Literature DB >> 7562466

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.

A Molleman1, H J Little.   

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)

Entities:  

Mesh:

Substances:

Year:  1995        PMID: 7562466

Source DB:  PubMed          Journal:  J Pharmacol Exp Ther        ISSN: 0022-3565            Impact factor:   4.030


  4 in total

1.  Altered hippocampal synaptic function in transgenic mice with increased astrocyte expression of CCL2 after withdrawal from chronic alcohol.

Authors:  Jennifer G Bray; Kenneth C Reyes; Amanda J Roberts; Donna L Gruol
Journal:  Neuropharmacology       Date:  2018-02-27       Impact factor: 5.250

2.  Sustained ethanol inhibition of native AMPA receptors on medial septum/diagonal band (MS/DB) neurons.

Authors:  G D Frye; A Fincher
Journal:  Br J Pharmacol       Date:  2000-01       Impact factor: 8.739

3.  Increased AMPA receptor GluR1 subunit incorporation in rat hippocampal CA1 synapses during benzodiazepine withdrawal.

Authors:  Paromita Das; Scott M Lilly; Ricardo Zerda; William T Gunning; Francisco J Alvarez; Elizabeth I Tietz
Journal:  J Comp Neurol       Date:  2008-12-20       Impact factor: 3.215

Review 4.  Glutamatergic substrates of drug addiction and alcoholism.

Authors:  Justin T Gass; M Foster Olive
Journal:  Biochem Pharmacol       Date:  2007-06-30       Impact factor: 5.858

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.