the axon terminals of one neuron and the dendrites of another

Postsynaptic neuron: Transmits information away from the synaptic cleft, from its dendrites towards its soma.

What are neurotransmitters?: Chemicals that neurons release to communicate with each other. They bind into ion channels/receptors on the next cell, leading to ion influx into the cell. The binding of neurotransmitters to channels can lead to the generation of electrical impulses that can either lead to an AP or prevent AP from forming.

Components of a chemical Synapse:

Pre synaptic neuron

Synaptic cleft

Post synaptic neuron

Neurotransmitters

Synaptic vesicles: Contain neurotransmitters that are released in the synaptic cleft if an AP is developed in the presynaptic neuron.

Receptors

Open: A chemically-gated receptor opened by neurotransmitter binding, allowing ion movement and possibly triggering an action potential.

Closed: A receptor with no bound neurotransmitter, so it remains closed and does not allow ion flow.

The release from the neurotransmitters from the pre synaptic neuron:

AP reaches axon terminal an depolarizes the presynaptic membrane

Voltage gated Ca2+ channels open (located along the plasma membrane of the axon terminal and synapse)

Ca2+ enters the cell, triggering biochemical reactions that allow the synaptic vesicles to fuse with the presynaptic membrane

Neurotransmitters are released from the synaptic vesicle into the synaptic cleft

Neurotransmitters have several fates at this point:

Bind to receptors on the postsynaptic membrane:

Diffuse out of the synapse down concentration gradients

Broken down by enzymes located in the synaptic cleft or on the postsynaptic membrane

Re-uptake into the presynaptic cell to be recycled

Neurotransmitters bind to ligand-gated receptors on the postsynaptic membrane. These are receptors that respond when a molecule/ligand binds to them. They can be ion channels or can trigger events that lead to the opening of ion channels

The binding of neurotransmitters to receptors can lead to depolarization or hyperpolarization of the postsynaptic cell, depending on which channels open

What is a ligand-gated receptor/channel?:Receptors that open or trigger events when a ligand (like a neurotransmitter) binds to them, allowing ions to enter or exit the cell. There are also ligand-gated receptors that are not ion channels themselves, but lead to the opening of ion channels when the neurotransmitter binds to them.

What happens to neurotransmitters already in the synaptic cleft if release stops?:

Detach from receptors

Diffuse out

Get degraded

Undergo reuptake by the pre-synaptic cell

Excitatory and inhibitory synapses

What are graded potentials?: Small, sub-threshold changes in membrane potential that do not trigger an action potential on their own.

What happens to the membrane during a graded potential?: The membrane becomes slightly depolarized (more positive), but not enough to reach the threshold for an AP.

Can graded potentials vary in size?: Yes, they can be different in size and can add together (summation) to potentially reach a threshold.

What is the role of inhibitory signals in graded potentials?: Inhibitory signals hyperpolarize the membrane, making it harder to reach the threshold for an AP.

What are excitatory post-synaptic potentials (EPSPs)?: Sub-threshold depolarizations that do not produce an action potential but bring the neuron closer to one

Properties of EPSPs:

Do not produce AP

Are localized - depolarization is confined to one area of the plasma membrane

Can EPSPs be summed - stack up on top of each other to produce a larger depolarization. Multiple EPSPs are required to produce an AP.

Bring neuron closer to AP

What determines the magnitude of an EPSP?: The magnitude of the stimulus (EPSPs are graded). higher stimulus= larger depolarization

What happens to EPSPs as they move across the membrane?: They decay—the further from the stimulus, the smaller they become.

What kind of neurotransmitters produce EPSPs?: Neurotransmitters that open Na+ and K+ channels

What are inhibitory post-synaptic potentials (IPSPs)?: Sub-threshold hyperpolarizations that do not produce an action potential but move the neuron further from one.

What are inhibitory post-synaptic potentials (IPSPs)?: Hyperpolarizing, localized changes in membrane potentials that make neurons less likely to fire an action potential.

Are IPSPs graded or all-or-none?:Graded — the higher the stimulus, the larger the hyperpolarization.

Can IPSPs be summed?: Yes, multiple IPSPs can stack up to produce a larger hyperpolarization.

How do IPSPs affect the likelihood of an action potential?: They bring the neuron further away from the threshold, reducing the chance of an AP.

Do IPSPs propagate down the neuron?:No, they are localized and decay as they move across the membrane from the point of stimulus- the further from depolarization, the smaller they become

What ions are involved in generating IPSPs and how do they move?: IPSPs are produced by neurotransmitters that open K+; K⁺ moves out of the cell, Cl⁻ moves into the cell.

Size of stimulus lead to a larger change in membrane potential

EPSP and IPSPs

Can EPSPs and IPSPs be summed.

"Integration of EPSP and IPSP at the Neuronal Trigger Zone:

Can a post-synaptic neuron receive inputs from multiple pre-synaptic neurons?: Yes, it can receive multiple EPSPs and IPSPs simultaneously from different pre-synaptic cells.

What determines whether an action potential is generated in the post-synaptic neuron?: The sum of EPSPs and IPSPs at the axon hillock (trigger zone).

Where are EPSPs and IPSPs summed in a neuron?: At the axon hillock (trigger zone).

What happens to EPSPs and IPSPs as they travel toward the axon hillock?: They decay in size as they move across the membrane.

What happens if the summed input at the axon hillock does not reach threshold?: No action potential is generated.

Where must depolarization occur to trigger an action potential in a neuron?: At the axon hillock.

Why can't dendrites or the soma generate action potentials?: Because they lack voltage-gated channels needed to initiate an AP.

Why are voltage-gated channels essential for generating an action potential?: hey allow for rapid depolarization and propagation of the AP along the axon.

Where are voltage-gated channels highly concentrated in a neuron?: At the axon hillock and along the axon membrane.

What property of EPSPs makes it necessary for them to reach the axon hillock?: EPSPs are localized and only the axon hillock can initiate an AP.

What is decay in the context of EPSPs?: It is the reduction in intensity of depolarizations as they move away from the initial site on the dendrite.

Why must an EPSP be strong or large enough?: To depolarize the membrane at the axon hillock enough to open voltage-gated Na⁺ channels and trigger an action potential.

How to make EPSPs that are strong enough to reach the axon hillock?

temporal summation: The additive effect of many EPSPs generated at the same synapse by a series of high-frequency APs from one presynaptic neuron. One neuron fires repeatedly

Spatial summation: The additive effect of many EPSPs generated at different synapses on the same postsynaptic neuron at the same time. Many neurons fire at the same time.

Red line represents: They represent individual action potentials from the pre-synaptic neuron.

Where are neurotransmitters synthesized and stored before release?: Synthesized in the neuron and stored in synaptic vesicles.

What triggers the release of neurotransmitters from the axon terminal?: An action potential

What does an excitatory neurotransmitter do to a neuron?:It excites or "turns on" the neuron.

What does an inhibitory neurotransmitter do to a neuron?: It inhibits or "shuts off" the neuron.

TYPES OF NEUROTRANSMITTERS:

The neuromuscular junction

What is the role of the central nervous system (CNS) in skeletal muscle movement?: The CNS sends information to skeletal muscles to perform movements, often without conscious thought.

What is the pathway of neural signals from the CNS to skeletal muscle?: Signal goes from the primary motor cortex → upper motor neuron → spinal cord → lower motor neuron → skeletal muscle.

What happens at the synapse between the lower motor neuron and the muscle cell?: The neuron releases neurotransmitters into the synaptic cleft, which bind to receptors on the muscle cell to trigger an action.

The processes at the neuromuscular junction:

Action potential arrival: An action potential (AP) travels down the axon of the presynaptic neuron to the axon terminal or presynaptic terminal.

Calcium Influx: Change in voltage due the AP causes voltage-gated calcium channels on the presynaptic neuron to open. Then, calcium rushes into the presynaptic neuron

Neurotransmitter release: Calcium influx triggers synaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine (ACh) into the synaptic cleft.

Receptor binding and depolarization: ACh binds to receptors on the postsynaptic membrane, causing Na+ to enter and K+ to exit the cell, leading to depolarization.

ACh Breakdown and Recycling: Acetylcholinesterase degrades ACh into acetate and choline, with choline recycled to produce new ACh for future signals.

What type of receptor does ACh bind to at the neuromuscular junction?: Nicotinic receptors.

What happens when ACh binds to nicotinic receptors?: The receptors open, Na⁺ enters the muscle cell, causing depolarization.

What kind of transmission does ACh mediate at nicotinic receptors?: Fast transmission.

What kind of channels are nicotinic receptors?: Ligand-gated (chemical-gated) ion channels that open when ACh binds.

Key characteristic of nicotinic receptors:

Transmembrane, ligand-gated (ionotropic) receptors

Require acetylcholine to open.

Found at neuromuscular junctions and post-ganglionic cells in the autonomic nervous system

How does acetylcholine (ACh) act through muscarinic receptors, and how does it differ from nicotinic receptors?:

ACh binding to muscarinic receptors triggers slow transmission

Muscarinic receptors are not ion channels

They activate biochemical cascades that eventually open ion channels

Slower than nicotinic receptors, which directly open ion channels (fast transmission

What type of receptor is the muscarinic receptor and how does it work?: The muscarinic receptor is a ligand-gated G-protein coupled receptor that activates ion channels indirectly through biochemical reactions after ACh binds.

Where are muscarinic receptors found?: They are found on smooth and cardiac muscle cells.

What are metabotropic receptors?: Metabotropic receptors, are ligand-gated or chemically-gated receptors that require a ligand (e.g., acetylcholine, ACh) to activate.

What is the motor end plate?: It is the section of the skeletal muscle plasma membrane where the axon terminals communicate with the muscle.

What special structural features does the motor end plate have at the neuromuscular junction (NMJ)?: It has indentations and folds.

Why are the folds on the motor end plate important?: They are packed with nicotinic receptors, increasing the surface area for acetylcholine (ACh) binding.

Are the folds and nicotinic receptors on the motor end plate found throughout the muscle cell membrane?

What is the name of the graded current in skeletal muscle?: End plate current (EPC).

What does the end plate current (EPC) generate?: End plate potentials (EPPs).

Pathology of the NMJ

What is a common symptom of Myasthenia Gravis?: Generalized muscle weakness and fatigue, including Cogan's eyelid twitch.

: What is Cogan's eyelid twitch?: An abnormal eyelid movement where the eyelid twitches as the eyes move side to side.

What confirms the diagnosis of Myasthenia Gravis?: Presence of antibodies against nicotinic ACh receptors in the blood.

What type of disease is Myasthenia Gravis?: A chronic autoimmune neuromuscular disease causing skeletal muscle weakness.

What is the effect of reduced nicotinic receptors at the NMJ?: Less ACh binds, leading to less muscle excitation and muscle weakness.

How does the motor end plate differ in Myasthenia Gravis?: It has fewer folds and fewer receptors, reducing surface area for ACh binding.

What is one therapeutic approach for managing Myasthenia Gravis symptoms?: Acetylcholinesterase blockers, which prevent the breakdown of ACh, increasing its availability at the neuromuscular junction.

How do acetylcholinesterase blockers help in Myasthenia Gravis?: They slow ACh breakdown, keeping it in the synaptic cleft longer, which increases binding to cholinergic (nicotinic) receptors and reduces muscle weakness.

WEEK 3.1

Structure of Skeletal Muscle

What is a whole muscle, like the bicep, made of?: Bundles of fascicles.

What are muscle cells also called?: Muscle fibers.

What shape do skeletal muscle cells have?: Long and cylindrical.

: What is the length range of skeletal muscle cells?: From 1 to 12 cm.

: What is the appearance of skeletal muscle cells under the microscope?: They have a striated (banding) appearance.

How many nuclei do skeletal muscle cells have?: They are multinucleated.

What organelle is abundant in skeletal muscle cells?: Mitochondria.

Does the number of muscle fibers in a muscle stay the same across all muscles?: No, it depends on the size of the muscle.

What is the plasma membrane of a skeletal muscle cell called?: Sarcolemma.

What are the indentations in the sarcolemma called?: Transverse tubules (T-tubules).

Where are the T-tubules located in relation to the sarcoplasmic reticulum?: Near the end sections of the sarcoplasmic reticulum, called terminal cisternae.

What forms the structure known as the triad in skeletal muscle fibers?: One T-tubule and two terminal cisternae.

What are the bundles of organelles found in skeletal muscle fibers called?: Myofibrils.

How does the sarcoplasmic reticulum appear under the sarcolemma?: branches out like a spider web over and between the myofibrils.

What flanks each T-tubule in the muscle fiber?: The terminal cisternae of the sarcoplasmic reticulum.

What are myofibrils made of?: Bundles of myofilaments.

What are myofilaments?: Proteins that vary in thickness and appear darker or lighter under the microscope.

What types of myofilaments are found in skeletal muscle?: Thin myofilaments and thick myofilaments.

What are sarcomeres?: Repeating units of contractile proteins that make up the contractile unit of the myofibril.

What separates sarcomeres from one another?: A line of proteins called the Z-disc or Z-line.

Types of myofilament:

Thin myofilament: made of

Actin: Globular proteins linked into helical strands that form the backbone of the thin myofilament. They are arranged like twisted strands of beads. Each actin molecule has a myosin binding site. Associated with tropomyosin and troponin.

Tropomyosin: A rod-shaped protein found in the grooves of actin strands. At rest, Partially covers the myosin binding site on actin.

Troponin: A three-protein complex attached to actin and tropomyosin. At rest, hold tropomyosin over the myosin binding site on actin.

Troponin A: Binds to actin

Troponin C: Binds to calcium

Troponin T: Binds to tropomyosin

Thick myofilament: made of

Myosin: It has a long tail and two heads. An actin binding site and an ATP binding site are found in its head. Its binding site contains ATPase, an enzyme that breaks down ATP. Under contraction, its head Undergoes a conformational change to generate contraction.

What is the sarcomere?: The contractile unit of the myofibril.

: What is the sarcomere made of?: Alternating bands of thin and thick filaments.

How are sarcomeres connected to each other?: Through structural proteins that form the Z-line or Z-disc.

The zones of the sarcomere:

Thin myofilament- the thin myofilament is anchored to the Z-line. At rest, it partially overlaps with the thick myofilament

Thick myofilament - the thick myofilament is anchored to the M-line and attached to the Z-line via a protein called titin (not shown)

Z-line - structural proteins that delineate sarcomeres and provide support for the contractile proteins

M-line- provides support for the thick myofilament

I-band- area between the Z-line and the start of the thick myofilament. Made entirely of the thin myofilament

A-band- spans the length of the thick myofilament, with various degrees of overlap from the thin myofilament

H-band (not shown) - represents the distance between two thin myofilaments. It spans the M-line

What happens to the sarcomere during a muscle contraction?: It becomes shorter

What causes the sarcomere to shorten during contraction?: Increased overlap between thin and thick myofilaments.

Does the length of the thick myofilament change during contraction?:No, it remains unchanged.

Does the length of the thin myofilament change during contraction?: No, it remains unchanged.

What happens to the I-band during a muscle contraction?:It shortens.

What happens to the A-band during a muscle contraction?: It does not change in length.

What happens to the Z-discs during a muscle contraction?: They get closer together.

Sliding filament theory and excitation contraction coupling

What is the contractile unit of the myofibril?:The sarcomere

What happens to the sarcomere during contraction?: It shortens, bringing the Z-discs/Z-lines closer together.

Do the thin and thick myofilaments change length during contraction?: No, their length remains unchanged.

What causes the sarcomere to shorten?: An increased overlap between thin and thick myofilaments.

How does the overlap between filaments increase during contraction?: The thin myofilament slides over the thick myofilament toward the M-line.

What forms the cross-bridge during contraction?: The myosin head binds to the myosin-binding site on actin in the thin myofilament.

What happens after the myosin head binds to actin?: It changes shape and performs a power stroke.

What is a power stroke?: The myosin head propels the thin filament toward the M-line.

What is the result of repeated power strokes?: The thin myofilament slides past myosin, pulling Z-lines closer and shortening the sarcomere.

Why is labeling the thin myofilament solely as "actin" a misnomer?: Because it also includes tropomyosin and troponin, not just actin.

When a contraction is started, the overlap between the actin and myosin increases. Here is the sequence of events:

Contraction Begins → Actin and myosin overlap increases.

Cross-Bridge Forms → Myosin head binds to actin (like hands catching a surfboard).

Power-Stroke Occurs → Myosin changes shape, propelling actin forward.

Filament Sliding → Thin filament moves past thick filament toward M-line.

Z-Discs Move Closer → Muscle shortens as contraction completes.

What is excitation-contraction coupling?:It’s the process where an action potential on the sarcolemma triggers calcium release from the sarcoplasmic reticulum, leading to muscle contraction.

What triggers the release of calcium from the sarcoplasmic reticulum?:An action potential on the sarcolemma.

What does calcium release lead to during excitation-contraction coupling?:Cross-bridge formation, power-stroke, and muscle contraction.

What triggers the start of excitation-contraction coupling in skeletal muscle?: An action potential on the sarcolemma.

What does the action potential cause the sarcolemma to do?: It propagates over the sarcolemma and down the T-tubules.

What structure detects the action potential in the T-tubules?: Voltage sensors.

What happens when the voltage sensors detect the action potential?: They change shape and open Ca²⁺ release channels on the SR.

What happens when Ca²⁺ is released from the SR?:Ca²⁺ binds to troponin, which pulls tropomyosin off the myosin-binding sites on actin.

What forms after the myosin-binding sites are exposed?: Crossbridges form between myosin and actin.

What causes the muscle to contract?:The power stroke pulls thin filaments over thick filaments, shortening sarcomeres.

How does the muscle relax after contraction?: Ca²⁺ is pumped back into the SR by Ca²⁺ ATPase, and tropomyosin blocks myosin-binding sites again.

What happens when Ca²⁺ is removed from the sarcoplasm?: Muscle contraction stops and the muscle relaxes.

What are the two key binding sites on the myosin head?: An actin binding site and an ATPase binding site.

What does the actin binding site on myosin do?: It binds to actin to form a cross-bridge.

What does the ATPase binding site on myosin do?: It binds and breaks down ATP to power myosin movement.

How does ATP help in muscle contraction?: ATP is broken down by myosin ATPase to power the myosin head movement that slides actin toward the M-line.

What other ATPase was mentioned in excitation-contraction coupling?: Calcium ATPase, which pumps Ca²⁺ back into the SR to stop contraction.

Q: What happens when ATP binds to the ATPase site on the myosin head?

A: ATP is hydrolyzed to ADP and Pi, releasing energy that energizes the myosin head into position to bind actin.

Q: During the energized state, what stays bound to the myosin ATPase site?

A: ADP and inorganic phosphate (Pi) remain bound.

Q: What allows the myosin head to bind to actin?

A: Calcium binds to troponin C, moving tropomyosin and exposing the myosin binding site on actin.

Q: What happens if calcium is absent in the muscle cell?

A: The myosin binding site on actin remains blocked by tropomyosin, preventing cross-bridge formation and contraction.

Q: What triggers the power stroke in muscle contraction?

A: Release of Pi from the myosin ATPase site causes a conformational change, pulling actin toward the M-line and shortening the sarcomere.

Q: What is released from the myosin ATPase site after the power stroke?

A: ADP is released.

Q: How does the myosin head detach from actin?

A: A new ATP molecule binds to the ATPase site, causing the myosin head to detach and return to a low-energy state.

Q: What restarts the ATP-myosin cycle after detachment?

A: Hydrolysis of the newly bound ATP re-energizes the myosin head for another cycle.

Q: What is rigor mortis?

A: A post-death condition where muscles become stiff due to permanent actin-myosin cross-bridges.

Q: Why does rigor mortis occur after death?

A: Because oxygen is no longer available, so ATP production stops.

Q: Why does the lack of ATP cause muscles to stay contracted?

A: ATP is required to detach myosin from actin; without it, they stay fused.

Q: What happens to calcium during rigor mortis?

A: Calcium remains in the cytoplasm because ATP is needed to pump it back into the SR.

Q: How does calcium contribute to rigor mortis?

A: It binds to troponin C, exposing myosin binding sites and allowing more cross-bridges to form.

Q: What two key events lead to the muscle locking in rigor mortis?

A: Cross-bridges can't detach due to lack of ATP, and calcium stays in the cytoplasm, allowing continuous binding.

Is rigor mortis permanent?

A: No, rigor mortis is not permanent; it lasts for about 24–72 hours after death.

Aya is given a medication that, as a side effect, blocks the activity of the calcium ATPase on the sarcoplsamic reticulum. What is a likely skeletal muscle symptom that Aya would experience?: muscle stiffness

The motor unit and graded muscle contractions

What makes up a motor unit?: A motor neuron and all the muscle fibers it innervates.

What happens if an action potential is generated in the purple neuron?: An action potential will be generated in all the purple skeletal muscle cells it innervates.

Does the same action potential rule apply to all motor units?: Yes, it also applies to the orange and blue motor units.

What does each motor unit consist of in the image?: A neuron (purple, blue, or orange) and the skeletal muscle cells it innervates.

Which muscle fibers are innervated by the purple neuron?: The purple muscle fibers.

Which muscle fibers are innervated by the blue neuron?: The blue muscle fibers.

Which muscle fibers are innervated by the orange neuron?: The orange muscle fibers.

What forms the muscle fascicle shown in the image?: A bundle of blue, orange, and purple muscle fibers.

Why is the intermingled arrangement of muscle fibers in a fascicle important?: It ensures a uniform muscle contraction, regardless of which motor unit contracts.

What is the effect of one action potential in a motor neuron?: It causes one action potential in all the muscle fibers it innervates.

What is a muscle twitch?: A contraction in response to one action potential on the motor neuron.

Periods of a muscle twitch:

Latent period

Contraction period

Relaxation period

What is the latent period in a muscle twitch?: A short 1-2 ms delay from the muscle cell action potential to measurable muscle tension.

Why does the latent period occur?: Because calcium is released from the sarcoplasmic reticulum, binds to troponin C, causes tropomyosin to shift, and allows cross-bridge formation.

What happens during the contraction period of a muscle twitch?: The muscle generates tension due to cycling of the cross-bridges.

What is the relaxation period in a muscle twitch?: The period during which the muscle returns to its normal length.

Why do our muscles move smoothly despite individual twitches?: Because motor units are arranged interspersed and fire asynchronously.

How does the interspersed arrangement of motor units help smooth muscle contraction?: It ensures the muscle contracts smoothly even though not all motor units contract at the same time.

What happens if all motor units contract simultaneously?: The movement would be jerky.

What does it mean that motor units fire asynchronously?: Not all motor units fire at the same time; some relax while others contract.

How does asynchronous firing contribute to smooth movement?: The relaxation period of one motor unit overlaps with the contraction period of another.

In a muscle twitch, which period is longer: contraction or relaxation?: The relaxation period is longer than the contraction period.

Why is the relaxation period of a muscle twitch longer than the contraction period?: Because it takes longer to pump calcium back into the sarcoplasmic reticulum (SR) than to release it.

What enzyme is responsible for pumping calcium back into the SR?: Calcium ATPase.

Why does calcium return to the SR more slowly than it is released?: Because it is pumped against its concentration gradient using ATP, while release occurs down its concentration gradient.

What happens during contraction regarding calcium?: Calcium is released from the SR and binds to troponin C, exposing myosin-binding sites on actin.

What is a graded muscle contraction: An increase in muscle contraction force through motor unit recruitment and/or summation of twitches.

How does motor unit recruitment increase muscle force?:More motor units are recruited as load increases, causing more muscle fibers to contract.

Do muscle fibers from different motor units contract at the same time?:No, they contract asynchronously.

Do muscle fibers from the same motor unit contract at the same time?: yes

What happens when one action potential occurs in a motor neuron?: An action potential is triggered in all the skeletal muscle fibers it innervates.

Why do motor units fire asynchronously?:To ensure the muscle contraction is smooth.

How can a muscle generate more power?: By recruiting more motor units.

How does lifting progressively heavier weights affect motor units?: It trains the muscle to recruit more motor units.

What happens when more motor units are recruited?:The muscle generates more force, leading to increased strength.

What is muscle summation?: When action potentials occur more frequently and twitches stack up before full relaxation, generating more force.

How does summation increase muscle force?: The force from each twitch adds to the previous one, resulting in greater total force.

tension changes when muscle twitches are summed:

Muscle Twitches: Each twitch follows an action potential and fully relaxes before the next twitch, producing equal tension.

Summed twitches: Increased action potential frequency prevents full relaxation, leading to higher tension due to summation.

Unfused tetanus: Further increase in frequency results in a stair-like rise in contraction (treppe), with partial relaxation between twitches.

Complete tetanus: Extremely high action potential frequency eliminates relaxation, creating a smooth, sustained contraction.

What happens in Step 1 of muscle twitch summation?: Each twitch fully relaxes before the next begins, so all twitches generate the same tension.

What is seen in Step 2: Summed Twitches?: Twitches begin to overlap; the third twitch doesn’t fully relax before the next starts, increasing total tension.

What causes summation of muscle twitches?: An increase in the frequency of action potentials.

What is unfused tetanus?: When action potential frequency increases and twitches partially relax between contractions, creating a stair-like tension pattern.

What is complete tetanus?: When action potential frequency is so high that no relaxation occurs between twitches, resulting in a smooth, sustained contraction.

What is treppe?: A stair-like increase in contraction strength due to repeated stimulation.

Integration lecture- Lab activity

Where on the muscle were the electrodes placed in the video and why? : The electrodes were placed on the NMJ. Stimulation at the NMJ ensures that an AP develops in the muscle of interest. If an AP develops, then we can record a twitch.

Why did the muscle respond at 3 mAmp of stimulation but not at 1 mAmp?: The muscle responded to 3 mAmp of current that was necessary to elicit an AP in the muscle. 1 mAmp was too low to cause depolarization of the muscle cells to reach threshold and produce AP

Did the mAmp value change after we increased the frequency of the stimulation?:The mAmp value did not change after the frequency of the stimulation was increased

What happened to the twitches when we increased the frequency of the stimulation? Explain your answer in terms of contraction and relaxation periods.: When the frequency of the stimulation was increased, the time between twitches decreased. Therefore, the twitches got closer together

Was complete tetanus reached? Justify your answer.:Complete tetanus was not reached because there was still a small period of relaxation between the twitches

What happened to the tension generated by the muscle when the frequency of the stimulation was increased even further at the end of the video? Explain how this phenomenon occurred: When the frequency of the stimulation was increased at the end of the video, the tension generated by the muscle increased. This occurred because of summation, as the next twitch was occurring before the previous one had achieved complete relaxation.

WEEK 3.2

Somatic Motor System

What does the somatic motor system control?: Voluntary muscle movements by sending and receiving information between the brain and muscles.

What are the key components involved in voluntary muscle movement?: The brain (for control), spinal tracts (to send info), and muscles (which also send sensory feedback).

How is information exchanged during movement, such as running?: The brain and muscles rapidly and efficiently send signals back and forth to adjust posture, tone, and force.

What is the main function of the somatic motor system?: To coordinate voluntary movement by controlling skeletal muscles.

What part of the nervous system is the somatic motor system part of?: The peripheral nervous system (PNS).

What do motor neurons in the somatic motor system do?: They carry signals from the CNS to skeletal muscles at the neuromuscular junction.

What is the other part of the PNS besides the somatic motor system?: The autonomic nervous system.

What are the three main motor areas in the higher brain involved in the motor system?: The supplementary motor area, the premotor area, and the primary motor cortex.

Besides the motor areas of the brain, what other structures are part of the motor system?: The basal ganglia, spinal pathways, motor nerves, and muscle receptors.

What is the role of the motor areas of the brain?: To activate and control muscles.

What is proprioception?: The process by which muscle receptors send information to the brain about limb position.

What is the main function of the premotor cortex?: To develop the strategy and sequence for voluntary movements.

What happens if the premotor cortex is damaged?: A person may struggle to choose an appropriate movement strategy, like reaching incorrectly for an object.

What does the supplementary motor cortex do?: It programs the muscle sequences for complex and repetitive movements like typing.

What happens when the supplementary motor cortex is damaged?: A person may be unable to coordinate fine finger movements, like picking up a peanut properly.

Where is the primary motor cortex located?: On the precentral gyrus in the frontal lobe, just behind the premotor cortex.

What is the motor homunculus?: A map on the primary motor cortex representing body parts, showing which area controls each muscle.

What is the order of body parts in the motor homunculus from medial to lateral?: Foot, ankle, knee, thigh, trunk, shoulder, elbow, wrist, hand, fingers, face, lips, jaw, tongue.

What happens if a stroke affects the hand region of the motor cortex?: The brain’s image of the hand becomes unclear, affecting control, but can be improved with physiotherapy.

What is the function of the primary somatosensory cortex?: It receives sensory information about temperature, touch, proprioception, texture, and pain.

Why are the lips and fingertips especially sensitive?: Because large areas of the somatosensory cortex are dedicated to them.

What is mirror box therapy used for?: It's used for patients with amputated hands, chronic hand pain, or carpal tunnel syndrome.

How does mirror box therapy work?: The patient moves the unaffected limb while watching its reflection in a mirror, creating the illusion that the affected limb is also moving.

What is the goal of mirror box therapy?: To "convince" the brain that the affected or missing limb is moving, which can reduce pain or help retrain the brain.

What is another name for the corticospinal tract?: The pyramidal tract.

Where does the corticospinal tract begin?: In the primary motor cortex.

What happens at the medulla in the corticospinal tract?: 80% of the nerve fibers cross to the contralateral side; 20% stay ipsilateral.

Where do the corticospinal tract fibers synapse with lower motor neurons?: At the level of the spinal cord where they exit to innervate muscles.

What happens to the ipsilateral fibers once they reach the spinal cord?: They cross to the contralateral side before synapsing with lower motor neurons.

Muscle spindles and the reflex arc

What is proprioception?

A: Proprioception is the sense of knowing the position and movement of your limbs without needing to see them, allowing accurate control of muscle movement.

Q: How can you demo proprioception?

A: Close your eyes, extend both arms, and touch your index fingers together—your brain knows where your limbs are through proprioceptive signals.

Q: What muscle receptors enable proprioception?

A: Muscle spindles and Golgi tendon organs.

Q: What do muscle spindles detect?

A: Muscle spindles detect muscle stretch, length, and the rate of change in length.

Q: Where are muscle spindles located?

A: They are located within skeletal muscles, between muscle fibers.

Q: What is the protective role of muscle spindles?

A: They sense overstretching and signal the brain to increase muscle force to prevent damage.

Q: How does the brain increase muscle force based on spindle signals?

A: By increasing action potential frequency in motor neurons (twitch summation) and/or recruiting more motor units.

Q: What do Golgi tendon organs detect?

A: Muscle tension and force produced by muscle contraction.

Q: Where are Golgi tendon organs located?

A: At the junction between muscle and tendon.

Q: What is the function of Golgi tendon organs?

A: They monitor muscle tension for fine control and act as a protective inhibitory mechanism to prevent muscle overload.

Q: How do Golgi tendon organs interact with muscle spindles?

A: They can override spindle signals to fine-tune muscle tension and prevent damage from excessive force.

: What are muscle spindles?

A: Collections of 6-8 specialized fibers located within the muscle that signal changes in muscle length and the rate of those changes.

Q: Do muscle spindles generate force?

A: No, they do not generate force; they detect changes in muscle length.

Q: What are intrafusal fibers?

A: Fusiform-shaped specialized muscle fibers inside muscle spindles.

Q: What are extrafusal fibers?

A: The majority of muscle fibers that generate force in muscles.

Q: What does "fiber" mean in muscle terminology?

A: Another name for a muscle cell.

Q: What does "fusal" refer to?

A: The shape of the muscle fiber (fusiform or spindle-shaped).

Q: What does "intra-" and "extra-" refer to in muscle fibers?

A: Their location inside (intrafusal) or outside (extrafusal) the muscle spindle.

Q: What happens in the sensory region of muscle spindles when the muscle stretches?

A: The sensory region stretches, triggering action potentials in the sensory nerve.

Q: How does the frequency of action potentials relate to muscle stretch?

A: The more the muscle stretches, the higher the frequency of action potentials sent to the CNS.

Q: What does the brain do with information from muscle spindles?

A: It interprets muscle stretch and knows the position of the limb in space.

Q: What is proprioception?

A: The brain's awareness of limb position in space based on muscle spindle input.

Q: How does the brain respond to information from muscle spindles?

A: It may increase motor unit activation and action potential frequency to adjust muscle contraction.

Q: Where is the Golgi tendon organ located?

A: Between the muscle fiber and the tendon, in series with the muscle.

Q: How is the Golgi tendon organ different in location compared to muscle spindles?

A: Muscle spindles are parallel to extrafusal fibers; Golgi tendon organs are in series with the muscle.

Q: What does the Golgi tendon organ detect?

A: The load or force applied to the muscle.

Q: What is the Golgi tendon organ made of?

A: A capsule containing collagen fibers.

Q: What type of nerve fibers innervate the Golgi tendon organ?

A: Primary afferent nerves called Ib fibers.

Q: What happens when force is applied to the muscle in relation to the Golgi tendon organ?

A: The Golgi tendon organ is stretched, collagen fibers squeeze the afferent nerve endings, causing depolarization and action potentials.

Q: What does the Golgi tendon organ signal to the CNS?

A: Information about the amount of force applied to the muscle.

Q: What do muscle spindles signal?

A: Muscle length and velocity (rate of change of length).

Q: How do the locations of muscle spindles and Golgi tendon organs relate to their functions?

A: Muscle spindles detect stretch (length changes) because they are parallel; Golgi tendon organs detect force because they are in series with the muscle and tendon.

Q: Why do muscle spindles stretch along with extrafusal fibers?

A: Because muscle spindles are located parallel to the extrafusal fibers.

Q: What information do muscle spindles signal?

A: Changes in muscle length and the velocity (rate of change) of these length changes.

Q: How is sensory information from muscle spindles sent to the CNS?

A: Through two types of specialized sensory fibers that innervate intrafusal fibers.

Q: What are the two types of sensory fibers that innervate muscle spindles?

A: Primary afferents (Ia) and secondary afferents (II).

Q: What do primary afferents (Ia) detect and how do they respond?

A: They provide information about length changes and velocity; they fire at a high rate during stretching, with firing rate depending on the rate of change of muscle length.

Q: How do primary afferents (Ia) firing rates change when the muscle stops stretching?

A: Their firing decreases.

Q: What do secondary afferents (II) detect?

A: Changes in muscle length only, not velocity.

Q: How do secondary afferents (II) firing rates behave during stretching?

A: Their firing rate increases steadily, depending only on the immediate muscle length, not the rate of change.

Q: Why are these sensory fibers called afferent fibers?

A: Because they send sensory information from the muscle spindle to the CNS.

Q: What does the brain do with the information sent by the afferent fibers?

A: It interprets the position, stretch, and frequency of muscle length changes to place limbs in space.

Q: What are the two types of motor neurons that send signals from the CNS to muscles?

A: Alpha motor neurons and gamma motor neurons.

Q: What do alpha motor neurons innervate?

A: Extrafusal muscle fibers, which generate muscle contraction and power.

Q: What do gamma motor neurons innervate?

A: Intrafusal muscle fibers within muscle spindles.

Q: What is the main function of gamma motor neurons?

A: To keep muscle spindles sensitive to stretch by causing slight contraction of intrafusal fibers.

Q: Why is alpha-gamma coactivation important?

A: It allows muscle spindles to stay active during muscle contraction, continuously sending proprioceptive information to the brain.

Q: What happens if there is no alpha-gamma coactivation?

A: Extrafusal fibers contract but intrafusal fibers go slack, stopping sensory feedback, so the brain loses information about muscle position and contraction force.

Q: How do gamma motor neurons maintain spindle sensitivity during muscle contraction?

A: They cause intrafusal fibers to contract slightly, maintaining stretch on the sensory region to keep sending signals.

Q: Does contraction of intrafusal fibers by gamma motor neurons generate significant force?

A: No, their contraction is slight and does not contribute significantly to muscle force.

Q: What continuous information do muscle spindles send to the brain thanks to alpha-gamma coactivation?

A: Information about muscle length, stretch, and limb position.

Q: What do afferent pathways do?

A: They carry information from organs or tissues to the CNS for integration.

Q: What are efferent pathways also known as?

A: Motor pathways.

Q: What is the function of efferent pathways?

A: They send information from the CNS to effector organs, such as muscles.

Q: How can you remember the difference between afferent and efferent pathways?

A: Efferent pathways carry signals from the CNS to the Effector organ (both start with E), so afferent pathways must send signals from organs to the CNS.

Q: What is the stretch reflex an example of?

A: A reflex arc.

Q: What happens when the patellar tendon is tapped during a doctor’s checkup?

A: It causes a small stretch in the quadriceps muscle.

Q: What triggers the action potential in the stretch reflex?

A: Stretching of the muscle spindles in the quadriceps.

Q: Where does the sensory (afferent) neuron send its signal in the stretch reflex?

A: To the spinal cord.

Q: What happens after the sensory neuron synapses in the spinal cord during the stretch reflex?

A: It activates the motor neuron of the quadriceps and inhibits the hamstring motor neuron (reciprocal innervation).

Q: What is reciprocal innervation?

A: When contraction of one muscle causes relaxation of its antagonist (opposing muscle).

Q: What is the result of the stretch reflex in the leg?

A: The quadriceps contracts, the hamstring relaxes, and the lower leg kicks out.

Q: Does the brain control the muscle contraction in the stretch reflex?

A: No, the brain is not involved; it’s a simple reflex mediated by the spinal cord.

The stretch reflex:

Tapping the patellar tendon stretches the quadriceps muscle.

Muscle spindles within the quadriceps detect the stretch.

Sensory (afferent) neurons generate an action potential and send signals to the spinal cord.

The afferent neuron synapses onto the motor neuron controlling the quadriceps in the spinal cord.

The quadriceps motor neuron is activated, while inhibition of the hamstring occurs via reciprocal innervation.

Quadriceps contracts, hamstring relaxes, and the lower leg kicks forward.

Cerebellum and the lymbic system

Q: What does the word "cerebellum" literally mean?

A: "Little brain."

Q: Does the cerebellum have fewer neurons because it is smaller?

A: No, it contains more neurons than the rest of the brain combined.

Q: What are the main functions of the cerebellum?

A: It contributes to accurate limb movement, corrects ongoing movements, modifies some reflexes, helps learn new muscle movements, and is involved in the vestibular ocular reflex (VOR).

Q: What two sources of information does the cerebellum receive to assist in movement?

A: The motor cortex (signals sent to muscles) and proprioceptors (position of limbs in space).

Q: How does the cerebellum use information from the motor cortex and proprioceptors?

A: It compares the intended movement from the motor cortex with the actual limb position from proprioceptors to ensure accuracy.

Q: What happens if the cerebellum detects a movement error?

A: It modifies the signals from the primary motor cortex to adjust the movement.

Q: What role does sensory feedback (e.g., from the visual system) play in cerebellar function?

A: It provides additional information to help the cerebellum fine-tune movement adjustments.

Q: Describe the pathway of motor information involving the cerebellum.

A: Motor cortex sends signals through the cerebellum, which integrates information from proprioceptors, adjusts commands, and then sends corrected signals to muscles.

Q: What is the primary function of the limbic system?

A: It is the emotional center of the brain.

Q: What key role does the hypothalamus play within the limbic system?

A: It regulates homeostasis and hormone release.

Q: What behaviors can be triggered by stimulation of the hypothalamus and limbic system?

A: Eating, drinking, locomotion, changes in heart rate and blood pressure, sexual behaviors, and memory.

Q: What types of effects do the limbic system and hypothalamus coordinate?

A: Autonomic, hormonal, and motor effects related to maintaining the internal environment and coordinating emotional behaviors.

Q: What is the amygdaloid body (amygdala) responsible for?

A: Emotional responses like fear, anger, anxiety, and pleasure; also influences how strongly memories linked to emotions are stored.

Q: How does the amygdala affect memory?

A: It determines how strongly memories attached to strong emotions like fear or anxiety are stored.

Q: Who is Alex Honnold and why is he significant in studying fear?

A: A solo climber known for fearlessness; researchers studied his brain to understand his lack of fear.

Q: What was observed about Alex Honnold's amygdala response compared to other climbers?

A: His amygdala showed a reduced or different response to fear-inducing stimuli like images from the top of a mountain.

Q: Why might Alex Honnold’s amygdala response explain his adventurous behavior?

A: A less reactive amygdala could explain his reduced fear and willingness to take risks.

Q: Where is the hypothalamus located in the brain?

A: At the base of the brain, just anterior to the brain stem.

Q: Name some key functions of the hypothalamus.

A: Temperature control, body water regulation, food intake regulation, cardiovascular and circadian clock regulation, coordinating emotional behaviors, and controlling hormones released from the pituitary.

Q: What type of control system does the hypothalamus mainly use?

A: Negative feedback control.

Q: In the negative feedback loop involving the hypothalamus, what role does it play?

A: It acts as the control center.

Q: How does the hypothalamus regulate body temperature during exercise?

A: By detecting the temperature rise and triggering sweating and vasodilation to promote heat loss.

Q: What is the typical body temperature set point maintained by the hypothalamus?

A: Approximately 37°C.

Q: Why does the hypothalamus raise the temperature set point during a fever?

A: To protect the body from infection by bacteria or viruses.

Q: What mechanisms does the hypothalamus induce to raise body temperature during a fever?

A: Shivering of skeletal muscles and vasoconstriction in peripheral blood vessels.

Q: Why do hands and feet feel cold during a fever?

A: Because of vasoconstriction to conserve heat.

Q: What happens when the fever breaks and the set point returns to normal?

A: The hypothalamus triggers heat loss mechanisms like sweating and vasodilation.

Autonomic nervous System

Q: What is the main function of the sympathetic division (SYN) of the ANS?

A: It activates body functions involved in "fight, flight, or freeze" responses, increasing heart rate, blood flow to muscles, and airway dilation while reducing gut activity.

Q: What does the parasympathetic division (PSYN) of the ANS do?

A: It conserves energy by slowing heart rate, lowering blood pressure, and directing blood flow toward digestion during rest and relaxation.

Q: How do the sympathetic and parasympathetic divisions generally interact?

A: They often have opposing effects but work together, with one being more active than the other depending on the body's needs.

Q: Name an organ that receives only sympathetic innervation and no parasympathetic input.

A: The adrenal glands or blood vessels.

Q: How do the sympathetic and parasympathetic divisions work in the genitalia?

A: They work together to contribute to sexual arousal.

Q: What is the enteric nervous system?

A: A third division of the ANS that controls gut motility independently from the CNS.

Q: Is the ANS under voluntary control?

A: No, it controls involuntary functions like heart rate, pupil size, smooth muscle in blood vessels, and gland secretions.

Q: What role does the hypothalamus play in the ANS?

A: It acts as the control center, integrating sensory information and deciding whether to activate the sympathetic or parasympathetic pathways.

Q: How does the hypothalamus send signals to effector organs?

A: Through efferent nerve fibers via either the sympathetic or parasympathetic pathways.

Q: Does the hypothalamus completely shut down one division of the ANS when activating the other?

A: No, both divisions work simultaneously but with varying levels of activity.

Q: What is the difference in myelination between sympathetic preganglionic and postganglionic neurons?

A: Preganglionic neurons are myelinated, but true postganglionic neurons that communicate with target tissues are unmyelinated.

Q: What advantage does myelination provide to neurons?

A: It increases the speed of nerve signal conduction.

: Where are the cell bodies of preganglionic neurons located in both the sympathetic and parasympathetic divisions?

A: In the central nervous system (CNS).

Q: What is an autonomic ganglion?

A: A group of nerve cell bodies where the preganglionic neuron synapses to relay information to postganglionic neurons.

Q: What neurons synapse onto the target organ in the ANS pathways?

A: Postganglionic neurons.

Q: Are neurotransmitters used in both autonomic ganglia and target tissues for the SYN and PSYN?

A: Yes, neurotransmitters are used in both locations.

Q: Is the neurotransmitter used in the autonomic ganglion the same for both SYN and PSYN?

A: Yes, it is the same for both.

Q: Are the neurotransmitters at the target tissues the same or different for SYN and PSYN?

A: Different.

Q: Where do sympathetic nerves exit the spinal cord?

A: Thoracic and lumbar regions.

Q: Where do parasympathetic nerves exit the spinal cord?

A: Brain stem and lower sacral region.

Q: Which division has a shorter preganglionic neuron axon?

A: Sympathetic division.

Q: Which division has the autonomic ganglion closer to the CNS?

A: Sympathetic division.

Q: Which division has the autonomic ganglion closer to the target organ?

A: Parasympathetic division.

Q: Are postganglionic neurons myelinated or unmyelinated in both divisions?

A: Unmyelinated in both.

Q: Which division has a longer postganglionic neuron?

A: Sympathetic division.

Q: What are the main neurotransmitters at the target organs for the sympathetic division?

A: Epinephrine and noradrenaline (except sweat glands, where acetylcholine is released).

Q: What neurotransmitter does the parasympathetic division release at target organs?

A: Acetylcholine.

Q: What neurotransmitter do preganglionic neurons release in both sympathetic (SYN) and parasympathetic (PSYN) divisions?

A: Acetylcholine (ACh).

Q: Where does acetylcholine released by preganglionic neurons bind in the autonomic nervous system?

A: To nicotinic receptors on dendrites of postganglionic neurons in the autonomic ganglion.

Q: How do nicotinic receptors respond to acetylcholine binding?

A: They open quickly, allowing ions to rush in and depolarize the cell (fast transmission).

Q: What is the difference in structure between nicotinic receptors at the autonomic ganglion and those at the neuromuscular junction (NMJ)?

A: They are slightly different in structure, but this is beyond the current scope.

Q: Besides nicotinic receptors, what other type of receptor does ACh bind to in the ANS?

A: Muscarinic receptors.

Q: How do muscarinic receptors transmit signals?

A: They activate biochemical reactions via G-proteins that open ion channels indirectly (slow transmission).

Q: Where are muscarinic receptors found?

A: On the target organs of the autonomic nervous system.

Q: What type of receptor is the nicotinic receptor?

A: A ligand-gated ion channel (ionotropic receptor) that spans the plasma membrane.

Q: Where are nicotinic receptors located?

A: At the neuromuscular junction (NMJ) and on postganglionic neurons in the autonomic nervous system.

Q: What type of receptor is the muscarinic receptor?

A: A ligand-gated receptor that is a G-protein coupled receptor (metabotropic receptor).

Q: What happens when ACh binds to muscarinic receptors?

A: It triggers biochemical reactions inside the post-synaptic cell that lead to the opening of ion channels.

Q: On which types of cells are muscarinic receptors found?

A: Smooth muscle and cardiac muscle cells.

Q: Which neurotransmitter mainly mediates sympathetic signaling at target organs?

A: Norepinephrine.

Q: Which neurotransmitter is released by sympathetic innervation of sweat glands?

A: Acetylcholine (ACh).

Q: What hormones does the adrenal gland release, and in what proportions?

A: 80% epinephrine and 20% norepinephrine.

Q: What are the two main types of adrenergic receptors?

A: Alpha adrenergic receptors and beta adrenergic receptors.

Q: What effect do alpha adrenergic receptors have?

A: They cause smooth muscle contraction and vasoconstriction.

Q: What effect do beta adrenergic receptors have?

A: They cause vasodilation, smooth muscle relaxation, bronchodilation, and excitatory cardiac function.

Q: How does the adrenal medulla function differently from other sympathetic ganglia?

A: It has no parasympathetic innervation and no postganglionic neuron; it releases epinephrine directly into the bloodstream.

Q: What do the sympathetic and adrenal pathways release that binds to adrenergic receptors?

A: Epinephrine and norepinephrine