{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T01:28:59Z","timestamp":1777858139037,"version":"3.51.4"},"reference-count":59,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2000,7,1]],"date-time":"2000-07-01T00:00:00Z","timestamp":962409600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Psychopharmacol"],"published-print":{"date-parts":[[2000,7]]},"abstract":"<jats:p>The hypothesis that long-lasting potentiation (LLP) in amygdala efferents to the periacqueductal gray (PAG) of the right hemisphere mediates initiation of lasting increases in defensive response to rats induced by FG-7142 was supported in this study. GABA transmission was potentiated with Vigabatrin (gamma vinyl GABA, GVG), a suicide inhibitor of GABA transaminase. It was predicted that increasing GABA transmission would interfere with LLP and behavioural changes. The hypothesis was confirmed, for the most part. GVG given 1 day prior to FG-7142 prevented increased defensive response to rats as well as LLP in right amygdala efferent transmission to the PAG. It did not prevent LLP in the left amygdalo-PAG pathway, although LLP duration was shortened. Nor did it prevent LLP in the right amygdalo-ventromedial hypothalamic (VMH) pathway, and LLP in this pathway was associated with a slightly increased response to vocal threat, but not to rats. GVG given without FG-7142 had no behavioural effects, although it did potentiate transmission in the left amygdalo-PAG pathway. The effects of increasing GABA transmission are consistent with the hypothesis that FG-7142 changes behaviour by inducing a failure of GABA transmission, which in turn facilitates NMDA transmission and NMDA dependent limbic LLP. Finally, the hypothesis that altering GABA tone would change the efficacy of Flumazenil from a neutral antagonist to an inverse agonist was tested on limbic transmission. The hypothesis was confirmed in the left amygdalo-VMH pathway, but no other. It wasa concluded that mechanisms other than a change in GABA tone account for the drug-dependent reversal of LLP in the right amygdalo-PAG by Flumazenil. The findings of the present study suggest that response to FG-7142 may be a useful model of the effects of traumatic stressors on limbic system function in anxiety.<\/jats:p>","DOI":"10.1177\/026988110001400418","type":"journal-article","created":{"date-parts":[[2009,4,1]],"date-time":"2009-04-01T19:04:54Z","timestamp":1238612694000},"page":"323-339","source":"Crossref","is-referenced-by-count":14,"title":["Evidence that long-lasting potentiation of amygdala efferents in the right hemisphere underlies pharmacological stressor (FG-7142) induced lasting increases in anxiety-like behaviour: role of GABA tone in initiation of brain and behavioural changes"],"prefix":"10.1177","volume":"14","author":[{"given":"Robert E.","family":"Adamec","sequence":"first","affiliation":[{"name":"Department of Psychology, Memorial University, 232 Elizabeth Avenue, St Johns, NF, A1B 3X"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2000,7,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1177\/026988119100500107"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1177\/026988119300700302"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1016\/0031-9384(93)90247-D"},{"key":"atypb4","doi-asserted-by":"crossref","first-page":"391","DOI":"10.1177\/074823379401000513","volume":"10","author":"Adamec R","year":"1994","journal-title":"Toxicol Industr Health"},{"key":"atypb5","doi-asserted-by":"publisher","DOI":"10.1016\/S0149-7634(96)00055-3"},{"key":"atypb6","doi-asserted-by":"publisher","DOI":"10.1177\/026988119801200202"},{"key":"atypb7","doi-asserted-by":"crossref","first-page":"129","DOI":"10.1177\/026988119801200203","volume":"12","author":"Adamec R","year":"1998","journal-title":"J Psychopharmacol"},{"key":"atypb8","doi-asserted-by":"crossref","first-page":"227","DOI":"10.1177\/026988119801200301","volume":"12","author":"Adamec R","year":"1998","journal-title":"J Psychopharmacol"},{"key":"atypb9","doi-asserted-by":"crossref","first-page":"133","DOI":"10.1016\/S0006-8993(99)01731-X","volume":"839","author":"Adamec R","year":"1999","journal-title":"Brain Res"},{"key":"atypb10","volume":"14","author":"Adamec R","year":"2000","journal-title":"Role of benzodiazepine receptors J Psychopharmacol"},{"key":"atypb11","doi-asserted-by":"publisher","DOI":"10.1016\/S0163-1047(80)91256-X"},{"key":"atypb12","unstructured":"American Psychiatric Association (1994) Diagnostic and statistical manual of mental disorders, 4th edn, pp. 424\u2013426. 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