The entry of calcium into a cell triggers many biochemical and biophysical actions (113, 114). This major second-messenger effect of calcium has been clearly linked to the regulation of neuronal excitability and cell metabolism (109, 114, 115). Thus, controlling calcium entry into the cell is the first major step in regulating the effect of calcium as a second messenger.
Depolarization-dependent action potentials are typically mediated by large sodium currents into the cell. Calcium simultaneously enters the cell during depolarization. Recently, the importance of this calcium entry during action potential generation has been more clearly understood. Accumulation of increased concentrations of calcium within a neuron is related to SRF of neurons, which can occur in vitro or during epileptic activity. Calcium entry is also regulated by specific excitatory amino acid receptors. This type of calcium channel is opened or closed in response to binding of excitatory amino acids (EAA) to specific calcium channel-linked receptors. The ability of these channels to produce tonic, long-lasting excitability changes in hippocampal neurons and in other cortical neurons has implications for long-term potentiation, memory, and excitability.
In conceptualizing the role of calcium in neuronal excitability and anticonvulsant drug action, one must consider both voltage-regulated and excitatory amino acid-modulated calcium channels. The regulation of calcium channels, like the regulation of the chloride channel, by the benzodiazepines, barbiturates, and convulsant drugs may play an important role in modifying neuronal excitability.
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