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All of the most commonly used antianxiety drugs (the benzodiazepines, the barbiturates, ethanol) selectively enhance only GABA-mediated synaptic transmission. Furthermore, the relative affinities of pharmacologically active benzodiazepines for the benzodiazepine receptor correlate well with their ability to antagonize GABA-modulin (the endogenous inhibitor of GABA receptors) in vitro, as well as with their ability to potentiate GABA-mediated electrically evoked cortical inhibition in vivo. Finally, it is of interest for the neurophysiology of anxiety that repetitive stimulation of the recurrent inhibitory GABAergic pathway in the rat hippocampus leads to a remarkable reduction of the effectiveness of GABA; this elimination of GABAergic \u201cinhibition\u201d is counteracted by antianxiety drugs. On the basis of the above a neurophysiological model of anxiety is proposed.<\/jats:p>","DOI":"10.1177\/070674378402900614","type":"journal-article","created":{"date-parts":[[2017,4,26]],"date-time":"2017-04-26T04:39:08Z","timestamp":1493181548000},"page":"520-529","source":"Crossref","is-referenced-by-count":33,"title":["Gabaergic Mechanisms and Anxiety: An Overview and a New Neurophysiological Model"],"prefix":"10.1177","volume":"29","author":[{"given":"Joannis N.","family":"Nestoros","sequence":"first","affiliation":[{"name":"Athens Tower Institute of Research in Neuropsychology, Athens, Greece. 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