depolarization inducing an open conformation of the channel, the initial phase is caused by a rapid increase in the permeability of Na+ through voltage-sensitive Na+ channels. The result is inward movement of Na+ and a rapid depolarization from the resting potential, which continues to a positive overshoot. The second phase results from the rapid inactivation of the Na+ channel and the delayed opening of a K+ channel, which permits outward movement of K+ to terminate the depolarization.

The transmembrane ionic currents produce local circuit currents around the axon. As a result, adjacent resting channels in the axon are activated, exciting an adjacent portion of the axonal membrane and causing propagation of the AP without decrement along the axon. The region that has undergone depolarization remains momentarily in a refractory state. In myelinated fibers, permeability changes occur only at the nodes of Ranvier, thus causing a rapidly progressing type of jumping, or saltatory, conduction. The puffer fish poison tetrodotoxin and a congener found in shellfish, saxitoxin, selectively block axonal conduction by blocking the voltage-sensitive Na+ channel and preventing the increase in Na+ permeability associated with the rising phase of the AP. In contrast, batrachotoxin, a potent steroidal alkaloid secreted by a South American frog, produces paralysis through a selective increase in permeability of the Na+ channel, which induces a persistent depolarization. Scorpion toxins are peptides that cause persistent depolarization by inhibiting the inactivation process. For more details on Na+ and Ca2+ channels, see Chapters 14, 31, and 34.

JUNCTIONAL TRANSMISSION The arrival of the AP at the axonal terminals initiates a series of events that trigger transmission of an excitatory or inhibitory impulse across the synapse or neuroeffector junction (see Figure 6-2):

1. Release of stored neurotransmitter; prejunctional regulation. Nonpeptide (small molecule) neurotransmitters are largely synthesized in the axonal terminals and stored there in synaptic

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