The septohippocampal system has been implicated in the cognitive deficits associated with ethanol consumption, but the cellular basis of ethanol action awaits full elucidation. In the MS/DB, a muscarinic tone, reflective of firing activity of resident cholinergic neurons, regulates that of their non-cholinergic, putatively GABAergic, counterparts.
Here we tested the hypothesis that ethanol alters this muscarinic tone.
The spontaneous firing activity of cholinergic and non-cholinergic MS/DB neurons were monitored in acute MS/DB slices from C57Bl/6 mice.
Exposing the entire slice to ethanol increased firing in both cholinergic and non-cholinergic neurons. However, applying ethanol focally to individual MS/DB neurons increased firing only in cholinergic neurons. The differential outcome suggested different mechanisms of ethanol action on cholinergic and non-cholinergic neurons. Indeed, with bath-perfused ethanol, the muscarinic antagonist methyl scopolamine prevented the increase in firing in non-cholinergic, but not cholinergic, MS/DB neurons.
Thus, the effect on non-cholinergic neuronal firing was secondary to ethanol's direct action of acutely increasing muscarinic tone.
We propose that the acute ethanol-induced elevation of muscarinic tone in the MS/DB contributes to the altered net flow of neuronal activity in the septohippocampal system that underlies compromised cognitive function.
Request Reprint E-Mail: hermes.yeh@dartmouth.edu
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