Neuroreceptors and Ion Channels as Targets of Alcohol

Narahashi, Toshio; Kuriyama, Kinya; Illéš, Peter; Wirkner, Kerstin; Fischer, Wolfgang B.; Mühlberg, Katja S.; Scheibler, Peter; Allgaier, Clemens; Minami, Kouichiro; Lovinger, David M.; Lallemand, Frédéric; Ward, Roberta J.; DeWitte, P.; Itatsu, Tomoko; Takei, Yoshiyuki; Oide, Hirosumi; Hirose, Miyoko; Wang, X. E.; Watanabe, Sumio; Tateyama, Michihiro; Ochi, Rikuo; Sato, Nobuhiro

doi:10.1111/j.1530-0277.2001.tb02394.x

Cited by 52 publications

(31 citation statements)

References 46 publications

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“…In contrast to this potentiation of I Gly , 10 mM ethanol depressed glutamate-evoked current to 74 Ϯ 3% (n ϭ 10) of control (Fig. 6C), in agreement with previous reports (Narahashi et al, 2001).…”

Section: C and D)supporting

confidence: 75%

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Ethanol Suppresses Fast Potentiation of Glycine Currents by Glutamate

Zhu

Krnjević²,

Jiang³

et al. 2002

J Pharmacol Exp Ther

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Excitatory (glutamate) and inhibitory (GABA A and glycine) receptor/channels coexist in many neurons. To assess effects of ethanol on the interaction of glutamate and glycine receptors, glycineinduced current (I Gly ) was recorded by a whole-cell patch-clamp technique from neurons freshly dissociated from the ventral tegmental area of rats. A conditioning prepulse of glutamate (1-3 s, 1 mM) significantly and reversibly potentiated responses to a pulse of glycine. This potentiation was increased when extracellular calcium was raised to 12 mM and reduced by including 10 mM 1,2-bis-(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid in the internal recording medium. It was not affected by 5 (KN-62), a selective inhibitor of calcium/calmodulin-dependent protein kinase II. In a concentration-response analysis, a conditioning pulse of glutamate significantly lowered the EC 50 for glycine and increased the maximal I Gly . Kinetic analysis of the currents indicated that glutamate slowed deactivation of glycinegated chloride channels; therefore, glutamate may increase the affinity of glycine receptors for glycine. When coapplied with glycine, ethanol (10 mM) potentiated I Gly in 35% of neurons from the ventral tegmental area. In contrast, when coapplied with glutamate and glycine, ethanol suppressed the glutamate-induced potentiation of I Gly in these neurons. This suppression was also observed when ethanol and glycine were coapplied after a glutamate prepulse. A similar effect was observed when ethanol alone did not potentiate I Gly . These findings suggest that glutamate-induced calcium influx modulates glycine receptors by a mechanism that can be blocked by ethanol.

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Section: C and D)supporting

confidence: 75%

“…There is now compelling evidence that ethanol directly and/or indirectly affects many receptor/ion channels, including N-methyl-D-aspartate (NMDA), non-NMDA (AMPA), GABA A , glycine, 5-HT 3 , and nicotinic acetylcholine receptors (Narahashi et al, 2001). Modulation of these receptors by ethanol may be responsible for its behavioral effects.…”

mentioning

confidence: 99%

Ethanol Suppresses Fast Potentiation of Glycine Currents by Glutamate

Zhu

Krnjević²,

Jiang³

et al. 2002

J Pharmacol Exp Ther

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“…Among the multiple targets of acute and chronic alcohol, GABA A receptors and ionotropic glutamate receptors are particularly important in the mechanisms of alcohol addiction (Narahashi et al, 2001;Koob, 2004;Siggins et al, 2005). Behavioral studies have demonstrated that the CeA is the most sensitive brain site for GABA A receptor antagonists to reduce alcohol consumption in rodent models (Hyytia and Koob, 1995;Koob, 2004).…”

Section: Role Of Cea Non-nmdar In Alcohol Rewardmentioning

confidence: 99%

Involvement of Non-NMDA Glutamate Receptors in Central Amygdala in Synaptic Actions of Ethanol and Ethanol-Induced Reward Behavior

Zhu

Bie

Pan³

2007

J. Neurosci.

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“…As lipotropic agent, ethanol is able to change the essential physico -chemical properties of cell membranes, which is reflected in the current foetal brain synaptogenesis to establish the nature of this effect, have been made now study [12,13].…”

Section: Introductionmentioning

confidence: 99%

Cortical Synaptogenesis in the Human Brain in Conditions of Prenatal Alcoholization

TV¹,

Av²

2016

Autism Open Access

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Objective: Shaping synaptic contact is one of the leading processes during which largely determine the future integrative brain capabilities. Prenatal exposure to ethanol may have an impact on synaptogenesis in the brain of the embryo and foetus. The purpose of this study -identify the features of synaptogenesis in the brain of embryos and fetuses in conditions of prenatal alcoholization. Materials and Methods:33 embryos and fetuses were obtained from female alcoholic patients. Alcoholic patients were aged 26-39 years and the duration of illness was 3-13 years. In all cases, grade II alcoholism was diagnosed F10.202). The control group consisted of embryos and fetuses from healthy women numbering 30 people with no history of neurological or mental illnesses.The method of electron microscopy and morphometry have been used to study peculiarities in formation of the structure of human embryo and fetus brain synapses at early stages (7 to 12 weeks) of development at mother alcoholization.Results: Electron microscopy of material obtained from alcoholic women has shown slowing -down of formation of synaptic structure. Morphometry has revealed that under the influence of prenatal alcoholization the formation of components of synaptic brain contacts slows down at studying stages of development: the area of presynaptic terminals and their perimeter decreases, and the perimeter of postsynaptic densities decreases as well. Conclusions:The data showed a significant effect of prenatal exposure to ethanol on the development of synaptic structures -reduction of morphometric parameters, slowing the formation of synaptic contacts on the background of reduction of their formation in the brain of the fetus in the early stages of development compared with the norm, which is reflected on during synaptogenesis in the developing brain and can lie the basis of severe disorders in the unborn child. Graphical AbstractMethods of electron microscopy and morphometry have been used to study peculiarities in formation of the structure of human embryo and fetus brain synapses at early stages of development at mother alcoholization.

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Neuroreceptors and Ion Channels as Targets of Alcohol

Cited by 52 publications

References 46 publications

Ethanol Suppresses Fast Potentiation of Glycine Currents by Glutamate

Ethanol Suppresses Fast Potentiation of Glycine Currents by Glutamate

Involvement of Non-NMDA Glutamate Receptors in Central Amygdala in Synaptic Actions of Ethanol and Ethanol-Induced Reward Behavior

Cortical Synaptogenesis in the Human Brain in Conditions of Prenatal Alcoholization

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