Seven-day variable-stress regime alters cortical β-adrenoceptor binding and immunologic responses: Reversal by imipramine

Basso, Ana M.; Depiante-Depaoli, M; Cancela, Liliana Marina; Molina, Vı́ctor A.

doi:10.1016/0091-3057(93)90522-u

Cited by 34 publications

(16 citation statements)

References 39 publications

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“…The increase, rather than decrease, in DTH following chronic restraint was somewhat surprising, given previous reports that chronic stress is detrimental to immune function (Basso et al, 1993;Bonneaud et al, 2004;Dhabhar and McEwen, 1997); however, a few studies have reported that some aspects of immune function are enhanced and some are suppressed by chronic stress (Cunnick et al, 1988;Mizoguchi et al, 2001;Nakano, 2004;Van Raaij et al, 1996). There were also notable differences between the current study and previous experiments documenting the suppressive influence of chronic stress on DTH responses (Dhabhar and McEwen, 1997).…”

Section: Discussioncontrasting

confidence: 55%

Stressor-specific alterations in corticosterone and immune responses in mice

Bowers

Bilbo

Dhabhar

et al. 2008

Brain, Behavior, and Immunity

197

122

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Different stressors likely elicit different physiological and behavioral responses. Previously reported differences in the effects of stressors on immune function may reflect qualitatively different physiological responses to stressors; alternatively, both large and subtle differences in testing protocols and methods among laboratories may make direct comparisons among studies difficult. Here we examine the effects of chronic stressors on plasma corticosterone concentrations, leukocyte redistribution, and skin delayed-type hypersensitivity (DTH) and the effects of acute stressors on plasma corticosterone and leukocyte redistribution. The effects of several commonly used laboratory stressors including restraint, forced swim, isolation, and low ambient temperatures (4°C) were examined. Exposure to each stressor elevated corticosterone concentrations, with restraint (a putative psychological stressor) evoking a significantly higher glucocorticoid response than other stressors. Chronic restraint and forced swim enhanced the DTH response compared to the handled, low temperature, or isolation conditions. Restraint, low temperature, and isolation significantly increased trafficking of lymphocytes and monocytes compared to forced swim or handling. Generally, acute restraint, low temperature, isolation, and handling increased trafficking of lymphocytes and monocytes. Considered together, our results suggest that the different stressors commonly used in psychoneuroimmunology research may not activate the physiological stress response to the same extent. The variation observed in the measured immune responses may reflect differential glucocorticoid activation, differential metabolic adjustments, or both processes in response to specific stressors.

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Section: Discussioncontrasting

confidence: 55%

Stressor-specific alterations in corticosterone and immune responses in mice

Bowers

Bilbo

Dhabhar

et al. 2008

Brain, Behavior, and Immunity

197

122

View full text Add to dashboard Cite

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“…Stress-induced downregulation of beta-adrenoceptors has also been previously reported for the rat cortex (Stone and Platt 1982). However, while a positive correlation between downregulation and adaptation to stress seemed to exist in the above-mentioned study, other investigators found that chronic stress induced an increase in beta-adrenergic binding sites in the rat brain (Basso et al 1993). On the basis of these inconsistent findings and from data raised with a learned helplessness rat model, it was recently concluded that beta-adrenergic receptor changes may depend on the kind of stress and on test parameters (Brannan et al 1995).…”

Section: Beta-adrenoceptors In the Prefrontal Cortexmentioning

confidence: 71%

Monoamine receptors in the prefrontal cortex of Tupaia belangeri during chronic psychosocial stress

Flügge

Ahrens

Fuchs

1997

Cell and Tissue Research

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The prefrontal cortex has been reported to be involved in the regulation of emotional behaviour by integrating cognitive, emotional and autonomic information processes, and impairments of its functions are implicated in psychopathologies such as depression. Neuronal functioning in the prefrontal cortex is under the control of the noradrenergic and the serotonergic system which are both activated during stress. The present study aimed to quantify the effect of chronic psychosocial stress on alpha2-adrenoceptors, beta-adrenoceptors, and serotonin1A receptors in the prefrontal cortex. Male tree shrews (Tupaia belangeri) were subjected to subordination stress for 2, 10, 21 and 28 days, and binding sites for the alpha2-adrenergic antagonists 3H-rauwolscine and 3H-RX821002, for the beta-adrenergic antagonist 125I-iodocyanopindolol, and for the 5-hydroxytryptamine (5HT)1A receptor agonist 3H-8-hydroxy-2-(di-n-propylamino)tetralin were quantified by in vitro receptor autoradiography. Chronic psychosocial stress induced time-dependent receptor down- and upregulations. Beta-adrenoceptors were transiently reduced in numbers after just 2 days of psychosocial stress which is interpreted as agonist-mediated downregulation induced by high local concentrations of noradrenaline released from terminals originating from the locus coeruleus. Alpha2-adrenoceptors were transiently downregulated after 10 days, and upregulated after 28 days of psychosocial stress. These data indicate that the noradrenergic system adapts to the stress by counterbalancing its receptor numbers. 5HT1A receptors were only downregulated after 28 days of psychosocial stress, and thus react later than the noradrenergic receptors. In summary, our results show that monoaminergic receptors in the prefrontal cortex of tree shrews undergo dynamic changes during chronic psychosocial stress. These alterations probably have an impact on neuronal activity, and might contribute to the behavioural changes which have been previously described in subordinate male tree shrews.

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“…Other stressors, for example, chronic footshock stress (Kellar et al, 1981;Cohen et al, 1986) or rapid eye movement sleep deprivation did not modify beta-adrenergic receptor binding sites in the cortex. Uncontrollable shock (Pandey et al, 1995), seven-day variable-stress regime (Basso et al, 1993) or series of unpredictable stressors (Molina et al, 1990) upregulated B-adrenergic sites. In the current study we utilized a control group which was exposed to the experimental stress conditions, i.e.…”

Section: Discussionmentioning

confidence: 99%