مدلسازی حملات هراس
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|75389||2001||13 صفحه PDF||سفارش دهید||7265 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Neuroscience & Biobehavioral Reviews, Volume 25, Issues 7–8, December 2001, Pages 647–659
The isomorphism of dorsal periaqueductal gray-evoked defensive behaviors and panic attacks was appraised in the present study. Thresholds of electrically induced immobility, trotting, galloping, jumping, exophthalmus, micturition and defecation were recorded before and after acute injections of anxiolytic, anxiogenic and antidepressant drugs. Antidepressant effects were further assessed 24 h after injections of 7–14- and 21-day treatments. Chronic administration of clomipramine (CLM, 5–10 mg/kg) a clinically effective antipanic drug increased the thresholds of immobility (24%), trotting (138%) galloping (75%), jumping (45%) and micturition (85%). The 21-day treatment with fluoxetine (FLX, 1 mg/kg) virtually abolished galloping without changing the remaining responses. Galloping thresholds were also increased by 5 mg/kg acute injections of CLM (19%) and FLX (25%). In contrast, chronically administered maprotiline (10 mg/kg), a noradrenaline (NE) selective reuptake inhibitor, selectively increased the thresholds of immobility (118%). Diazepam (1.8 mg/kg) and midazolam (MDZ, 2.5 mg/kg) failed in attenuating the somatic defensive responses. Yet, the sedative dose of MDZ (5 mg/kg) attenuated immobility. The panicogenic drug, pentylenetetrazole (50 mg/kg), markedly decreased the thresholds of galloping (−51%) and micturition (−66%). These results suggest that whereas immobility is a NE-mediated attentional response, galloping is the panic-like behavior best candidate.