Differential effects of chronic ethanol administration on GABAA receptor α1 and α6 subunit mRNA levels in rat cerebellum

Morrow, A. Leslie; Herbert, James S.; Montpied, Pascale

doi:10.1016/1044-7431(92)90045-4

Cited by 98 publications

(63 citation statements)

References 34 publications

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“…Likewise, examination of drugs affecting GABA A receptor function implicated differing brain regions for self-administration and ethanol discrimination of ethanol (Hyytia and Koob, 1995;McBride et al, 1999;Roberts et al, 1996;Rodd et al, 2004Rodd et al, , 2005. In further support of a regional specificity of ethanol on GABA transmission, work demonstrated that chronic ethanol treatment altered expression of GABA A receptor subunit mRNAs in some brain regions, but not others Grobin et al, 2000a, b;Montpied et al, 1991;Morrow et al, 1992;Mhatre and Ticku, 1992;Papadeas et al, 2001). electrophysiological recording of spontaneous activity of neurons in anesthetized animals across a variety of brain regions.…”

Section: Regional Specificity Of Ethanol On Functions Altered By Gabamentioning

confidence: 96%

“…After chronic ethanol, an alteration in the expression of a 4 -receptor subunit occurs in some, but not all, brain regions (Grobin et al, 2000a, b;Kumar et al, 2002;Montpied et al, 1991;Papadeas et al, 2001) and the a 6 -receptor subunit is increased in the cerebellum (Mhatre and Ticku, 1992;Morrow et al, 1992). In respect to the increase in the expression of the a 4 -and a 6 -receptor subunits following chronic ethanol exposure, there is often a concomitant downregulation of the a 1 -receptor subunit (Grobin et al, 2000a, b;Mhatre and Ticku, 1992;Morrow et al, 1992;Papadeas et al, 2001).…”

Section: Argument For An Action Of Ethanol On Bzd-insensitive Gaba a mentioning

confidence: 99%

“…In respect to the increase in the expression of the a 4 -and a 6 -receptor subunits following chronic ethanol exposure, there is often a concomitant downregulation of the a 1 -receptor subunit (Grobin et al, 2000a, b;Mhatre and Ticku, 1992;Morrow et al, 1992;Papadeas et al, 2001). While the underlying basis of the shift in these alpha-subunits for GABA A receptors after chronic ethanol is unknown, this change in GABA A receptor subunits is consistent with a close relationship between ethanol action in vivo and GABA function.…”

Section: Argument For An Action Of Ethanol On Bzd-insensitive Gaba a mentioning

confidence: 99%

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A Conceptualization of Integrated Actions of Ethanol Contributing to its GABAmimetic Profile: A Commentary

Criswell

Breese

2005

Neuropsychopharmacol

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Early behavioral investigations supported the contention that systemic ethanol displays a GABAmimetic profile. Microinjection of GABA agonists into brain and in vivo electrophysiological studies implicated a regionally specific action of ethanol on GABA function. While selectivity of ethanol to enhance the effect of GABA was initially attributed an effect on type-1-benzodiazepine (BZD)-GABA A receptors, a lack of ethanol's effect on GABA responsiveness from isolated neurons with this receptor subtype discounted this contention. Nonetheless, subsequent work identified GABA A receptor subtypes, with limited distribution in brain, sensitive to enhancement of GABA at relevant ethanol concentrations. In view of these data, it is hypothesized that the GABAmimetic profile for ethanol is due to activation of mechanisms associated with GABA function, distinct from a direct action on the majority of postsynaptic GABA A receptors. The primary action proposed to account for ethanol's regional specificity on GABA transmission is its ability to release GABA from some, but not all, presynaptic GABAergic terminals. As systemic administration of ethanol increases neuroactive steroids, which can enhance GABA responsiveness, this elevated level of neurosteroids is proposed to magnify the effect of GABA released by ethanol. Additional factors contributing to the degree to which ethanol interacts with GABA function include an involvement of GABA B and other receptors that influence ethanol-induced GABA release, an effect of phosphorylation on GABA responsiveness, and a regional reduction of glutamatergic tone. Thus, an integration of these consequences induced by ethanol is proposed to provide a logical basis for its in vivo GABAmimetic profile.

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Section: Regional Specificity Of Ethanol On Functions Altered By Gabamentioning

confidence: 96%

Section: Argument For An Action Of Ethanol On Bzd-insensitive Gaba a mentioning

confidence: 99%

Section: Argument For An Action Of Ethanol On Bzd-insensitive Gaba a mentioning

confidence: 99%

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A Conceptualization of Integrated Actions of Ethanol Contributing to its GABAmimetic Profile: A Commentary

Criswell

Breese

2005

Neuropsychopharmacol

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“…The administration of the inverse benzodiazepine agonist, FG 7142, for several days increased al and 3'2, while treatment with diazepam resulted in decreased levels [56]. Furthermore, the long term administration of ethanol, a positive modulator of GABAAR mediated functions, also decreased the expression of several a class members in the neocortex [44,49]. These data suggest that a long-lasting activation of GABAARS is followed by a response at the mRNA level, presumably to compensate for the altered receptor efficacy.…”

Section: Gaba Ar Subunit Mrna Expression In Other Models Of Synaptic mentioning

confidence: 99%

“…By altering the expression pattern of GABAAR subunit encoding genes, neurons may have the ability to fine tune their GABAergic signal transduction pathway in response to changing conditions. Changes in subunit expression profile during development [30] and in response to transient cerebral ischemia [33], chronic GABAA/benzodiazepine receptor agonists/antagonists [15,25,42,56,63,80] or ethanol treatment [41,44,49] may underly functional changes of GABAARS. Modified GABAAR subunit mRNA levels were also described in rats that were subjected to repeated electrical stimulations with short interstimulus intervals resuiting in recurrent epileptiform seizures (rapid kindling procedure) [27].…”

Section: Introductionmentioning

confidence: 99%

Expression of GABAA receptor subunit mRNAs in hippocampal pyramidal and granular neurons in the kindling model of epileptogenesis: an in situ hybridization study

Kamphuis

Rijk

Silva

1995

Molecular Brain Research

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Expression of GABA-A receptor subunit in mRNAs in hippocampal pyramidal and granular neurons in the kindling model of epileptogenesis: an in situ hybridization study. Kamphuis, W.; de Rijk, T.C.; Lopes da Silva, F.H. Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Accepted 24 January 1995 AbstractTo investigate the molecular changes underlying kindling epileptogenesis in the rat hippocampus, the expression levels of the genes encoding for 13 different y-aminobutyric acid type-A receptor (GABAAR) subunits were measured in hippocampal principal neurons using in situ hybridization techniques and semi-quantitative analysis of the autoradiograms. Schaffer collateral-commissural pathway kindled rats were investigated at three different stages of kindling acquisition, at 24 h after the last seizure and at long-term (28 days) after termination of kindling stimulations. Changes were distinct for the different subunits in the three analyzed regions (CA1, CA3, fascia dentata) and also different for the various kindling stages. In all hippocampal areas at the early phases of kindling epileptogenesis, before the appearance of generalized seizures, an increase was found of those transcripts that constituted the majority of the expressed variants in control animals (al, a2, a4, /31, /32, /33, y2/y2L mRNA). In these stages, the increased levels of different variants in the granular neurons of the fascia dentata were more pronounced when compared to the pattern of changes in pyramidal cells of CA1 and CA3. In fully kindled animals, the expression levels of several subunits returned to control levels, whereas/33 and y2/y2L mRNA expression was still significantly enhanced in all areas. At long-term, few changes were encountered. The long-splice variant of 3,2 was decreased within pyramidal and granular neurons while the total level of y2 mRNA was not different from controls. The increased GABAAR subunit expression in the fascia dentata may underly the reported increased GABAAR ligand binding and the increased GABA mediated inhibition. However, the decreased GABAAR binding and the attenuation of GABAergic inhibition in CA1, could not be explained by a decrement of receptor subunit expression.

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Cortical γ-Aminobutyric Acid Type A–Benzodiazepine Receptors in Recovery From Alcohol Dependence

Staley¹,

Gottschalk²,

Petrakis³

et al. 2005

Arch Gen Psychiatry

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These data demonstrate time-dependent regulation of cortical GABA(A)-benzodiazepine receptors associated with the recovery from alcohol dependence. Higher GABA(A)-benzodiazepine receptor levels during acute withdrawal may reflect a compensation for reduced receptor function, which is thought to contribute to alcohol tolerance and withdrawal. The subsequent decline may reflect "normalization" of GABA(A) receptor function with sobriety. Smoking may attenuate GABA(A) receptor adaptations associated with alcohol dependence and may contribute to the comorbidity between alcoholism and smoking.

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Differential effects of chronic ethanol administration on GABAA receptor α1 and α6 subunit mRNA levels in rat cerebellum

Cited by 98 publications

References 34 publications

A Conceptualization of Integrated Actions of Ethanol Contributing to its GABAmimetic Profile: A Commentary

A Conceptualization of Integrated Actions of Ethanol Contributing to its GABAmimetic Profile: A Commentary

Expression of GABAA receptor subunit mRNAs in hippocampal pyramidal and granular neurons in the kindling model of epileptogenesis: an in situ hybridization study

Cortical γ-Aminobutyric Acid Type A–Benzodiazepine Receptors in Recovery From Alcohol Dependence

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