Voltage-gated Na channels

Figure 8. A schematic for the toxin binding sites on the voltage-gated Na channel. Toxin-free open and closed conformations are drawn at the left and center. Separate sites are depicted within the membrane for activators such as BTX, VTD (A), and brevetoxin (B) these are coupled to each other and to the a-peptide toxin site (a), which is kinetically linked to the -peptide toxin site (P see ref. 20). Near the outer opening of the pore is a site (G) for STX and TTX which is affected by binding at site A and which can modify inactivation gating.

Na+ channels are primarily a single family. There are ten human genes encoding voltage-gated Na+ channels (Table 6-2), and at least nine of the ten encode members of a single family (Navl.l-1.9) [38], These Na+ channels are expressed in different tissues and cells but their function is almost always to initiate action potentials in response to membrane depolarization. 

Phase 2 This portion of the curve demonstrates the rapid rise in membrane potential to a peak of + 30 mV as voltage-gated Na+ channels allow rapid Na+ entry into the cell. 

In response to stimulation, the neuronal membrane becomes more permeable to Na+, which is drawn into the neuron down the electrical and chemical diffusion gradients. This depolarizes the neuron and makes the membrane further permeable to Na+. If sufficiently depolarized, a threshold of excitation is reached (approximately -60 mV), where voltage-gated Na+ channels open and the membrane becomes highly permeable... 

The process starts with the opening of voltage-gated Na" channels (see p. 222). Due to their high equilibrium potential (see A), Na" ions flow into the cell and reverse the local membrane potential (depolarization). 

The Clinicah-Molecular Interface Epilepsy and Voltage-Gated Na Channels... 

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