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  • 1
    Electronic Resource
    Electronic Resource
    Genetic factors in addiction: QTL mapping and candidate gene studies implicate GABAergic genes in alcohol and barbiturate withdrawal in mice (2001)
    Oxford, UK : Carfax Publishing, part of the Taylor & Francis Group
    Addiction 96 (2001), S. 0 
    Details
    ISSN: 1360-0443
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine , Psychology
    Notes: Quantitative trait locus (QTL) mapping has allowed dramatic progress toward the detection and chromosome mapping of minor and major gene loci involved in murine responses to alcohol and other drugs of abuse. Here we focus on the identification of QTLs for one particular trait relevant to addiction, drug withdrawal following acute or chronic drug administration. To date, five significant QTLs ( p 〈 5 × 10-5) and six suggestive QTLs (p 〈 0.001) have been mapped to specific murine chromosomes for alcohol and pentobarbital withdrawal, indicating the presence of a relevant gene or genes at each location. Overlapping QTLs for alcohol withdrawal and pentobarbital withdrawal are identified on murine chromosomes 1, 4, and 11, and may detect the influence of common genes. For many QTLs, candidate genes with relevant neurobiological function lie within the mapped region. Notably, several QTLs for alcohol and pentobarbital withdrawal are in proximity to genes that directly or indirectly affect GABAA receptor-mediated transmission, which has been implicated in some of the actions of alcohol and other drugs. These include a cluster of GABAA receptor genes and genes encoding the enzymes steroid 5α-reductase-1 (involved in biosynthesis of the neuroactive steroid allopregnanolone) and glutamic acid decarboxylase-1 (involved in GABA biosynthesis). This paper will discuss data that examines the involvement of GABAergic genes in withdrawal and other drug responses, including genetic variation in gene sequence, expression and function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1360-0443.2001.96113910.x
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  • 2
    Electronic Resource
    Electronic Resource
    Abnormal adaptations to stress and impaired cardiovascular function in mice lacking corticotropin-releasing hormone receptor-2 (2000)
    [s.l.] : Nature America Inc.
    Nature genetics 24 (2000), S. 403-409 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The actions of corticotropin-releasing hormone (Crh), a mediator of endocrine and behavioural responses to stress, and the related hormone urocortin (Ucn) are coordinated by two receptors, Crhr1 (encoded by Crhr) and Crhr2 (refs 4,5). These receptors may exhibit distinct functions due to unique ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/74255
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  • 3
    Electronic Resource
    Electronic Resource
    Reduced lethality from ethanol or ethanol plus pentobarbital in mice exposed to 1 or 12 atmospheres absolute helium-oxygen (1985)
    Springer
    Psychopharmacology 86 (1985), S. 409-412 
    Details
    ISSN: 1432-2072
    Keywords: Ethanol ; Pentobarbital ; Ethanol antagonists ; LD50 ; Lethality ; Hyperbaric ; Helium-oxygen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present experiments investigated the effects of 1 and 12 atmospheres absolute (ATA) helium-oxygen on potentially lethal doses of ethanol given alone or in combination with pentobarbital. Drug-naive, male C57BL/6J mice were injected IP with 5.4–6.5 g/kg ethanol, 4.5–6.9 g/kg ethanol plus 20 mg/kg pentobarbital, or 50–110 mg/kg pentobarbital plus 2.5 g/kg ethanol. Following injection, the mice were placed into chambers and exposed to environments of 1 ATA air, 1 ATA helium-oxygen, or 12 ATA helium-oxygen. Exposure to 1 or 12 ATA helium-oxygen significantly reduced the lethal effect (percent mortality at given doses and LD50) of ethanol given alone or with 20 mg/kg pentobarbital when compared to animals exposed to 1 ATA air. The pattern and degree of reduction in lethality for the 1 and 12 ATA helium-oxygen treatments were similar, suggesting that the antagonism resulted from increased helium or decreased nitrogen and not from increased atmospheric pressure. Exposure to these environments did not reduce lethality in mice given 2.5 g/kg ethanol in combination with relatively high doses (50–110 mg/kg) of pentobarbital. These findings suggest that helium-oxygen breathing mixtures may be useful in the treatment of some overdose patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427900
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  • 4
    Electronic Resource
    Electronic Resource
    In vivo and in vitro hyperbaric studies in mice suggest novel sites of action for ethanol (1999)
    Springer
    Psychopharmacology 141 (1999), S. 339-350 
    Details
    ISSN: 1432-2072
    Keywords: Key words Hyperbaric exposure ; Helium-oxygen gas mixture ; γ-Aminobutryic acid (GABA) ; N-Methyl-d-aspartate (NMDA) ; 4 ; 5 ; 6 ; 7-Tetrahydroisoxazolo-pyridin-3-ol (THIP) ; 3α-Hydroxy-5β-pregnan-20-one (3α ; 5β-P) ; Loss of righting reflex (LORR) ; Anticonvulsant effect ; GABA-activated chloride ion uptake ; Central nervous system ; Benzodiazepines ; Barbiturates ; Neuroactive steroid ; C57BL/6 mice ; Ethanol antagonist ; GABAA receptor complex ; Ligand-gated ion channels ; Allosteric coupling hypothesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The present study uses increased atmospheric pressure as an ethanol antagonist to test the hypothesis that allosteric coupling pathways in the GABAA receptor complex represent initial sites of action for ethanol. This was accomplished using behavioral and in vitro measures to determine the effects of pressure on ethanol and other GABAergic drugs in C57BL/6 and LS mice. Behaviorally, exposure to 12 times normal atmospheric pressure (ATA) of a helium-oxygen gas mixture (heliox) antagonized loss of righting reflex (LORR) induced by the allosteric modulators ethanol and pentobarbital, but did not antagonize LORR induced by the direct GABA agonist 4,5,6,7-tetrahydroisoxazolo-pyridin-3-ol (THIP). Similarly, exposure to 12 ATA heliox antagonized the anticonvulsant effects verses isoniazid of ethanol, diazepam and pentobarbital. Biochemically, exposure to 12 ATA heliox antagonized potentiation of GABA-activated 36Cl– uptake by ethanol, flunitrazepam and pentobarbital in LS mouse brain preparations, but did not alter GABA-activated 36Cl– uptake per se. In contrast to its antagonist effect versus other allosteric modulators, pressure did not antagonize these behavioral or in vitro effects induced by the neuroactive steroid, 3α-hydroxy-5β-pregnan-20-one (3α,5β-P). These findings add to evidence that pressure directly and selectively antagonizes drug effects mediated through allosteric coupling pathways. The results fit predictions, and thus support the hypothesis that allosteric coupling pathways in GABAA receptors represent initial sites of action for ethanol. Collectively, the results suggest that there may be common physicochemical and underlying structural characteristics that define ethanol sensitive regions of receptor proteins and/or their associated membranes that can be identified by pressure within (e.g., GABAA) and possibly across (e.g., GABAA, NMDA, 5HT3) receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050843
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  • 5
    Electronic Resource
    Electronic Resource
    Glutamate uptake in mice bred for ethanol withdrawal severity (1999)
    Springer
    Psychopharmacology 143 (1999), S. 174-182 
    Details
    ISSN: 1432-2072
    Keywords: Key words Glutamate ; Convulsion ; Ethanol ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rationale: Withdrawal seizure-prone and withdrawal seizure-resistant mice were selectively bred to exhibit differences in handling-induced convulsion severity during ethanol withdrawal. The glutamatergic system has been implicated in seizure activity as well as ethanol withdrawal symptoms. Objective: This study assessed L-[3H]glutamate uptake into hippocampal synaptosomes prepared from withdrawal seizure-prone and- resistant mice. Methods:Glutamate uptake was characterized following repeated handling-induced convulsions, during acute intoxication, and during peak withdrawal following chronic ethanol exposure. Results: Hippocampal synaptosomal L-[3H]glutamate uptake did not differ between convulsion- and ethanol-naive withdrawal seizure-prone and- resistant mice. Furthermore, exposure to convulsions or to a hypnotic dose of ethanol (4 g/kg) did not alter L-[3H]glutamate uptake. However, withdrawal from 72 h of ethanol exposure significantly increased L-[3H]glutamate uptake in both mouse lines as compared to their respective ethanol-naive controls. Conclusions:These data suggest that glutamate uptake is influenced by chronic ethanol exposure similarly in both withdrawal seizure-prone and- resistant mice. The observed increases in glutamate uptake during withdrawal may be associated with compensatory mechanisms triggered by chronic intoxication and are independent of the selected differences for withdrawal severity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050933
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