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[Abstract Title]. - Society for Neuroscience

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Support: NIH grant AA14973<br />

<strong>Title</strong>: Ethanol increases spontaneous action potential firing frequency of cerebellar Golgi<br />

neurons via membrane depolarization<br />

Authors: *P. BOTTA, C. F. VALENZUELA;<br />

Neurosci, Univ. New Mexico HSC, Albuquerque, NM<br />

<strong>Abstract</strong>: Cerebellar Golgi neurons (GNs) are spontaneously firing GABAergic interneurons<br />

situated in the cerebellar granule layer. These neurons play a pivotal role in filtering mossy fiberdependent<br />

excitation of granule cells. We have previously shown that acute ethanol (EtOH)<br />

exposure enhances GN spontaneous action potential firing (Carta et al. J Neurosci. 24:3746-51,<br />

2004) and that this effect can be observed in presence of antagonists of ionotropic glutamate,<br />

mGluR2, GABA-A, GABA-B and glycine receptors (Program No. 909.10. <strong>Neuroscience</strong><br />

Meeting Planner. San Diego, CA: SFN 2007). These findings indicate that EtOH enhances GN<br />

firing by affecting intrinsic conductances rather than changing synaptic inputs. The goal of this<br />

study was to further characterize the action of EtOH at GNs. Parasagittal cerebellar vermis slices<br />

(200 micrometer-thick) were prepared from 23-25 day-old male Sprague-Dawley rats. GN firing<br />

was recorded using the per<strong>for</strong>ated-patch current-clamp configuration (Iinject = 0 pA) at 32 o C. The<br />

artificial cerebrospinal fluid contained antagonists of the above-mentioned neurotransmitter<br />

receptors. EtOH (40 mM) reversibly increased the spontaneous action potential firing frequency<br />

(ctrl = 3.9 ± 0.9 Hz; EtOH = 4.6 ± 0.9 Hz; n = 9; p

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