title: Increases in non-N-methyl-D-aspartate glutamatergic transmission, but no change in gamma-aminobutyric acidB transmission, in CA1 neurons during withdrawal from in vivo chronic ethanol treatment.
abstract: Evoked fast excitatory postsynaptic potentials and slow inhibitory postsynaptic potentials were measured in mouse CA1 neurons in hippocampal slices after chronic ethanol treatment in vivo. Intracellular recordings were made 2, 4 and 6 hr after ethanol withdrawal, i.e., after the beginning of slice preparation. The resting membrane potentials were standardized to -60 mV by using constant current injection. The fast excitatory postsynaptic potentials were isolated by adding DL-2-amino-5-phosphonopentanoic acid, bicuculline and nitrendipine to the bathing solution and injecting QX-314 into the recording cell; stimulation then evoked a monophasic depolarization with a maximum of 16.3 mV at about 30 msec after stimulation, which was inhibited by 6-cyano-7-nitroquinozaline-2,3-dione. At 4 and 6 hr after withdrawal, but not at 2 hr, the estimated fast excitatory postsynaptic potential conductance in slices from ethanol-treated mice was significantly larger than in those from control animals. There were no changes in stimulus/response relation or voltage-dependency of the depolarization. In the presence of these blocking agents, the thresholds for elicitation of field potentials was decreased at 6 hr from withdrawal. The slow inhibitory postsynaptic potentials were isolated by adding DL-2-amino-5-phosphonopentanoic acid, 6-cyano-7-nitroquinozaline- 2,3-dione and bicuculline to the bathing solution; stimulation of the Schaffer collateral fibers then evoked a monophasic hyperpolarization with a maximum of 5.7 mV at about 180 msec after stimulation, which was inhibited by the gamma-aminobutyric acidB antagonist saclofen. At the three time points, the stimulus/response relation, voltage dependency of the hyperpolarization and estimated slow inhibitory postsynaptic conductance in ethanol-treated mice did not differ from control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Pharmacology Department, Medical School, University of Bristol, UK.
authors.forename: A
authors.initials: A
authors.lastname: Molleman
authors.forename: H J
authors.initials: HJ
authors.lastname: Little
mesh_terms: D000818:Animals; D000431:Ethanol / Q000009:adverse effects*; D005071:Evoked Potentials; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016202:N-Methylaspartate / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000187:drug effects*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D000431:Ethanol; D005680:gamma-Aminobutyric Acid; D016202:N-Methylaspartate