Organismal Physiology Exam 2

EPSP

• Excitatory Postsynaptic Potentials (EPSPs): Temporary depolarizations of the postsynaptic membrane driven by the influx of positive ions (like Na+ or Ca2+). Triggered by excitatory neurotransmitters like glutamate, an EPSP shifts the membrane potential closer to the action potential threshold.

IPSP

• Inhibitory Postsynaptic Potentials (IPSPs): Temporary hyperpolarizations caused by the influx of Cl- or efflux of K+. Driven by neurotransmitters like GABA, an IPSP moves the membrane potential further from the threshold, suppressing neuron firing.

Spatial Summation

Multiple different presynaptic neurons release neurotransmitters at the same time across separate locations on the postsynaptic dendrites or soma. Their individual potentials combine; if the combined depolarization reaches the threshold, an action potential fires.

EX: Feeling a light touch on your fingertip.

• While spatial summation relies on coordination across multiple synapses, temporal summation relies on rapid repetition from a single synapse.

Temporal Summation

A single presynaptic neuron fires multiple action potentials in rapid succession. Because the first EPSP has not fully decayed by the time the next arrives, the potentials stack sequentially over time to reach the firing threshold.

EX: A single pain fiber firing rapidly to signal an intense stimulus.

• While spatial summation relies on coordination across multiple synapses, temporal summation relies on rapid repetition from a single synapse.

Absolute Refractory Period (ARP)

What happens: During this phase, it is physically impossible for the neuron to fire another action potential, regardless of how strong the incoming stimulus is.

As the action potential peaks, voltage-gated sodium (Na+) channels rapidly transition from an open state to an inactivated state.

Relative Refractory Period (RRP)

What happens: Immediately following the absolute refractory period, a new action potential can be triggered, but only by a stronger-than-normal stimulus.

• By this point, the Na+ channels have reset to their resting (closed) state and can open again.

• However, voltage-gated potassium (K+) channels are still slow to close, leading to a temporary hyperpolarization (the membrane potential dips below resting, often reaching -80 mV).

Conduction Velocity

1. Axon Diameter

• The reason: A larger cross-sectional area offers less internal resistance to the flow of electrical current (ions moving down the axon). Think of it like a wide pipe versus a narrow straw: water flows more freely and quickly through the wider pipe.

2. Myelination

• How it works: Myelinated axons conduct impulses significantly faster than unmyelinated ones.

• The reason: The myelin sheath acts as an electrical insulator. Instead of continuous conduction along the entire membrane, the action potential "jumps" from one gap in the myelin (the node of Ranvier) to the next in a process called saltatory conduction. This skips large stretches of membrane and drastically speeds up transmission.

3. Temperature

• The reason: Temperature affects the kinetic energy of ions and the rate at which voltage-gated channels open and close. Warm temperatures allow ions to diffuse faster and channels to react quicker, speeding up the impulse. (However, this only applies within normal physiological limits; extreme heat can disrupt protein function).

Key Takeaway: The fastest nerve fibers in the body are large and heavily myelinated (such as those controlling rapid skeletal muscle movement or sharp touch), whereas small, unmyelinated fibers transmit slower signals (such as dull, aching pain).

Trans-membrane resistance and conductance affect how far local potentials travel.

How far a local (graded) potential travels along a dendrite or axon depends on electrotonic conduction—the passive spread of electrical current. As the current moves, it gradually fades because charge leaks out through the cell membrane.

High Trans-Membrane Resistance (Low Conductance)

• What happens: When the membrane has high resistance (few open ion channels), it acts like a well-insulated pipe.

Low Trans-Membrane Resistance (High Conductance)

• What happens: When the membrane has low resistance (many open ion channels), it acts like a leaky garden hose with holes punched in it.

Sequence of Events in Synaptic Transmission

Step-by-Step Breakdown

• 1. Arrival of the Action Potential: The action potential propagates down the axon and depolarizes the membrane of the presynaptic terminal (the axon terminal or synaptic knob).

• 2. Opening of Voltage-Gated Calcium Channels: The change in membrane voltage causes voltage-gated calcium Ca2+ channels on the presynaptic membrane to open.

• 3. Influx of Calcium Ions: Because extracellular calcium concentration is much higher than intracellular concentration, Ca2+ rapidly rushes into the presynaptic terminal down its electrochemical gradient.

• 4. Vesicle Docking and Fusion (Exocytosis): The surge of internal Ca2+acts as a trigger. It interacts with specialized proteins (such as synaptotagmin and the SNARE complex) that cause synaptic vesicles—which are packed with neurotransmitters—to fuse with the presynaptic cell membrane.

• 5. Release of Neurotransmitters: Once the vesicles fuse, they rupture and dump their neurotransmitter cargo into the synaptic cleft via exocytosis.

• 6. Receptor Binding on the Postsynaptic Membrane: The neurotransmitter molecules diffuse across the narrow synaptic cleft and bind to specific receptor proteins embedded in the postsynaptic membrane. This binding causes ion channels to open or close, generating a local potential (an EPSP or IPSP).

• 7. Signal Termination: To prevent continuous stimulation, the neurotransmitter is quickly cleared from the synaptic cleft through three mechanisms: enzymatic degradation (e.g., acetylcholinesterase breaking down acetylcholine), cellular reuptake by the presynaptic neuron or surrounding astrocytes, or simple diffusion away from the cleft.

Key Takeaway: Synaptic transmission converts an electrical signal (the action potential) into a chemical signal (neurotransmitter release), which is then converted back into an electrical signal (local potential) on the receiving cell.

Core Criteria for Neurotransmitters

• Synthesis Within the Neuron: The substance must be synthesized inside the presynaptic neuron, typically through enzymatic reactions involving precursor molecules.

• Storage in Vesicles: Once made, the chemical must be packaged and stored in synaptic vesicles within the presynaptic terminal, ready for action.

• Calcium-Dependent Release: The substance must be released from the terminal in response to presynaptic depolarization and the influx of calcium ions Ca2+.

• Specific Postsynaptic Receptors: Upon release, it must bind to specific receptor proteins on the postsynaptic membrane to exert a biological effect (either excitatory or inhibitory).

• Exogenous Mimicry: If the substance is applied experimentally from the outside (exogenously) to the synapse, it must produce the exact same physiological response as natural, endogenous release.

• Rapid Removal and Termination: There must be an active mechanism in place to clear or deactivate the chemical from the synaptic cleft quickly (via enzymatic degradation, cellular reuptake, or diffusion) to prevent continuous, unwanted signaling.

Key Takeaway: While neuromodulators can drift more widely and alter the general sensitivity of brain regions, classic neurotransmitters act swiftly and directly at targeted synapses to pass precise electrical-to-chemical messages.

Ionotropic Receptors (Ligand-Gated Ion Channels)

• Structure: These are fast, multi-subunit protein complexes that combine a neurotransmitter-binding site directly with an ion channel pore.

• Mechanism: When a neurotransmitter binds, the channel opens instantly, allowing specific ions (such as Na+, K+, or Cl-) to rush directly across the membrane.

• Speed and Duration: Extremely fast (operating in milliseconds) with a short-lived effect. They are ideal for rapid-fire communication like reflex arcs.

Key Takeaway: Ionotropic receptors provide rapid, digital-like on/off communication, whereas metabotropic receptors act more like an analog dimmer switch, modulating cellular activity and shaping broader neural states.

Metabotropic Receptors (G-Protein-Coupled Receptors)

• Structure: These are single protein chains that span the membrane and are not directly attached to an ion channel.

• Mechanism: Neurotransmitter binding activates an intracellular G-protein, which detaches and triggers a cascade of second messengers (such as cAMP or protein kinases) inside the cell. These messengers can indirectly open or close distant ion channels or even alter gene expression.

• Speed and Duration: Slower to onset (hundreds of milliseconds to minutes) but produce much longer-lasting, widespread metabolic and structural effects.

Key Takeaway: Ionotropic receptors provide rapid, digital-like on/off communication, whereas metabotropic receptors act more like an analog dimmer switch, modulating cellular activity and shaping broader neural states.

Sarcolemma

The specialized cell membrane of the muscle fiber. It maintains the resting membrane potential and is capable of propagating electrical action potentials just like a neuron.

Transverse Tubules (T-tubules)

Narrow, finger-like tunnels formed by the sarcolemma that dive deep into the cell. They ensure that an electrical action potential travels rapidly from the surface deep into the core of the fiber simultaneously.

Sarcoplasm

The cytoplasm of the muscle fiber. It contains a high concentration of glycogen (for energy storage) and myoglobin (an oxygen-binding protein similar to hemoglobin).

Sarcoplasmic Reticulum (SR)

A specialized network of smooth endoplasmic reticulum that wraps around every myofibril. Its primary job is to store, sequester, and release calcium ions Ca2+, which act as the molecular "on switch" for muscle contraction. Terminal cisternae are enlarged chambers of the SR that abut the T-tubules.

Myofibrils

ong, cylindrical organelle bundles that fill nearly 80% of the muscle fiber's volume. They give skeletal muscle its striated (striped) appearance.

Sarcomeres

The repeating, fundamental functional and contractile units of a myofibril, stretching from one Z-line to the next.

• Thin Filaments (Actin): Anchored to the Z-lines, containing regulatory proteins like troponin and tropomyosin.

• Thick Filaments (Myosin): Centered in the sarcomere, featuring heads that pull on the actin filaments during contraction.

Tropomyosin: The Physical Blockade

• What it is: A long, thread-like protein molecule that winds helically around the actin filament.

• Its Role at Rest: In a relaxed muscle, tropomyosin sits right over the myosin-binding sites on the actin chain. By physically blocking these sites, it prevents the myosin heads from attaching to actin, ensuring the muscle stays relaxed.

Tropomyosin acts as a safety gate blocking muscle contraction, and troponin acts as the lock that opens that gate only when calcium ions arrive.

Troponin: The Calcium Switch

• What it is: A small, globular protein complex anchored to both actin and tropomyosin. It consists of three specific subunits:

  • TnT: Binds to tropomyosin to position it correctly.

  • TnI: The inhibitory subunit that helps hold tropomyosin tightly over the binding sites.

  • TnC: The calcium-binding site.

Tropomyosin acts as a safety gate blocking muscle contraction, and troponin acts as the lock that opens that gate only when calcium ions arrive.

The Cross-Bridge Cycle (The Molecular Rowing Motion

The interaction between actin and myosin operates through a continuous, repeating cycle powered by ATP. This sequence is known as the cross-bridge cycle:

• 1. Cross-Bridge Formation (Binding): With the myosin-binding sites on actin now exposed by calcium, the high-energy myosin head binds firmly to actin, forming a cross-bridge.

• 2. The Power Stroke: Once attached, the myosin head releases its stored energy, pivots, and bends. This pulls the actin filament toward the center of the sarcomere (the M-line), generating tension and shortening the muscle. During this pivot, ADP and inorganic phosphate are released.

• 3. Detachment: A new molecule of ATP binds to the myosin head. This binding breaks the bond between myosin and actin, causing the myosin head to detach from the thin filament.

• 4. Cocking of the Myosin Head: The myosin head splits the newly bound ATP into ADP and Pi, using that released energy to "re-cock" or reset its position back to an upright, high-energy state, ready to bind to actin again further down the line.

This cycle repeats rapidly over and over, like a crew team pulling oars, as long as calcium and ATP are available.

SO Fibers (Slow Oxidative / Type I)

• Overview: Often called "slow-twitch" fibers, these are optimized for endurance and sustained, lower-power contractions.

• Metabolism: Entirely aerobic. They contain a high density of mitochondria, rich blood capillary networks, and high levels of myoglobin (an oxygen-storing protein that gives them a dark red color).

• Performance: They contract slowly and generate modest tension, but they are extremely resistant to fatigue, allowing them to work for hours without tiring.

• Example Activity: Maintaining posture or running a marathon.

FOG Fibers (Fast Oxidative-Glycolytic / Type IIa / often shortened to FO)

• Overview: Often referred to as "intermediate" or fast oxidative fibers, these act as the "switch-hitters" or bridge between endurance and explosive strength.

• Metabolism: They use a hybrid metabolic profile, combining aerobic respiration with anaerobic glycolysis. They have high concentrations of myoglobin and mitochondria, alongside good glycogen stores.

• Performance: They contract rapidly and generate high tension, with a moderate resistance to fatigue. (With specialized training, they can adapt to take on more oxidative or glycolytic traits).

• Example Activity: Middle-distance running (like an 800-meter race) or high-intensity circuit training.

FG Fibers (Fast Glycolytic / Type IIx)

• Overview: Known as "pure fast-twitch" or white fibers, these are built for short, maximum-intensity bursts of power.

• Metabolism: Strictly anaerobic. They have very few mitochondria or blood vessels, low myoglobin (making them paler in color), but massive reserves of stored glycogen and phosphocreatine.

• Performance: They contract at the fastest velocity and produce the greatest amount of raw physical force. However, they fatigue extremely quickly due to rapid lactic acid accumulation.

• Example Activity: A 100-meter sprint, a heavy 1-rep-max lift, or a sudden jump.

shaker muscle differs from standard skeletal muscle

The tail shaker muscle of a rattlesnake is one of the most extreme examples of muscular specialization in the animal kingdom. It can vibrate at astonishing frequencies—up to 90 Hz (90 contractions per second)—and maintain this pace continuously for hours without tiring.

Compared to standard skeletal muscle, which would tetanize (lock up in a continuous contraction) or fatigue almost instantly at such speeds, the rattlesnake's shaker muscle features distinct structural and physiological adaptations.

Bird Muscle Performance vs. Human Muscle

Feature	Humans	Hummingbirds	Migratory Birds
Primary Fuel Source	Mixed (Carbohydrates & Fats depending on intensity)	Exogenous Sugars (Glucose & Fructose)	Stored Fatty Acids (Lipids)
Aerobic Capacity	Moderate (optimized for terrestrial endurance/walking)	Extreme (highest known among vertebrates)	Extreme (optimized for continuous multi-day flight)
Mitochondrial Density	Moderate	Exceptionally High	Exceptionally High
Energy Storage Strategy	Modest glycogen & fat reserves	Relies on continuous nectar intake	Massive fat accumulation (up to 50%+ of body weight)

Key Takeaway: While human muscles are built for versatile terrestrial movement and fatigue relatively quickly under high-intensity stress, avian muscles are hyper-specialized biochemical engines—burning raw nectar for instant power in hummingbirds, or running on ultra-dense fat stores for multi-day endurance in migratory species.

Open vs. Closed Circulatory Systems

Open Circulatory Systems

In an open circulatory system, the blood (technically called hemolymph) is not enclosed in a continuous loop of blood vessels.

Closed Circulatory Systems

In a closed circulatory system, blood is completely confined to a continuous, closed network of vessels (arteries, capillaries, and veins) at all times.

The Flow of Blood Through the Mammalian Heart

1. Entering the Right Side: Deoxygenated blood from the body returns via the superior and inferior vena cava and empties into the right atrium.

2. Into the Right Ventricle: Blood passes through the tricuspid valve into the right ventricle.

3. To the Lungs: The right ventricle contracts, pushing blood through the pulmonary semilunar valve into the pulmonary trunk and pulmonary arteries, which carry it to the lungs to pick up oxygen and release carbon dioxide.

4. Returning to the Left Side: Newly oxygenated blood returns from the lungs via the pulmonary veins and enters the left atrium.

5. Into the Left Ventricle: Blood flows through the bicuspid (mitral) valve into the left ventricle.

6. To the Body: The powerful left ventricle contracts, forcing blood through the aortic semilunar valve into the aorta, which distributes it to the entire body.

Calculating Cardiac Output

Cardiac output (CO) is the total volume of blood pumped by each ventricle per minute. It is a key indicator of how effectively the cardiovascular system is meeting the body's metabolic demands.

The Formula

$$\text{CO} = \text{HR} \times \text{SV}$$

• $\text{HR}$ (Heart Rate): The number of heartbeats per minute (typically around 70 beats/min at rest).

• $\text{SV}$ (Stroke Volume): The volume of blood pumped out by a single ventricle with each heartbeat (typically around 70 mL/beat at rest).

Example Calculation (Resting State)

$$\text{CO} = 70 \text{ beats/min} \times 70 \text{ mL/beat} = 4,900 \text{ mL/min}$$