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[Abstract Title]. - Society for Neuroscience

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co-variation in alcohol and sweet intake remain to be determined, recent findings indicate that<br />

sweet taste substrates are involved in alcohol intake and preference in C57BL/6J mice (Brasser et<br />

al., 2006; Blednov et al., 2008), suggesting that the processing of alcohol‟s sweet taste<br />

component may be influencing its ingestion. The present study compared self-initiated<br />

orosensory responding to alcohol and prototypic sweet, bitter, and oral trigeminal stimuli among<br />

P, NP, and non-selected Wistar rat lines to assess the relationship between genetically-influenced<br />

alcohol preference and orosensory sensitivity to these stimuli. Rats were tested <strong>for</strong> immediate<br />

short-term lick responses to alcohol (3, 5, 10, 15, 25, 40%), sucrose (0.01, 0.03, 0.06, 0.1, 0.3, 1<br />

M), quinine (0.01, 0.03, 0.1, 0.3, 1, 3 mM) and capsaicin (0.003, 0.01, 0.03, 0.1, 0.3, 1 mM) in a<br />

brief-access paradigm designed to index orosensory-mediated behavior while minimizing the<br />

influence of post-ingestive factors. P rats displayed elevated short-term lick responses to both<br />

alcohol and sucrose relative to NP and Wistar lines across a wide range of concentrations of each<br />

stimulus. There were no line differences in orosensory avoidance of capsaicin, and Wistar rats<br />

showed a moderately greater aversion to quinine compared to P and NP lines, which did not<br />

differ in quinine sensitivity. These data indicate that genetic selection <strong>for</strong> alcohol preference in P<br />

rats is associated with enhanced sensory responses to alcohol and sweet stimuli, consistent with<br />

prior evidence that differences in sweet taste processing may contribute to differences in alcohol<br />

intake.<br />

Disclosures: B.C. Silbaugh, None; M. Ketchum, None; S.M. Brasser, None.<br />

Poster<br />

257. Alcohol Intake and Preference<br />

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

Program#/Poster#: 257.10/Z27<br />

Topic: C.16.a. Alcohol<br />

Support: NIH-NIAAA R56AA012386 GDF<br />

<strong>Title</strong>: Do GABAARs containing alpha 2/3/5 subunits contribute to synaptic dysfunction after<br />

early postnatal binge-ethanol exposure in medial septum / diagonal band (MS/DB) neurons?<br />

Authors: *G. D. FRYE, H. WANG;<br />

Neurosci & Exptl. Therap, Texas A&M Univ. Syst Hlth. Sci. C, College Station, TX<br />

<strong>Abstract</strong>: „Binge-like‟ ethanol exposure on PD 4-9 exaggerates allopregnanolone and blunts<br />

zolpidem potentiation of GABAA receptor (GABAARs) mediated miniature postsynaptic<br />

current (mPSC) decay kinetics in MS/DB neurons in brain slices prepared on PD 11-16 (Wang<br />

and Frye SfN Abst, 34: 329.2, 2006; Wang et al., EB Abst, 1439:1127.12 2008). This treatment

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