{"title":"Anxiety as a state of diminished gabaergic neurotransmission resulting from too frequent recruitment of gabaergic neurons: A neurophysiological model","authors":"Joannis N. Nestoros","doi":"10.1016/0364-7722(81)90053-9","DOIUrl":null,"url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. All of the most commonly used antianxiety drugs (benzodiazepines, barbiturates, ethanol) selectively enhance GABA-mediated neurotransmission.</p></span></li><li><span>2.</span><span><p>2. The degree of GABA-potentiation produced by benzodiazepines correlates well with their relative affinities for the benzodiazepine receptor.</p></span></li><li><span>3.</span><span><p>3. Repetitive stimulation of the recurrent inhibitory GABAergic pathway in rat hippocampus leads to a remarkable reduction of the effectiveness of GABA; this “disinhibition” is counteracted by antianxiety drugs.</p></span></li><li><span>4.</span><span><p>4. A neurophysiological model is proposed, conceptualizing anxiety as the by-product of hypervigilance occurring in frequencies higher than those that the GABAergic system can accommodate, before “fading” or “desensitization” occurs.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90053-9","citationCount":"8","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Progress in neuro-psychopharmacology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0364772281900539","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 8
Abstract
1.
1. All of the most commonly used antianxiety drugs (benzodiazepines, barbiturates, ethanol) selectively enhance GABA-mediated neurotransmission.
2.
2. The degree of GABA-potentiation produced by benzodiazepines correlates well with their relative affinities for the benzodiazepine receptor.
3.
3. Repetitive stimulation of the recurrent inhibitory GABAergic pathway in rat hippocampus leads to a remarkable reduction of the effectiveness of GABA; this “disinhibition” is counteracted by antianxiety drugs.
4.
4. A neurophysiological model is proposed, conceptualizing anxiety as the by-product of hypervigilance occurring in frequencies higher than those that the GABAergic system can accommodate, before “fading” or “desensitization” occurs.
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