Module 2 Study Guide

Its job is to change voltage on purpose. Precise control over which ions cross, when, and how fast takes many channel types: leak channels to set rest, ligand-gated channels for graded potentials, voltage-gated channels for action potentials. A non-excitable membrane only needs a steady potential. (M2 slide 3)

Depolarization (up): positive ions enter, as Na⁺ influx. Hyperpolarization (down below baseline): positive ions leave or negative ions enter, as K⁺ efflux or Cl⁻ influx. Repolarization: return to baseline, typically K⁺ efflux after a depolarization. (M2 slide 3)

Pain receptors in the fingertip (somatic receptors) → sensory, afferent neurons → CNS (spinal cord and brain) integrates → somatic motor, efferent neurons → skeletal muscle (effector) pulls the hand away. (M2 slide 7)

Both are structures sensitive to their environment. Module 1: a membrane protein that binds a ligand, such as a G protein-coupled receptor binding norepinephrine. Module 2: a specialized cell that turns a stimulus into an electrical signal, such as a thermoreceptor or baroreceptor. (M2 slide 8)

Na⁺: chemical in (more outside), electrical in (positive ion drawn to the negative inside), electrochemical strongly in. K⁺: chemical out (more inside), electrical in, electrochemical out because the chemical gradient is slightly stronger. (M2 slide 12)

E_K becomes less negative. K⁺ dominates resting conductance, so resting potential moves the same way: less negative, closer to threshold, more excitable. (M2 slides 14, 23)

It assumes the membrane is permeable to only one ion. Real membranes are permeable to several ions at once. Nernst potentials are still useful because they show which way each ion wants to move at a given V_m, and the chord conductance and Goldman equations are built from them. (M2 slide 15)

Driving force is V_m − E_Cl = −70 − (−47) = −23 mV. The inside is more negative than chloride’s equilibrium, so electrical repulsion of the negative ion outweighs its inward chemical gradient and Cl⁻ moves out. The lecture’s “more negative than E_X means it flows in” rule is written for cations; flip it for an anion. (M2 slide 16)

K⁺ leak channels: many, always open, steady K⁺ loss makes the inside negative. The main contributor. Na⁺ leak channels: few, a small trickle in that keeps V_m slightly above E_K. Na⁺-K⁺ pump: restores the gradients and, being electrogenic (3 out, 2 in), adds a little negativity. (M2 slide 22)

Each term is weighted by that ion’s share of total conductance, and at rest most open channels are K⁺ leak channels, so K⁺'s weight is about 0.70. If g_Na matched g_K, the two weights would be equal and V_m would land between E_K and E_Na: in the Assignment 2 neuron, about −21 mV, a large depolarization. (M2 slide 23)

Spatial summation of an EPSP and an IPSP. If they are equal in size they cancel and V_m barely changes; otherwise the net change is their sum (for +4 and −5 mV, −1 mV). (M2 slides 30, 32)

Graded potentials decay with distance because nothing refreshes them. A signal far out on a dendrite has more membrane to cross before reaching the axon hillock, so it arrives smaller and is less likely to meet threshold. (M2 slide 31)

Spatial: several synapses fire at the same time. Temporal: one synapse fires repeatedly before earlier potentials decay. Both together: two excitatory terminals each firing in rapid bursts, as in panel 4 of slide 32 (A A B B), which reaches threshold. (M2 slide 32)

Rest: both closed, Na⁺ channels resting and ready. Threshold: Na⁺ channels begin opening, K⁺ still closed. Depolarization: many Na⁺ open, K⁺ closed. Peak (+30 mV): Na⁺ inactivating, K⁺ finally opening. Repolarization and hyperpolarization: Na⁺ inactivated then resetting, K⁺ open then slowly closing. (M2 slide 38)

Voltage-gated K⁺ channels are slow to close. K⁺ keeps leaving after V_m reaches resting, carrying it below −70 mV until the channels close. (M2 slides 38–39)

At the peak, Na⁺ channels close with the activation gate open and the inactivation gate closed. In that state they cannot open again whatever the voltage or stimulus strength. Only when they reset to resting and ready (activation closed, inactivation open) can a new action potential start. (M2 slides 38–39)

Na⁺ spreading from an active patch reaches both neighbors, but the patch behind is still refractory and cannot fire. Only the patch ahead can, so the signal moves away from the axon hillock. (M2 slide 40)

Velocity falls sharply. Without myelin, membrane resistance drops, current leaks out, the length constant shrinks, and the action potential must regenerate at every patch of membrane. Voltage-gated channels are concentrated at the nodes, so a stripped internode may fail to conduct at all. (M2 slides 41–42)

Thick and myelinated fastest, then thin and myelinated, then thick and unmyelinated, assuming the thin axon is above about 1 µm where myelin helps and temperature is equal. Myelin gives the largest gain (10–150 against 0.5–2 m/s); diameter adds to it. (M2 slides 41–42)

The action potential only opens voltage-gated Ca²⁺ channels at the terminal. Ca²⁺ entry is the signal for vesicles to undergo exocytosis. Block the channels and the electrical signal never becomes a chemical one, so nothing reaches the next cell. (M2 slide 43)