Expression of N-methyl-D-aspartate receptor-dependent long-term potentiation in the neostriatal neurons in an in vitro slice after ethanol withdrawal of the rat.
To examine changes in corticostriatal synaptic transmission in rats with ethanol withdrawal syndrome, intracellular and extracellular responses to subcortical white matter stimulation were recorded in neostriatal slice preparations. The resting membrane potential, input resistance and depolarizing postsynaptic potentials to single cortical white matter stimulation were similar in the neostriatum of naive and ethanol withdrawal rats. Repetitive stimulation of the white matter induced more pronounced N-methyl-D-aspartate receptor-mediated postsynaptic potentials in ethanol withdrawal than naive rat neostriatum. In intracellular recording, tetanic stimulation (50 Hz, 20 s) induced more pronounced post-tetanic potentiation of depolarizing postsynaptic potentials in the neostriatum of ethanol withdrawal than naive rats. However, in extracellular recording, tetanic stimulation induced smaller post-tetanic depression of population spikes in the neostriatum of ethanol withdrawal than naive rats. Tetanic stimulation of the subcortical white matter induced long-term potentiation of postsynaptic potentials and population spikes in the ethanol withdrawal rat neostriatum, while long-term depression was evoked in the naive rat neostriatum. The induction of long-term potentiation was blocked by D-2-amino-5-phosphonovaleric acid or 7-chlorokynurenic acid, N-methyl-D-aspartate receptor antagonists, but not by (RS)-methyl-4-carboxyphenyl-glycine, a metabotropic glutamate receptor antagonist. Dopamine also significantly depressed the induction of long-term potentiation in ethanol withdrawal rat neostriatum and this depressant effect was antagonized by the D2 antagonist L-sulpiride but not by the D1 antagonist SCH23390. These results indicate that the N-methyl-D-aspartate component of the corticostriatal glutamatergic responses, which might be necessary for induction of long-term potentiation, was enhanced in ethanol withdrawal rats. The depression of long-term potentiation induction by activation of D2 receptor suggests that corticostriatal N-methyl-D-aspartate response or intracellular mechanisms involving in the induction of the long-term potentiation can be suppressed by D2 activation and that the D2 effects are inhibited in the neostriatum of ethanol withdrawal rats.
Yamamoto
Y
Y
Department of Pharmacology, Faculty of Dentistry, Kyushu University, Fukuoka, Japan.
Nakanishi
H
H
Takai
N
N
Shimazoe
T
T
Watanabe
S
S
Kita
H
H
D000818:Animals; D002492:Central Nervous System Depressants / Q000009:adverse effects*; D065127:Dopamine D2 Receptor Antagonists; D000431:Ethanol / Q000009:adverse effects*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D017072:Neostriatum / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D017447:Receptors, Dopamine D1 / Q000037:antagonists & inhibitors; D018094:Receptors, Metabotropic Glutamate / Q000037:antagonists & inhibitors; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000502:physiology*; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000187:drug effects
D002492:Central Nervous System Depressants; D065127:Dopamine D2 Receptor Antagonists; D018691:Excitatory Amino Acid Antagonists; D017447:Receptors, Dopamine D1; D018094:Receptors, Metabotropic Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D000431:Ethanol