Final answer:
While ethanol can affect neurotransmitter systems that ultimately influence Ca2+ dynamics in neurons, the specific action of ethanol on voltage-gated Ca2+ channels is not clearly indicated in the provided literature. Ethanol is known to interact with other receptors and channels that can indirectly affect calcium signaling.
Step-by-step explanation:
Alcohol's interaction with ion channels is complex, but the literature provided does not explicitly discuss ethanol's effect on voltage-gated Ca2+ channels. However, we know that ethanol can alter neuronal communication and may interact indirectly with Ca2+ channels through modulation of other receptors and ion channels.
For example, ethanol can block NMDA receptors, which are known to permit Ca2+ influx once the inhibitory Mg2+ is removed following depolarization.
The dysfunction of ATPases after ischemic events can impair neurons' ability to maintain low intracellular calcium concentrations, leading to activation of voltage-dependent calcium channels and potentially contributing to excitotic damage.
In cases like stroke, an upregulation of calcium-permeable AMPA receptors without the GluA2 subunit has been observed, potentially increasing Ca2+ entry. In this scenario, the role of ethanol remains uncertain without specific evidence linking it to direct stimulation of voltage-gated Ca2+ channels.