Ethanol prevents the glutamate release induced by in the rat striatum

Carboni, Susanna; Isola, Raffaella; Gessa, Gian Luigi; Rossetti, Zvani L.

doi:10.1016/0304-3940(93)90501-b

Cited by 80 publications

(49 citation statements)

References 25 publications

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“…Our observations that EtOH depressed mEPSC frequency supported previous reports showing that it inhibited NMDAmediated glutamate release in the rat striatum (Carboni et al 1993) and suppressed high-K ϩ -evoked release of endogenous glutamate and aspartate in the hippocampal slice (Martin and Swartzwelder 1992). The finding that EtOH increased mIPSC frequency was similar to the increased frequency of glycinergic mIPSCs in postnatal hypoglossal motoneurons (Eggers et al 2000) but contradicted its inhibitory effect on high-K ϩ -evoked GABA release in the hippocampus (Martin and Swartzwelder 1992).…”

Section: Dual Etoh Actions On Neurotransmitter Releasesupporting

confidence: 89%

“…EtOH inhibits NMDAR-mediated glutamate release in the rat striatum (Carboni et al 1993), and in the hippocampus, it suppresses high-K ϩ -evoked release of endogenous glutamate, aspartate, and GABA (Martin and Swartzwelder 1992). In contrast, EtOH increases the frequency of action potential-independent glycinergic currents in hypoglossal motoneurons, implying that it increases presynaptic glycine release (Eggers et al 2000).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ethanol Dual Modulatory Actions on Spontaneous Postsynaptic Currents in Spinal Motoneurons

Ziskind-Conhaim

Gao

Hinckley

2003

Journal of Neurophysiology

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. Recently we have shown that acute ethanol (EtOH) exposure suppresses dorsal root-evoked synaptic potentials in spinal motoneurons. To examine the synaptic mechanisms underlying the reduced excitatory activity, EtOH actions on properties of action potential-independent miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs) were studied in spinal motoneurons of newborn rats. Properties of mEPSCs generated by activation of N-methyl-D-aspartate receptors (NMDARs) and non-NMDA receptors and of mIPSCs mediated by glycine and ␥-aminobutyric acid-A receptors (GlyR and GABA A R) were examined during acute exposure to 70 and 200 mM EtOH. In the presence of 70 mM EtOH, the frequency of NMDARand non-NMDAR-mediated mEPSCs decreased to 53 Ϯ 5 and 45 Ϯ 7% (means Ϯ SE) of control values, respectively. In contrast, the frequency of GlyR-and GABA A R-mediated mIPSCs increased to 138 Ϯ 15 and 167 Ϯ 23% of control, respectively. Based on the quantal theory of transmitter release, changes in the frequency of miniature currents are correlated with changes in transmitter release, suggesting that EtOH decreased presynaptic glutamate release and increased the release of both glycine and GABA. EtOH did not change the amplitude or rise and decay times of either mEPSCs or mIPSCs, indicating that the presynaptic changes were not associated with changes in the properties of postsynaptic receptors/channels. Acute exposure to 200 mM EtOH increased mIPSC frequency two-to threefold, significantly higher than the increase induced by 70 mM EtOH. However, the decrease in mEPSC frequency was similar to that observed in 70 mM EtOH. Those findings implied that the regulatory effect of EtOH on glycine and GABA release was dose-dependent. Exposure to the higher EtOH concentration had opposite actions on mEPSC and mIPSC amplitudes: it attenuated the amplitude of NMDAR-and non-NMDAR-mediated mEPSCs to ϳ80% of control and increased GlyR-and GABA A R-mediated mIPSC amplitude by ϳ20%. EtOH-induced changes in the amplitude of postsynaptic currents were not associated with changes in their basic kinetic properties. Our data suggested that in spinal networks of newborn rats, EtOH was more effective in modulating the release of excitatory and inhibitory neurotransmitters than changing the properties of their receptors/channels.

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Section: Dual Etoh Actions On Neurotransmitter Releasesupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Ethanol Dual Modulatory Actions on Spontaneous Postsynaptic Currents in Spinal Motoneurons

Ziskind-Conhaim

Gao

Hinckley

2003

Journal of Neurophysiology

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“…Acute ethanol injection, 2 g/kg to either naive rats (Carboni et al 1993;Dahchour et al 1994;Selim and Bradberry 1996) or rats receiving two injections per day for 8 days (Dahchour et al 1996), does not significantly increase glutamate extracellular content. Such results were confirmed in this present study in the two groups of rats which received an acute dose of ethanol during the microdialysis experiments.…”

Section: Discussionmentioning

confidence: 96%

Changes in the amygdala amino acid microdialysate after conditioning with a cue associated with ethanol

Quertemont¹,

Neuville²,

Witte³

1998

Psychopharmacology

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The excitatory amino acid neurotransmission within the amygdala has been implicated in learning associations between external stimuli and intrinsic reward values such that it may play a key role in conditioned drug effects. In the present studies, the responses of the excitatory amino acids, aspartate and glutamate together with the neuromodulatory sulphonated amino acid taurine, within the basolateral amygdala, to an odor cue repeatedly associated with acute ethanol injections (2g/kg, IP) have been investigated by a microdialysis technique combined with HPLC-EC analysis. After presentation of the ethanol-conditioned stimulus, a single IP saline injection induced an immediate and significant increase in the taurine microdialysate content which could be related to the neuromodulatory action of taurine. Furthermore, when the conditioned stimulus was combined with the ethanol injection (2g/kg, IP), significant increases in both taurine and glutamate microdialysate content were observed and indicated a learned compensatory response to counteract the acute effects of ethanol. These results demonstrate that changes in amygdala extracellular glutamate and taurine concentrations can be conditioned to ethanol-associated stimuli and are therefore probably implicated in the phenomenon of environmental-dependent tolerance to ethanol.

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“…Ethanol is a well-known NMDA antagonist (Carboni et al, 1993), and the blocking action of ethanol on NMDA receptors can be reversed in a time-and concentration-dependent manner (McCown et al, 1986). Long-term blockade of NMDA receptors that results from chronic exposure of neurons to ethanol has been found to both increase NMDA receptor density (Gulya et al, 1991) and sensitize neurons to the excitotoxic effect of NMDA receptor activation (Chandler et al, 1993).…”

Section: Ethanol and Nmda Receptorsmentioning

confidence: 99%

Mismatch Negativity in Subjects at High Risk for Alcoholism

Zhang

Cohen

Porjesz

et al. 2001

Alcoholism Clin & Exp Res

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Background:Evidence from P300 studies in both alcohol-dependent and high-risk (HR) individuals suggests that the reduced P300 amplitudes that often characterize these individuals may reflect a deficit in inhibition (hyperexcitability) in the central nervous system. In this context, the mismatch negativity (MMN) was investigated in the male and female HR offspring of alcohol-dependent fathers and a mixed-sex, low-risk (LR) control group.Methods: As subjects read popular materials, they received a random sequence of 500 binaurally presented tones of 600 Hz and 1600 Hz. The designation of the rare stimulus (n ϭ 60 trials) and frequent stimulus (n ϭ 440 trials) was alternated across subjects.Recordings of MMN were made from 61 electrodes; risk group comparisons were restricted to the five frontal midline electrodes: Fpz, Afz, Fz, Fcz, and Cz. The MMN was obtained by calculating the integral of the area under the curve for both the frequent and rare waveforms over an interval from 100 to 190 msec and then subtracting the former from the latter.Results: The primary observation was that MMN responses in the HR group were significantly larger than those in the LR group. In addition, both LR and HR individuals manifested differential responses to the rare and frequent stimuli, and MMN responses in both groups were largest at Fcz and smallest at Fpz.Discussion: The results indicate that individuals at high risk for alcoholism differ electrophysiologically from LR controls. These differences were manifested as larger magnitudes of the MMN. The findings suggest the possibility that as measured by the MMN, individuals at high risk for alcoholism may be characterized by a deficit in inhibition (excessive neural excitation). The presence of these preexisting central nervous system states may lead to ethanol use for self-medication, which then may facilitate the development of both tolerance to and dependence on ethanol.

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Ethanol prevents the glutamate release induced by in the rat striatum

Cited by 80 publications

References 25 publications

Ethanol Dual Modulatory Actions on Spontaneous Postsynaptic Currents in Spinal Motoneurons

Ethanol Dual Modulatory Actions on Spontaneous Postsynaptic Currents in Spinal Motoneurons

Changes in the amygdala amino acid microdialysate after conditioning with a cue associated with ethanol

Mismatch Negativity in Subjects at High Risk for Alcoholism

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