Catecholamine depletion in mice upon reexposure to stress: Mediation of the escape deficits produced by inescapable shock.

Abstract

Immediately following exposure to 60 inescapable shocks, Swiss-Webster mice had significantly reduced hypothalamic norepinephrine (NE). Within 24 hr NE levels returned to control values. Reexposure to as few as 10 shocks 24 hr after initial stress exposure resulted in a significant decline of hypothalamic NE. Moreover, at this interval after inescapable shock, escape performance was severely disrupted, with a large proportion of mice exhibiting numerous failures to escape shock. Increasing brain dopamine (DA) and NE by L-dopa treatment prior to inescapable shock prevented the escape deficits. Conversely, pairing five inescapable shocks with NE depletion by FLA-63, or both DA and NE depletion by a-methyl-p-tyrosine, disrupted escape performance 24 hr later. Residual drug effects, state dependence, or sustained amine turnover could not account for the behavioral changes observed. Data are discussed in terms of catecholamine mediation of escape performance through variations in response maintenance abilities. Furthermore, it is suggested that the long-term effects of inescapable shock may be due to sensitization effects or conditioned amine depletion.Exposure to inescapable shock has been shown to disrupt escape performance in a variety of animal species (see reviews in Maier & Seligman, 1976;Weiss, Glazer, & Pohorecky, 1976). The performance deficit is characterized not only by retarded escape latencies but by frequent failures to escape shock as well. In rodents the time course for the interference is dependent upon the shock parameters used during the initial stress session. Following long-duration shock of moderate intensity, a pronounced performance deficit is apparent as long as 1-7 days later; however, only a moderate deficit, if any, is seen at a 30-min interval (Glazer &

REM Sleep Deprivation Effect on Apomorphine-Induced Gnawing Is Reversed by Dexamethasone

“…Thus, in the present study, DEX administration may have relieved the depletion of NE engendered by 6 days on the small pedestals. This interpretation is consistent with reports that catecholamine (CA) system function is depressed following REM dep (21) and with reports of NE depletion following the longterm or repeated presentation of unavoidable noxious stimuli (22)(23)(24). Sleep deprivation and its inherent stress, however, have been reported to leave brain NE levels unchanged (20) or to increase NE function (25)(26)(27), so that DEX administration may well have produced the present results by further enhancing the already increased NE.…”

Evidence that the Pituitary-Adrenal Axis Does Not Cross-Adapt to Stressors: Comparison to Other Physiological Variables

“…Although the results obtained when the animals were ex posed to a novel acute stressor suggest that previous chron ic stress did not alter the physiological response to a novel stressor, it has been reported that previous exposure to stress induces a sensitization of the brain noradrenaline res ponse to a subsequent exposure to the same stressor [1,2]. More recently, we have observed that chronic exposure to various stress models enhanced basal and acute stress levels of brain serotoninergic activity.…”

Expositions récurrentes aux événements traumatiques: inoculation ou vulnérabilité croissante?

“…Ils ont établi que l'hyperactivité neurovégétative observée chez les sujets ayant un TSPT coïncidait avec une hypersensibilité des capteurs de la noradrenaline. Or, Anisman et al (1979) ont trouvé que de faibles chocs électriques n'ayant aucun effet mesurable sur des animaux naïfs, produisaient une diminution importante de la noradrenaline chez des animaux précédemment exposés à des chocs incontrôlables. Ainsi, l'exposition à une situation traumatique (des chocs incontrôlables) induirait cette hypersensibilité des capteurs noradrénergiques, ce qui supporte l'hypothèse de la vulnérabilité.…”