Inhibition of NMDA-evoked electrophysiological activity by ethanol in selected brain regions: evidence for ethanol-sensitive and ethanol-insensitive NMDA-evoked responses

Simson, Peter E.; Criswell, Hugh E.; Breese, George R.

doi:10.1016/0006-8993(93)91483-9

Cited by 124 publications

(46 citation statements)

References 22 publications

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“…We superfused ethanol (44 mM) after a stable baseline of NMDA responses had been obtained (10 -15 min). As predicted from the NMDARmediated EPSP and EPSC data and in accord with past studies showing ethanol inhibition of NMDA responses in other neuron types (Hoffman et al, 1989;Lovinger et al, 1989;Simson et al, 1993;Nie et al, 1994), acute ethanol decreased currents elicited by exogenous NMDA to 70 Ϯ 5% of baseline ( p Ͻ 0.05; n ϭ 4; Fig. 7) with recovery on washout.…”

Section: Effects Of Acute and Chronic Ethanol On Postsynaptic Nmdarssupporting

confidence: 90%

Acute and Chronic Ethanol Alter Glutamatergic Transmission in Rat Central Amygdala: anIn VitroandIn VivoAnalysis

Roberto¹,

Schweitzer²,

Madamba³

et al. 2004

J. Neurosci.

289

355

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Section: Effects Of Acute and Chronic Ethanol On Postsynaptic Nmdarssupporting

confidence: 90%

Acute and Chronic Ethanol Alter Glutamatergic Transmission in Rat Central Amygdala: anIn VitroandIn VivoAnalysis

Roberto¹,

Schweitzer²,

Madamba³

et al. 2004

J. Neurosci.

289

355

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“…# P < 0.05; significant difference from the synaptic potential immediately before the application of picrotoxin and suramin; * P < 0.05; significant difference from the synaptic potential immediately before the application of ethanol. + P < 0.05; significant difference from the synaptic potential immediately before the washout of ethanol combinations of subunits forming NMDA receptor subtypes (Simson et al 1993;Yang et al 1996). Native receptors appear to be heteromeric complexes of NMDAR1 and various NMDAR2 subunits.…”

Section: Discussionmentioning

confidence: 99%

Inhibition by ethanol of excitatory amino acid receptors in rat locus coeruleus neurons in vitro

Nieber

Poelchen

Sieler

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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Intracellular recordings were made in a pontine slice preparation of the rat brain containing the nucleus locus coeruleus (LC). In a first series of experiments, various parameters of spontaneous action potentials were evaluated. It turned out that ethanol (100 mM) does not alter the firing rate, the spike amplitude and the afterhyperpolarization following a spike. In subsequent experiments, the generation of action potentials was prevented by passing continuous hyperpolarizing current via the recording electrode. Under these conditions, ethanol (100 mM) had no effect on the membrane potential or input resistance. Pressure-applied N-methyl-D-aspartate (NMDA), (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and alpha,beta-methylene ATP (alpha,beta-meATP) reproducibly depolarized LC neurons. While ethanol (100 mM) depressed the NMDA- and AMPA-induced depolarization to a similar extent, it did not interact with alpha,beta-meATP. Lower concentrations of ethanol (10 and 30 mM) had no effect on depolarizing responses to NMDA or AMPA. Noradrenaline applied by pressure pulses reproducibly hyperpolarized LC cells. These hyperpolarizations were unchanged by ethanol (100 mM). Biphasic synaptic potentials consisting of early depolarizing (PSP) and late hyperpolarizing (IPSP) components were evoked by electrical stimulation. Ethanol (100 mM) depressed the PSP and increased the IPSP. Glutamatergic PSPs recorded in the combined presence of picrotoxin (100 microM) and suramin (100 microM) were also inhibited by ethanol (100 mM). However, IPSPs recorded under these conditions were insensitive to ethanol (100 mM). In conclusion, ethanol may interfere with the AMPA (or NMDA) receptor-mediated fraction of the PSP and slightly facilitate the alpha2 adrenoceptor-mediated fraction of the IPSP.

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“…The extended time required for the effect in hippocampus suggests that ethanol may have indirect actions on GABAA receptor a4 subunit peptide expression that are mediated via other mechanisms, possibly involving additional neurotransmitter systems. For example, the hippocampus contains glutamate receptors that are responsive to N-methyl-D-aspartate (NMDA) and are blocked by pharmacologically relevant concentrations of ethanol (Lovinger eta!., 1989;Simson et al, 1993). These receptors are localized to neurons containing GABAA receptors (Craig et al, 1994).…”

Section: Fig 2 Amentioning

confidence: 99%

Differential Regulation of GABA_A Receptor Gene Expression by Ethanol in the Rat Hippocampus Versus Cerebral Cortex

Matthews

Devaud

Fritschy

et al. 1998

Journal of Neurochemistry

103

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Abstract:Previous research has shown that chronic ethanol consumption dramatically alters GABAA receptor a, and a 4 subunit gene expression in the cerebral cortex and GABAA receptor a, and a6 subunit gene expression in the cerebellum. However, it is not yet known if chronic ethanol consumption produces similar alterations in GA-BAA receptor gene expression in other brain regions. One brain region of interest is the hippocampus because it has recently been shown that a subset of GABAA receptors in the hippocampus is responsive to pharmacologically relevant concentrations of ethanol. Therefore, we directly compared the effects of chronic ethanol consumption on GABAA receptor subunit gene expression in the hippocampus and cerebral cortex. Furthermore, we investigated whether the duration of ethanol consumption (14 or 40 days) would influence regulation of GABAA receptor gene expression in these two brain regions. Chronic ethanol consumption produced a significant increase in the level of GABAA receptor a4 subunit peptide in the hippocampus following 40 days but not 14 days. The relative expression of hippocampal GABAA receptor a1, a2, a3, /32/3, or Y2 was not altered by either period of chronic ethanol exposure. In marked contrast, chronic ethanol consumption for 40 days significantly increased the relative expression of cerebral cortical GABAA receptor a4 subunits and significantly decreased the relative expression of cerebral cortical GABAA receptor a, subunits. This finding is consistent with previous results following 14 days of chronic ethanol consumption. Hence, chronic ethanol consumption alters GABAA receptor gene expression in the hippocampus but in a different manner from that in either the cerebral cortex or the cerebellum. Furthermore, these alterations are dependent on the duration of ethanol exposure.

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Inhibition of NMDA-evoked electrophysiological activity by ethanol in selected brain regions: evidence for ethanol-sensitive and ethanol-insensitive NMDA-evoked responses

Cited by 124 publications

References 22 publications

Acute and Chronic Ethanol Alter Glutamatergic Transmission in Rat Central Amygdala: anIn VitroandIn VivoAnalysis

Acute and Chronic Ethanol Alter Glutamatergic Transmission in Rat Central Amygdala: anIn VitroandIn VivoAnalysis

Inhibition by ethanol of excitatory amino acid receptors in rat locus coeruleus neurons in vitro

Differential Regulation of GABA_A Receptor Gene Expression by Ethanol in the Rat Hippocampus Versus Cerebral Cortex

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Inhibition of NMDA-evoked electrophysiological activity by ethanol in selected brain regions: evidence for ethanol-sensitive and ethanol-insensitive NMDA-evoked responses

Cited by 124 publications

References 22 publications

Acute and Chronic Ethanol Alter Glutamatergic Transmission in Rat Central Amygdala: anIn VitroandIn VivoAnalysis

Acute and Chronic Ethanol Alter Glutamatergic Transmission in Rat Central Amygdala: anIn VitroandIn VivoAnalysis

Inhibition by ethanol of excitatory amino acid receptors in rat locus coeruleus neurons in vitro

Differential Regulation of GABAA Receptor Gene Expression by Ethanol in the Rat Hippocampus Versus Cerebral Cortex

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Differential Regulation of GABA_A Receptor Gene Expression by Ethanol in the Rat Hippocampus Versus Cerebral Cortex