Neuroscience 2005 Abstract
| Presentation Number: | 916.6 |
|---|---|
| Abstract Title: | Finasteride treatment partially prevents loss of zolpidem potentiation of GABAergic miniature postsynaptic currents in septal cultures after binge ethanol exposure. |
| Authors: |
Wang, H.*1
; Mieckowski, A. N.1
; Frye, G. D.1
1Dept Med Pharmacol & Toxicol, Texas A&M Univ. Syst. Health Sci. Ctr., Col. of Medicine, College Station, TX |
| Primary Theme and Topics |
Disorders of the Nervous System - Addiction and Drugs of Abuse -- Alcohol |
| Secondary Theme and Topics | Neural Excitability, Synapses, and Glia: Cellular Mechanisms<br />- Ligand-Gated Ion Channels<br />-- GABAa receptors: Physiology |
| Session: |
916. Alcohol: Effects on Development Poster |
| Presentation Time: | Wednesday, November 16, 2005 9:00 AM-10:00 AM |
| Location: | Washington Convention Center - Hall A-C, Board # VV15 |
| Keywords: | FETAL ALCOHOL SYNDROME, GABA RECEPTOR, ALCOHOL, SYNAPTOGENESIS |
Binge Ethanol exposure (DIV 6-11) consistently prolongs GABAA receptor (GABAAR)-mediated miniature postsynaptic current (mPSC) decay kinetics (DuBois et al., Dev.Br.Res. 152:199-212, 2004) and blunts potentiation by zolpidem, a positive modulator of *alpha*1 subunit-containing GABAARs (DuBois & Frye, SfN Abst. 33:108.1, 2003) on DIV 13-17 in rat septal neurons cultured on embryonic day 20. Previous studies showed that finasteride, a 5*alpha*-reductase inhibitor, can partially reverse some effects of ethanol (Morrow et al., Alc.Clin.Exp.Res. 23:1933-1940, 1999), including prolonged GABAergic mPSC decay caused by Binge Ethanol exposure (Mieckowski et al., SfN Abst. 34:913.8, 2004). The present study examined whether finasteride could prevent ethanol-induced blunting of zolpidem potentiation of GABAergic mPSC decay. Pretreatment with finasteride (1 *mu*M, on DIV 5 remaining in the media thru DIV 11) restored the potentiating action of acutely applied zolpidem (1 or 10 *mu*M) on DIV 13-18 in neurons receiving Binge Ethanol exposure (DIV 6-11). Surprisingly, finasteride pretreatment alone (DIV 5-11) when compared to DMSO (~0.1% vehicle control) treated cultures, blunted zolpidem potentiation of mPSC decay on DIV 11-16, similarly to Binge Ethanol exposure alone. These results suggest that Binge Ethanol exposure in developing septal neurons delays synaptic incorporation of *alpha*1 subunit-containing GABAARs, an action that finasteride pretreatment may prevent. In addition the data point to a possible role of 5*alpha*-reduced neurosteroid formation in the action of ethanol as well as in the development and maturation of synaptic GABAARs.
Supported by Supported in part by NIH AA12386 (GDF) & T32 MH65728 (ANM)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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