Pergamon Neuropharmoco/og~ Vol. 33. No. IO. pp. I203- 1209. I994 Copyright (0 1994 Elsevier Science Ltd Printed in Great Britain. All rights reserved ~28-3908/94 S7.00 + 0.00 Effect of Chronic Treatment with Ethanol and Withdrawal of Ethanol on Binding of [3H]SCH23390 to Dl Dopamine Receptor in Rat Visual Cortex and Hippocampus. An Autoradiographic Study E. GILMARTiN,’ A. FERNANDEZ-BRIERA,2 A. FERNANDEZ-LOPEZ3 and P. CALVO’* ~~epurtme~t 5f ~i5~ilen~istr~~ and ~o~ecufar Bioiogy, University of Lecin, 24007 Leh, Spain, ~DeFartmenI of Fundamental Biology, University of Ego, 32004 Uurense, Spain and ‘Department of Cellular Biolog>f and Anatomy, Univeristy of Lebn, 24007 Ledn, Spain (Accepted 14 June 1394) Summary-Male Wistar rats, treated with ethanolfor 8 weeks and pair-control animals, wereused to study the effectsof chronic treatment with ethanol,and withdrawalof ethanolfor 24 and 48 hr on [‘H]SCH23390 binding. The visual cortex (Laminae III-IV and Lamina VI), the superficial grey layer of the superior colliculus, and the molecular layer of the dentate gyrusof the hippocampus werethe cerebral areas analysed. Non significant changes were observed in hippocampus and Laminae III-IV of the visual cortex after treatments with alcohol.More interesting results were obtained from Lamina VI, where the chronictreatment with ethanol did not modify the binding of [‘HjSCH23390, whereas the withdrawal of ethanol produced a statisticallysignificant increase in binding values. In addition, superficial greylayer of the superior colliculus showed a significantincrease in binding values between 48 hr withdrawal and ethanol treated groups. The results herein reported suggest that some structures involved in visual functionsare relatedto responses of adaptation to ethanol. Keywords-D-I dopamine receptor,visual cortex, hippocampus, ethanol, withdrawal, autoradiography. Chronic abuse of ethanol is associated with a variety of impairments of brain function. Visual (hallucinations), motor (convulsions or rumf;ts, status epilepticus) and memory dysfunctions appear as the most typical symp- toms linked to intoxication with ethanol and withdrawal (Parson et al., 1987). Some of these disorders are accentuated during withdrawal of alcohol, and appear to be reversible during sobriety. Ethanol produces multiple biophysical and biochemi- cal actions on synaptosomal membranes (Guerri and Grisolia, 1983; Hoffman and Tabakoff, 1985; Polokoff et at., 1985; Taraschi et al., 1985; Hitzemann et al., 1986; Hock-and Taraschi, 1988), all of them tending to reduce neuronal excitability and neurotransmitter release. It has not yet been definitively established whether a specific receptor neurochemical disturbance is induced by ethanol. Currently, however, the implication of several central neurotransmitter systems in the response to ethanol exposure receives wide support (Ollat et al., *To whom correspondence shouldbe addressed. 1988).In this sense, a cerebellar y-aminobutyric receptor (GABA,) has been described as a hypothetical mediator of several alcohol motor disturbances (Liiddens et al., 1990). In addition to the GABAergic system, mesocorti- cal and mesolimbic dopaminergic pathways also seem to be involved in responses linked to ethanol toxicity (Myers, 1989; McBride et al., 1990; Koob, 1992a, b). These systems mediate the reinforcing properties of drug. abuse (Esposito et al., 1984) and the voluntary drinking of ethanol (Myers, 1989). Therefore, .brain dopamine (DA) neurons could act as a target for several drugs involved in promoting the drinking of ethanol, or in mediating the suppression of ethanol consumption (Myers and Privette, 1989; Privette and Myers, 1989). Likewise, dopaminergic receptors show several alterations in their binding parameters after treatment with ethanol. However, the available data concerning this topic are controversial.’ Results from different authors have addressed different numbers of binding sites, as well as receptor affinity (Leslie et al., 1986; Hruska, 1988; Lucchi et al., 1988; Russell et al., 1988). 1203