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The ad hoc genetic correlation between ethanol sensitivity and learning mechanisms in Drosophila could overemphasize a common process supporting both behaviors. To challenge directly the hypothesis that these mechanisms are singular, we examined the learning phenotypes of 10 new strains. Five of these have increased ethanol sensitivity, and the other 5 do not. We tested place and olfactory memory in each of these lines and found two new learning mutations. In one case, altering the tribbles gene, flies have a significantly reduced place memory, elevated olfactory memory, and normal ethanol response. In the second case, mutation of a gene we name ethanol sensitive with low memory (elm), place memory was not altered, olfactory memory was sharply reduced, and sensitivity to ethanol was increased. In sum, however, we found no overall correlation between ethanol sensitivity and place memory in the 10 lines tested. Furthermore, there was a weak but nonsignificant correlation between ethanol sensitivity and olfactory learning. Thus, mutations that alter learning and sensitivity to ethanol can occur independently of each other and this implies that the set of genes important for both ethanol sensitivity and learning is likely a subset of the genes important for either process.

We examined the interaction of ethanol with the [gamma]-aminobutyric acid (GABA)ergic system in neurons of slices of the rat central amygdala nucleus (CEA), a brain region thought to be critical for the reinforcing effects of ethanol. Brief superfusion of 11-66 mM ethanol significantly increased GABA type A (GAB[A.sub.A]) receptor-mediated inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) in most CeA neurons, with a low apparent E[C.sub.50] of 20 mM. Acute superfusion of 44 mM ethanol increased the amplitude of evoked GABAA IPSPs and IPSCs in 70% of CeA neurons. The ethanol enhancement of IPSPs and IPSCs occurred to a similar extent in the presence of the GABA type B (GAB[A.sub.B]) receptor antagonist CGP 55845A, suggesting that this receptor is not involved in the ethanol effect on CeA neurons. Ethanol superfusion also decreased paired-pulse facilitation of evoked GAB[A.sub.A] IPSPs and IPSCs and always increased the frequency and sometimes the amplitude of spontaneous miniature GAB[A.sub.A] IPSCs as well as responses to local GABA application, indicating both presynaptic and postsynaptic sites of action for ethanol. Thus, the CeA is the first brain region to reveal, without conditional treatments such as GAB[A.sub.B] antagonists, consistent, low-dose ethanol enhancement of GABAergic transmission at both pre- and postsynaptic sites. These findings add further support to the contention that the ethanoI-GABA interaction in CeA plays an important role in the reinforcing effects of ethanol. alcohol | GABA IPSP/Cs | paired-pulse facilitation | miniature synaptic current | electrophysiology

Single-cell extracellular recordings from dopaminergic neurons of the ventrotegmental region, coupled with antidromic identification from the nucleus accumbens, and microdialysis technique studies in the muscles accumbens were used to examine the activity of the mesolimbic dopaminergic system in rats withdrawn from chronic ethanol administration. The reduction of mesolimbic dopaminergic activity in the ethanol withdrawal syndrome is induced by the sudden stoppage of chronic ethanol administration.

Cells of Schizosaccharomyces pombe and Saccharomyces cerevisiae reveal an intracellular catalase activity and an intracellular cryptic activity. Both the cells were found to catalase into the medium. A study of the relationship between the two types of activities shows that both are influenced by prolonged aeration and are affected by the membrane permeability characteristic of the patent catalase activity. The catalase activities of substrates influencing catabolite repression, in activation or energizing cells, affect membrane permeability.