Neuronal Signaling: Action Potentials and synaptic integration

Na+ influx during an action potential

generates local depolarizing currents

Voltage-gated K+ channels

contribute to repolarization of the previously activated membrane

Direction of propagation

The refractory period prevents immediate re-esxcitation of the preceding membrane region, promoting forward propagation toward the axon terminal

Saltator conduction

Action potentials are regenerated at successive nodes of Ranvier rather tahn continuously along the axonal membrane

Larger axon diameter

Decreases axial resistance (Ri), allowing current to spread more easily

Thicker myelin sheath

increases membrane resistance (Rm) and decreases membrane capacitance, reducing current leakage and accelerating deporlarization

Internode length

Longer internodes can increase conduction speed up to an optimal distance; excessively long internodes may impair conduction

Strychnine

-blocks postsynaptic glycine receptors; prevents inhibitory signaling

-Receptors cannot respond to glycine

-causes severe muscle spasms and stimulus-triggered convulsions

Tetanus

-Caused by clostridium tetani, which produces tetanospasmin

-toxin blocks the release of inhibitory neurotransmitters (GABA and glycine) from inhibitory neurons; blocks presynaptic release

-results in sustained muscle rigidity and painful spasm

ESPSs

Depolarize the membrane, increasing the likelihood of an action potential

IPSPs

Reduce neuronal excitability, often through hyperpolarization