human phys final

what are the two types of receptors?

membrane-bound receptors: embedded to cell surface; binds to water-soluble ligands

• trigger rapid, short-lived responses via signal transduction cascades

• e.g., insulin, amino hormones-epinephrine, neurotransmitters-acetylcholine

intracellular receptor: located inside the cell (cytoplasm/nucleus); binds to lipid soluble ligands that can cross the membrane

• slow, but long-lasting genomic effects to inhibit/facilitate transcription + gene expression

• e.g., steroids-testosterone, estradiol, thyroid hormones, vitamin D

what is the difference between tight junctions and gap junctions?

tight junctions: creates a barrier to prevent leakage between cells

gap junctions: create channels to allow movement of molecules between cells (communication)

What is the functional division of the nervous system?

sensory (afferent) division: carries impulses from receptors to CNS; detects internal & external stimuli

motor (efferent) division: carries impulses from CNS to effectors

• somatic nervous system (SNS): control voluntary movements (e.g., skeletal muscles)

• autonomic nervous system (ANS): controls involuntary functions (e.g., smooth muscle, cardiac muscle)

  • sympathetic: “fight or flight”

  • parasympathetic: “rest and digest”

what are the types of glial cells in the CNS?

• oligodendrocytes

• microglia

• ependymal cell

• astrocyte

what are astrocytes?

• maintains blood brain barrier

• nourishes neurons w/ glycogen

• reuptake of neurotransmitters

• repair + regenerate neurons

• communicate changes in blood

• regulation of blood in extracellular brain

• maintain ion concentrations (K+)

what is the blood brain barrier?

• protective, selective barrier that separates the bloodstream from the brain tissue

• structure: Blood → Endothelial cell with tight junctions → Basement membrane → Astrocyte end-feet → Brain tissue

what factors influence ion movement across the membrane?

• concentration gradient (diffusion)

• ion channels (leak channels, gated channels)

• equilibrium potential (influenced by electrical gradient)

What is the resting membrane potential? What contributes to the resting membrane potential?

-70mV → excess positive ions outside of membrane

• more Na⁺ and Cl^- outside of cell

• more K⁺ inside of cell

Na⁺/K⁺ pump: 3 Na⁺ out, 2K⁺ in

K⁺ leaky channel: move K⁺ out of cell down its gradient

Describe the phases of action potential?

1. resting membrane potential (-70 mV)

2. stimulus causes membrane to reach threshold voltage (-50 mV)

3. depolarization: voltage-gated Na⁺ channels open causing influx of Na⁺ into the cell; membrane potential becomes more positive

4. at +30 mV: inactivation of Na⁺ channels & delayed opening of voltage-gated K⁺ channels

5. repolarization: voltage-gated K⁺ channel open causing K⁺ to leave the cell; helps membrane return towards -70mV resting potential

6. hyperpolarization (-80 mV): delayed closing of K⁺ channel causes membrane to be below resting membrane potential

7. voltage-gaated K⁺ channel closes & resting membrane potential is restored

what is the all-or-none principle?

• applies to action potential

• any stimulus that is strong enough to meet threshold potential will generate same strength action potential

• strength of stimulus does not affect strength of action potential

what is the refractionary period?

refractionary period: regulates # of action potentials that can occur during repolarization & hyperpolarization

absolute refractionary period: NO action potential can occur during refractionary period bc Na⁺ channel is inactivated

relative refractionary period: action potential can occur during hyperpolarization if strong enough to reach threshold bc Na⁺ channels are closed, not inactivated

how is an action potential self-propagating?

• local depolarization from Na⁺ influx at one segment of the membrane triggers depolarization in the adjacent Na⁺ channels of the next segment

• refractory period ensures action potential moving in one direction

• myelination allows depolarizing current to travel longer distance and speeds up conduction

what is myelin?

• insulator on axons that allows for fast propagation of action potential

• insulation stops leakages of ions → causes longer effective distance of ions to activate next segment of Na⁺ channels (aka longer depolarization)

• formed by oligodendrocytes (CNS) and schwann cells (PNS)

what is salutatory conduction?

axon potentials appears to jump from node to node due to Na⁺ channels located there

what are graded potentials? what are the key characteristics?

changes in membrane potential that are confined to relatively small region of plasma membrane (short-distance signaling)

• direction: stimulus can cause depolarization or hyperpolarization

• strength of stimulus affects intensity of graded potential

• short distance propagation from leaky membrane + unmyelinated axon

• summation of graded potentials can lead to action potentials

what are the types of graded potential summations?

temporal summation: consecutive depolarization events occurring at same location but diff times before neuron is able to return to resting membrane potential

spatial summation: depolarization events simultaneously occurring at diff locations but at same time

compare graded and action potentials

what is length constant? why might they differ between neurons?

• distance that ions travel until their voltage reaches 37% of original value

• increase in axon diameter = increase length constant

• myelination = increase length constant

What are the steps from action potential to neurotransmitter release?

1. action potential reaches presynaptic terminal

2. depolarization opens voltage-gated Ca²⁺ channels

3. influx of Ca²⁺ in presynaptic terminal

4. Ca²⁺ directly activates synaptotagmin (protein involved in neurotransmitter release) → activates SNARE protein → leads to vesicle docking and fusion

5. exocytosis—vesicle releases neurotransmitter into synaptic cleft

6. neurotransmitter diffusion across synaptic cleft and binds to receptors on postsynaptic membrane

7. postsynaptic potential generated

8. termination of signal: reuptake/diffusion/inactivation

Limitations on the maximum action potential firing frequency of neurons are determined by ____.

length of refractory periods

how does botulism/botox work?

destroys SNARE protein → no vesicle docking + fusion → no acetylcholine release from motor neuron → no muscle action potential → no DHP activation → no Ca²⁺ release from SR → no contraction

results in muscle weakness/paralysis

How can neurotransmitter concentration be regulated in a synaptic cleft?

• reuptake

• enzymatic degradation

• diffusion

what is the 3 step process of the somatosensory system?

1. reception: receptor detects stimulus

2. transduction: convert stimulus into signal (aka receptor potential)

3. perception: process + interpret signal in brain

what is a receptor potential?

• graded potential that occurs in sensory receptors in response to stimulus

• converts stimulus into electrical signal

• can trigger action potential if reaches action potential

what is adaptation? what are the two types of adaptors?

adaptation: diminishing activity in response to repeated or sustained stimuli

phasic receptors: fast-adapting; burst of action potential when stimulus is applied and removed; receptor potential does not persist when stimulus is applied

• e.g., slight touch (clothes on body), slight temperature (stepping in shower), smell

tonic receptors: slow-adapting; sustained signaling

• e.g., pain, vision

what is acuity?

degree of sharpness/precision to which you can sense a stimulus

how does two-point discrimination demonstrate acuity?

two-point discrimination: test that determines minimum distance at which a person can perceive two simultaneous touches as separate points instead of one.

• tests how well the nervous system can distinguish closely spaced stimuli

How does receptive field size impact acuity?

receptive field: area of skin that activates a single sensory neuron

smaller receptive field = neuron covers small area → stimuli activate diff neurons → high acuity

large receptive field = neuron covers large area → stimuli activate same neuron → brain perceives as one stimulus → low acuity

How does dendrite density impact acuity?

• high dendrite density (receptors) → high acuity

• low dendrite density (receptors) → low acuity

what does localization of a stimulus depend on?

• size of receptive field

• degree of receptive field overlap

what is receptive field overlap?

definition: when neighboring sensory neurons cover some of the same area of sensory space → single stimulus can activate more than one sensory neuron

**helps localize stimulus by comparing neuron firing activity

what is lateral inhibition?

definition: when neuron directly under the stimulus fires strongly and suppresses neighboring weaker responses; leads to increasing contrast between signals, which improves localization/acuity

how does rate of adaptation indirectly influence acuity?

tonic receptors (slow adaptation) → sustained signal → increase acuity

how does myelination indirectly influence acuity?

myelination → sustained signal → increase acuity

what factors influence the intensity of stimulus?

• recruitment of diff # of afferent neurons

• frequency of firing

• magnitude of receptor potentials

what are significant structures in spinal cord vertebrae?

• ventral horn = larger wings

• dorsal horn = smaller wings

• ventral root

• dorsal root

• dorsal root ganglion

where do afferent signals enter?

dorsal root

where do motor/efferent signals exit?

ventral root

what is the dorsal root ganglion?

cluster of sensory neuron cell bodies

what is the pathway from stimulus to spinal cord?

Stimulus → Receptor potential → Action potential → Peripheral afferent fiber → Dorsal root ganglion (cell body) → dorsal root

what are the two types of somatosensory pathways? how do they differ?

ascending anterolateral pathway: immediately synapse in spinal cord → crossover in spinal cord → ascend to brain through anterolateral column (side) → ascends to thalamus → reaches somatosensory cortex

dorsal column pathway: ascend to brain through dorsal column (back) → synapse in brain → crossover in brainstem → ascends to thalamus → reaches somatosensory cortex

what is the full somatosensory pathway, from sensory to motor command?

Receptor → sensory neuron (afferent pathway) → dorsal root ganglion → dorsal root → synapse at dorsal horn → ascends to brain → thalamus (relay center) → somatosensory cortex → motor cortex (generates motor response) → motor command travels down descending motor tract → motor neuron synapses in ventral horn → exits spinal cord via ventral root → muscle contracts

what is the somatosensory reflex arc pathway

*does not require brain (e.g., knee jerk reflex)

Receptor → sensory neuron → dorsal root → dorsal horn → interneuron → motor neuron (ventral horn) → ventral root → muscle

what are dermatomes? how do they relate to pathologies?

• areas of skin innervated by nerves in a segmented fashion; location of sensation is where the spinal cord will receive the signal

• ex: shingles—dormant virus in dorsal root ganglion; rash follows form of dermatome

• ex: spinal cord injury—loss of sensation in body can indicate which vertebrae has been injured

how do mechanoreceptors work?

1. direct activation due to lipid tension (membrane bilayer pulling receptor)

2. direct linkage via. intracellular and extracellular proteins (proteins pulling receptor)

3. indirect activation via. a system that activates the channel

how does threshold stimuli relate to sensitivity to touch?

low threshold = require little mechanical force to open mechanically-gated ion channels → high sensitivity (detect extremely subtle touch)

how does receptive field size influence sensitivity and acuity?

small receptive field size → high sensitivity + acuity

• detects fine detail

large receptive field size → broad detection + lower acuity

• usually detects pressure or vibration

how does adaptation affect touch?

phasic (rapidly adapting) → movement, texture, vibration

tonic (slowly adapting) → grip control, maintain continuous awareness of objects in hand

what are nociceptors?

pain receptors that respond to tissue damage, chemical, mechanical or thermal stimulation

what are the types of nociceptor fibers?

• Aδ (delta) fibers:

  • light myelinated, fast conducting →first pain

  • smaller receptive field size → increased acuity → sharp, localized pain

  • higher intensity pain for shorter period of time

• polymodal nociceptors (C fibers):

  • unmyelinated, slow conducting → second pain (dull, aching, throbbing, nonlocalized pain)

  • lower intensity pain for prolonged time

what is unique about sleeping nociceptors?

• activated by chemicals released during tissue damage

• located on C fibers (slow, chronic, dull second pain)

• ex: washing hand under water w/ cut

what neurotransmitters are involved in nociception?

• glutamate: primary fast transmitter; released from Aδ and C fibers

• substance P (neuropeptide): produce slower, prolonged excitation for chronic pain signaling; released mainly from C fibers

what are A-alpha fibers

• associated with tonic (slow adaptation) in muscle

what are A-beta fibers?

• associated with fast adaptation (phasic) in touch

what is the difference between mechanosensitive and mechanothermal receptors?

what is the difference between anesthesia and analgesics?

anesthesia: blocks all sensations

analgesic: blocks pain signaling

what are the subcategories of anesthesia?

• general anesthesia: induces total unconcsciousness; affects entire body

• local anesthesia: numbs specific small area

what are common forms of analgesics?

• opiods/oppiates

• cox inhibitors

what is hyperalgesia vs. hypoalgesia?

• hyperalgesia: increases pain sensitivity

• hypoalgesia: decreases pain sensitivity

what is the difference between first and second pain? how is it coded?

Describe the pain transduction pathway and how it relates to perception of pain.

1. Tissue injury → releases chemical signals (e.g., prostaglandins, histamine)

2. Nociceptor activation

3. Aδ and C fibers transmit signal

4. Synapse in dorsal horn

5. Cross in spinal cord

6. Ascend via anterolateral column

7. Thalamus relay

8. Cortex processes → conscious pain

How is hypoalgesia naturally activated?

stress → release serotonin + norepinephrine → releases opioids (e.g., beta-endorphins) → prevents release or binding of pain neurotransmitters from nociceptors (glutamate and substance P)

How is hyperalgesia naturally activated?

after tissue injury, inflammatory mediators are released (e.g., prostaglandins, histamine, cytokines) which lowers activation threshold of nociceptors → nociceptors fire more easily?

why does opioid addiction occur?

opioids bind to opiate receptors and inactivate GABA-ergic neuron → inhibits GABA release → allows dopamine release

what is the COX-1 pathway in nociception?

1. tissue injury releases inflammatory mediators (e.g., histamine, cytokines)

2. inflammatory mediators bind to GPCR on nociceptor

3. Gq activates PLC → cleaves PIP2 to IP3 + DAG → IP3 increases Ca²⁺, DAG activates PKC

4. activation of PLA₂ causes release of arachidonic acid

5. COX-1 converts arachidonic acid into prostaglandins & thromboxanes

6. sensitizes nociceptors & lowers activation threshold, leading to increased excitability and hyperalgesia

Compare COX-1 and COX-2

how do NSAIDs work?

• COX-1 inhibitor

• block COX pathway (*mainly prostaglandins) → reduced inflammation

• can cause stomach ulcers & kidney issues w/ prolonged use (bc COX-1 enzymes found in gastro + renal tract)

What are the parts of the brain that influence pain perception?

reticular alertness, arousal

thalamus: dull, poorly localized (chronic pain); main relay station that sends signals to cortex

cerebrum (cortex): localizes + characterizes pain

amygdala: emotions/memory, experience, suggestions

what is the cross-bridge cycle? List out the steps

• describes how myosin interacts with actin to generate contraction, with ATP, ADP, and Pi controlling each step

1. Ca2+ binds to troponin → induces conformational change

2. shifts tropomyosin on actin → exposes myosin-binding sites on actin

3. myosin (ADP + Pi bound—cocked state) binds to actin → forms cross-bridge

4. release of Pi leads to power stroke

5. ADP release leads to rigor state

6. ATP binds to myosin → detaches myosin from actin

7. ATP hydrolysis (ATP → ADP + Pi) leads to cocking (high energy state)

how is Ca²⁺ released into muscle cells, starting from motor neuron?

1. acetylcholine released from motor neuron

2. synapse on motor end plate

3. bind to acetylcholine receptors on sarcolemma of muscle cell and trigger action potential via. voltage-gated Na⁺ and K⁺ channels

4. action potential arrives at T-tubules and reaches DHP

5. DHP receptor (mechanical voltage receptor) detects voltage change and undergoes conformational change

6. DHP mechanically opens ryanodine receptor on sarcoplasmic membrane reticulum

7. Ca²⁺ release from sarcoplasmic reticulum

8. Ca²⁺ binds to troponin → shifts tropomyosin → muscle contraction

how does curare work?

• plant-derived toxin

• competitive antagonist of acetylcholine receptors → acetylcholine is released but does not bind to receptor → no end plate potential → no muscle action potential → no DHP activation → no Ca²⁺ release → no contraction → muscle weakness/paralysis

how does sarin (nerve gas) work?

• inhibit acetylcholinesterase (AChE) → acetylcholine not broken down → continuous stimulation of Ach receptors

• early phase: constant depolarization + Ca²⁺ release + sustained contraction → muscle spasms

• later phase: depolarization block, voltage gated Na⁺ channels inactivated, Ca²⁺ regulation disrupted → paralysis

what are the types of muscle contractions?

• isometric contraction: muscle tension increases but muscle length does not change (e.g., carrying groceries)

• isotonic contraction: muscle tension increases and muscle length changes

what are the two types of isotonic contractions?

• concentric contraction: muscle shortens while producing force; muscle force > external load (e.g., lifting dumbbells)

• eccentric contraction: muscle lengthens; muscle force < external load (e.g., lower dumbbells)

what is the difference between twitch and tetanus?

twitch: single contraction in response to one action potential

tetanus: repeated stimulation prevents Ca²⁺ from being fully removed, leading to summation of force and sustained contraction (e.g., maintaining posture, lifting weights)

what is the difference between unfused and fused tetanus?

unfused tetanus: incomplete; minimal relaxation; fluctuating elevated Ca²⁺

fused tetanus: complete; no relaxation; sustained high Ca²⁺

what factors can increase muscle tension?

1. stimulate more cross bridges by recruiting more sarcomeres + frequent stimulation (summation)

2. optimal degree of overlap to maximize cross bridge formation

3. larger diameter of muscle fibers → increase formation of cross bridges

what is a motor unit? how does it regulate muscle tension?

• single motor neuron and all the muscle fibers it innervates

• determines how much force is produced

• regulation: recruit motor unit by size & increase firing frequency for temporal summation

what are the three types of muscle fibers?

• type I: slow-oxidative; postural

• type IIa: faster-oxidative-glycolytic; endurance

• type IIb: fastest-glycolytic; speed

what are the pathways that muscles use to get ATP?

1. creatine phosphate + ADP → creatine + ATP (very fast ATP production)

2. glycolysis (generates atp fastest, anaerobic, amount of atp per waste product)

3. oxidative phosphorylation  (produces most atp but also most time consuming; requires lots of O₂—aerobic)

what are the causes of muscle fatigue?

• reduced motor neuron firing: K⁺ saturated T tubules causes hypoerpolarization → conduction failure of action potential

• lactic acid buildup → lower pH → troponin malfunction

• accumulation of ADP + Pi: inhibit cross bridge cycle & release of myosin from actin

what is the motor end plate?

• specialized region of the sarcolemma where motor neuron communicates with muscle cell at the neuromuscular junction

• results in Ca²⁺ release from sarcoplasmic reticulum & muscle contraction

what is the difference between central and peripheral fatigue?

central fatigue (brain-level): reduced motor neuron firing + reduced recruitment of motor units

peripheral fatigue (muscle-level): accumulation of ADP+Pi, troponin malfunction

what are key structural features of smooth muscle?

• gap junction (electrical coupling) vs. desmosomes (mechanical attachment)

• no sarcomeres → actin + myosin organized in lattice network instead of parallel bundles

• no troponin → use MLCK and MLCP instead

• actin + myosin filaments

• unique proteins: tropomyosin (different from skeletal), calponin, caldesmon

• dense bodies: actin (thin filaments) is anchored to dense bodies

• desmosomes: where two adjacent smooth muscle cells are physically attached to each other

what’s the difference between single-unit and multi-unit smooth muscle?

• single unit smooth muscle

  • structure: cells connected by gap junctions; few cells innervated

  • activation: myogenic (self-activation) triggered by stretch and local signals

  • ex: GI tract

• multi-unit smooth muscle

  • structure: little/no gap junction coupling; each cell acts independently + directly innervated

  • activation: neurogenic (nerve-controlled), allows for finer control

  • eyes adjusting light

what are the enzymes important for smooth muscle contractions?

MLCK (myosin light-chain kinase): phosphorylates myosin to allow myosin and actin to interact

MLCP (myosin light-chain phosphatase): removes phosphate from myosin

Rho-kinase: phosphorylates and inactivates MLCP so myosin stays phosphorylated

what are the steps of smooth muscle contraction?

1. agonist binds to GPCR on smooth muscle cells

2. activates PLC → IP₃ binds to receptors on sarcoplasmic reticulum → Ca²⁺ release

3. Ca²⁺ enters smooth muscle cell (graded)

4. Ca²⁺ binds + activates calmodulin

5. Ca2+-calmodulin binds + activates MLCK (myosin light-chain kinase)

6. **dependent on ratio of MLCK and MLCP

• contraction: MLCK phosphorylates MLC (uses ATP) to MLC-P → allows myosin and actin to bind → cross-bridge cycling (generates powerstroke) → smooth muscle contraction

• relaxation: MLCP (myosin light-chain phosphatase) dephosphorylates MLC-P to MLC → myosin isn’t able to bind to actin → no cross-bridge cycling → smooth muscle relaxation

7. Rho-kinase phosphorylates + inactivates MLCP → MLC-P stays phosphorylated → cross-bridge cycling occurs → allows muscle contraction

why are smooth muscle myosin ATPase slower than in striated muscle cells?

• provides a graded contraction

• leads to slow, sustained contraction (maintains tension) and low fatigue

what is latch state?

• when myosin stays latched into actin and can’t be released

• maintain muscle tension w/ minimal ATP use + lack of fatigue over longer periods of time

when does latch state occur?

when MLCP dephosphorylates myosin while myosin and actin are attached → myosin stays latched onto actin and can’t be released → allows muscle to maintain tension with very little energy

what needs to happen to release from latch state?

• decrease intracellular Ca²⁺ → stop cross-bridge cycling

• increase MLCP activity → promotes detachment

what are the two types of smooth muscle contractions?

phasic contraction: contraction followed by relaxation

• function: move things along

• ex: peristalsis

tonic contraction: sustained contraction for long period of time; very energy-efficient (latch state); little to no relaxation

• function: maintain pressure or resistance

• ex: bladder holding urine

What factors influence blood flow?

• directly proportional to pressure difference

• indirectly proportional to resistance

what factors influence resistance? which factor has the greatest influence on resistance?

• increase in viscosity (affected by water) → increase in resistance

• decrease in vessel radius** (affected by temp) → increase in resistance

• increase in length (affected by weight/height gain) → increase in resistance

what is the difference between increase vs. decrease vascular tone?

• vascular tone: degree of smooth muscle contraction in blood vessels (diameter of vessel)

• increase vascular tone = vasoconstriction (vessel narrowing, increase resistance, decrease bloodflow, increase blood pressure)

• decrease vascular tone = vasodilation (vessel widening, decrease resistance, increase bloodflow, decrease blood pressure

what drugs decrease vascular tone?

• decrease vascular tone (vasodilation) → treat hypertension

• L-type Ca²⁺ channel blockers

• K⁺ channel openers

• nitrodilators

• direct-acting vasodilators

• angiotensin pathway

• endothelin antagonists

• a-adrenoreceptor antagonists

what are the different mechanism pathways to decrease vascular tone?

• decrease vascular tone → muscle relaxation or decrease muscle contractions

• decrease Ca²⁺

• decrease MLCK activity

• increase MLCP activity

how does inhibiting the angiotensin pathway affect vascular tone?

• inhibiting angiotensin pathway → decrease vascular tone

• renin-inhibitor: block angiotensinogen → angiotensin I formation (earliest step)

• ACE inhibitor: block conversion of angiotensin I → angiotensin II 

• angiotensin receptor blockers (ARBs): block angiotensin receptor directly → Ang II present but no Gq → decrease Ca²⁺ signaling → vasodilation

what are the different types of adrenoreceptors? where are they located and how they relate to affinity?

• alpha adrenoreceptors: low affinity

  • a₁: smooth muscle vasculature → cause vasoconstriction

  • a₂: smooth muscle vasculature + neurons → decrease norepinephrine release → vasodilation

• beta adrenoreceptors: high affinity

  • b₁: heart → increase heart rate + myocardial contractions

  • b₂: smooth muscle vasculature → cause vasodilation

how does the a₁ adrenergic pathway work?

1. sympathetic nerve release epinephrine/norepinephrine

2. epinephrine/norepinephrine binds to a₁ receptor (G_q) on smooth muscle

3. activates IP₃-DAG pathway → releases Ca²⁺ → vasoconstriction