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[Abstract Title]. - Society for Neuroscience

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Support: This research was supported by a grant (#R13-2002-005-04001-0) from MRC <strong>for</strong> Cell<br />

Death Disease Research Center Program funded by the Ministry of Science and Technology of<br />

Republic of Korea.<br />

<strong>Title</strong>: Involvement of cannabinoid receptors on ethanol induced depression of corticostriatal<br />

synaptic transmission<br />

Authors: *H. CHO 1,3 , K. KIM 1,3 , S. JEUN 1,3 , S. CHOI 1,3 , S. HAHN 2,3 , K.-W. SUNG 1,3 ;<br />

1 Dept. of Pharmacol., 2 Dept. of Physiol., The Catholic Univ. of Korea, Seoul, Republic of Korea;<br />

3 MRC <strong>for</strong> Death Dis. Center, The Catholic Univ. of Korea, Seoul, Republic of Korea<br />

<strong>Abstract</strong>: It has been implicated that the dorsal striatum plays a key role in habit <strong>for</strong>mation, and<br />

compulsive alcohol or drug taking and seeking behavior. The dorsal striatum receives<br />

glutamatergic afferent inputs from the cortex and other brain areas, and these glutamatergic<br />

synaptic transmissions may play an important role in behavioral actions related to habit<br />

<strong>for</strong>mation. The purpose of this study was to examine the role of endogenous cannabinoid<br />

systems on ethanol induced depression of synaptic transmission in the rat dorsal striatum.<br />

Acute treatment of ethanol (10 - 150 mM) <strong>for</strong> 10 minute decreased the corticostriatal excitatory<br />

postsynaptic currents (EPSCs) in a dose-dependent manner. In the presence of AM 251 (5 κM), a<br />

selective cannabinoid 1 (CB1) receptor antagonist, the inhibition of corticostriatal EPSCs by<br />

ethanol was significantly attenuated. However, AM 404 (2 κM), an anandamide transport<br />

inhibitor, had no significant effect on the inhibition of corticostriatal EPSCs by ethanol. These<br />

results suggest that ethanol may not relate with endocannabinoid release, but might act directly<br />

on CB1 receptors. To further clarify our hypothesis, brain slices were pre-treated with WIN<br />

55,212-2 (1 κM), a CB1 receptor agonist, and ethanol did not inhibit corticostriatal EPSCs under<br />

this condition. This data indicates that when CB1 receptors are previously activated by its<br />

agonist, the effect of ethanol on corticostriatal EPSCs is blunted.<br />

Taken together, our results suggest that CB1 receptors are involved in the inhibition of<br />

corticostriatal synaptic transmission by ethanol and might be a direct target <strong>for</strong> ethanol.<br />

Disclosures: H. Cho, None; K. Kim, None; S. Jeun, None; S. Choi, None; S. Hahn, None; K.<br />

Sung, None.<br />

Poster<br />

274. Basal Ganglia: Transmitters and Neuromodulation II<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 274.8/JJ3<br />

Topic: D.15.a. Transmitters and neuromodulation

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