Practice Questions

Drugs like local anesthetics (e.g., lidocaine) or neurotoxins (e.g., tetrodotoxin) block voltage-gated Na⁺ channels, preventing the massive sodium influx required to generate and propagate an action potential.

The threshold potential (usually around -55 mV) is the tipping point where voltage-gated Na⁺ channels open en masse, triggering the explosive positive feedback loop of an action potential.

Following peak depolarization, voltage-gated K⁺ channels open and K⁺ rushes out of the cell down its electrochemical gradient, restoring the negative internal charge during repolarization.

Because a neuron cannot fire another action potential during the absolute refractory period regardless of stimulus strength, this period sets a strict upper limit on how frequently the neuron can fire.

Electrical synapses do not use neurotransmitters; instead, they utilize gap junctions (connexons) that physically connect the cytoplasm of adjacent cells, allowing instantaneous, bidirectional current flow.

Neuromuscular junctions (motor end plates) are the highly specialized synapses where motor neurons release acetylcholine to trigger skeletal muscle contraction.

Norepinephrine (and epinephrine from the adrenal medulla) acts on sympathetic target organs to mediate the 'fight or flight' stress responses, such as increased heart rate and bronchodilation.

Depolarization refers to any shift in membrane potential toward a less negative (or more positive) value, generally caused by the influx of positive ions like sodium.

Synaptic fatigue occurs when the rate of neurotransmitter release exceeds the rate of its synthesis and recycling, causing a temporary failure of synaptic transmission despite incoming action potentials.

Conduction velocity is positively correlated with both axon diameter (reducing internal electrical resistance) and the presence of myelination (allowing fast saltatory conduction).