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Sensorimotor gating of the SR occurs when the reflex is inhibited by a weak 'pre-pulse' that occurs 30-500 ms prior to the startling stimulus. Since 'pre-pulse inhibition' (PPI) of startle may be impaired in certain psychiatric and neurologic disorders (e.g. schizophrenia, schizotypal personality disorder and Huntington's disease), there has been considerable interest in determining the neural substrates of this form of startle plasticity. In rats, PPI is modulated by neural elements linking the limbic cortex with the striatum and pallidum. These substrates may include hippocampal glutamate efferents to the ventral striatum and striatal GABAergic efferents to the ventral pallidum. The striatal dopaminergic modulation of PPI appears to involve primarily D2, but not D1, receptors. Pallidal efferents may impinge directly on the 'primary' startle circuitry via projections to the mesencephalon or, indirectly, via projections to the thalamus. Evidence is reviewed for other neurochemical substrates of PPI\u2014including acetylcholine and opiates. Sensorimotor gating of the startle reflex appears to have a discrete and identifiable set of neural substrates that may be important for our understanding of neuropsychiatric disorders characterized by deficient suppression or 'gating' of sensory, cognitive or motor processes.<\/jats:p>","DOI":"10.1177\/026988119200600210","type":"journal-article","created":{"date-parts":[[2007,3,17]],"date-time":"2007-03-17T23:45:17Z","timestamp":1174175117000},"page":"176-190","source":"Crossref","is-referenced-by-count":318,"title":["The neural substrates of sensorimotor gating of the startle reflex: a review of recent findings and their implications"],"prefix":"10.1177","volume":"6","author":[{"given":"N.R.","family":"Swerdlow","sequence":"first","affiliation":[{"name":"0804, Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.B.","family":"Caine","sequence":"additional","affiliation":[{"name":"0804, Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.L.","family":"Braff","sequence":"additional","affiliation":[{"name":"0804, Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.A.","family":"Geyer","sequence":"additional","affiliation":[{"name":"0804, Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[1992,3,1]]},"reference":[{"key":"atypb1","first-page":"639","volume":"17","author":"Adler L.E.","year":"1982","journal-title":"Biol Psychiatr"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1016\/0091-3057(85)90014-0"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.1987.01800150017003"},{"key":"atypb4","author":"Bechara A.","year":"1989","journal-title":"Abstr Soc Neurosci"},{"key":"atypb5","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.1990.01810210048007"},{"key":"atypb6","doi-asserted-by":"publisher","DOI":"10.1016\/0006-3223(90)90648-L"},{"key":"atypb7","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(81)90519-1"},{"key":"atypb8","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.1990.01810140081011"},{"key":"atypb9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-8986.1978.tb01390.x"},{"key":"atypb10","first-page":"42","volume":"28","author":"Braff D.L.","year":"1989","journal-title":"Proc Am Coll Neuropsychopharmacol"},{"key":"atypb11","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.1992.01820030038005"},{"key":"atypb12","unstructured":"Bruyn G.W. 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