An action potential at a given stretch of a neuron's axon does not re-stimulate the neighboring region that was previously depolarized because in that region . Select one: O A. the voltage-gated K* channels are blocked by inactivation loops. B. there is an imbalance in the Nat and K* concentrations between the cell and the extracellular fluid. O C. the voltage-gated Na* channels are closed but not inactivated. O D. the voltage-gated Na* channels are open. O E. the voltage-gated sodium channels are inactivated.

Which of the following allows the cell to recover from hyperpolarization during an action potential?   A. Stimulus gated sodium channels B. voltage gated sodium channels C. voltage gated potassium channels D. sodium/potassium pump

Place the following events in chronological order from 1-8: Nat enters the cell, and depolarization occurs to approximately +30 mV. The voltage across the cell membrane is -70 mV, the resting membrane potential. Upon reaching the peak of the action potential, the VG Nat channels are inactivated by the closing of their inactivation gate and the activation gate of each VG K channel opens. VG K channels close by the closing of their activation gate, and the resting membrane potential is gradually restored. An excitatory post-synaptic potential depolarizes the membrane to threshold and the activation gate of VG Nat channels open. Upon returning to the resting membrane potential, VG Na channels are reset by opening of the inactivation gate and the closing of the activation gate. VG K+ channels are slow to close, resulting in an excess of K* efflux and hyperpolarization. Depolarization occurs as K+ flows out of the cell.

If TTX (tetrodotoxin) selectively binds voltage gated Na+ channels, and you tag TTX with a fluorescent marker and then you use it as a probe to label voltage-gated Na+ channels in various neurons in the CNS, would you expect the pattern of fluorescence to be different between myelinated and nonmyelinated axons? If so, how? If not, why not?