Brain Adrenergic receptors and resistance to stress

Stone, Eric A.; Platt, Jane

doi:10.1016/0006-8993(82)90452-8

Cited by 186 publications

(27 citation statements)

References 13 publications

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“…Therefore, the possibility exists that biochemical changes due to swim-induced stress may interact with the neuronal effects exerted by the various drugs, thus resulting in an anti-immobility action. Even if the effect of stress on immobility time is a matter of controversy Garcia-Marquez and Armario 1987a, b), other authors (Katz et al 1981 ;Platt and Stone 1982;Stone and Platt 1982;Duncan et al 1985;GarciaMarquez and Armario 1987b) have suggested an interaction between stress and antidepressant drug effects and our results agree with this hypothesis. This is also substantiated by the fact that desipramine exerted anti-immobility effects in rats exposed to types of stress (cold, restraint or footshock) different from forced swimming.…”

Section: Discussionsupporting

confidence: 92%

Discovery of antidepressant activity by forced swimming test may depend on pre-exposure of rats to a stressful situation

Borsini

Lecci

Sessarego³

et al. 1989

Psychopharmacology

109

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Antidepressant-induced anti-immobility effects have been assessed in animals exposed or not to a pretest session using the forced swimming test. Desipramine, maprotiline, mianserine (15 and 30 mg/kg), nomifensine (2.5 and 5 mg/kg), d-amphetamine (1 and 2 mg/kg) and muscimol (1 and 2 mg/kg), unlike imipramine (15 and 30 mg/kg), LY-171555 (0.1 and 0.2 mg/kg) and scopolamine (0.5 and 0.1 mg/kg), did not reduce immobility time in rats which had not received the pretest session. On the other hand, all of the drugs tested reduced immobility time in rats exposed to a pretest session. In addition, the degree of antiimmobility effects of desipramine (20 mg/kg) and nomifensine (5 mg/kg) increased proportionally with the level of water (0, 4, 15 and 30 cm) to which animals were exposed at the time of pretest. Furthermore, desipramine reduced immobility time in rats pre-exposed to types of stress different from forced swimming, cold, restraint or foot-shock. All drugs were injected intraperitoneally three times, 24, 5 and 1 h before testing. The present findings suggest that a stressful pretest session may reveal pharmacological properties of antidepressants in the forced swimming test. This is also substantiated by the fact that diazepam (2.5 and 5 mg/kg) administered 30 min before the swimming pretest antagonized the anti-immobility effect of 15 mg/kg desipramine.

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Section: Discussionsupporting

confidence: 92%

Discovery of antidepressant activity by forced swimming test may depend on pre-exposure of rats to a stressful situation

Borsini

Lecci

Sessarego³

et al. 1989

Psychopharmacology

109

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“…Chronic IMO induced anorexia and reduced body weight gain in all strains, confirming the severity of this chronic stress condition [20,22,49], Although some dif ferences among strains were found regarding changes in food intake and body weight caused by chronic IMO (ta ble 2), these differences were not related to HPA axis activity and, therefore, they are not further discussed. Chronic IMO increased ACTH levels in LEW, SHR and WKY but not in FIS and BN rats.…”

Section: Discussionmentioning

confidence: 83%

Hypothalamic-Pituitary-Adrenal Response to Chronic Stress in Five Inbred Rat Strains: Differential Responses Are Mainly Located at the Adrenocortical Level

Gómez

Lahmame

Kloet³

et al. 1996

Neuroendocrinology

248

137

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The effects of chronic stress on the hypothalamic-pituitary-adrenocortical (HPA) axis were studied in five inbred rat strains, i.e. Brown Norway (BN), Fischer (FIS), Lewis (LEW), Spontaneously Hypertensive (SHR) and Wistar Kyoto (WKY). Previously, these rat strains had been shown to display clear behavioral differences in the forced swimming test that presumably measures depression-like behavior, BN and WKY being more passive than the other strains. Here we test the hypothesis that the differences in behavioral immobility might be associated with an abnormal HPA response to chronic immobilization (IMO) stress. In stress-naive rats under basal conditions (morning) there were no differences among strains in adrenal weight, serum adrenocorticotropin hormone (ACTH) and corticosterone (B) levels, corticotropin-releasing factor (CRF) mRNA in the hypothalamic paraventricular nucleus (PVN) and hippocampal glucocorticoid and mineralocorticoid receptor (GR and MR) mRNA. After chronic IMO, basal serum ACTH levels were increased in LEW, SHR and WKY, but not in BN or FIS rats, whereas basal B levels were increased in BN, FIS, SHR and WKY rats, but not in LEW. The increase in adrenal weight was also strain dependent and correlated negatively with chronic IMO-induced hypercorticosteronemia. These peripheral differences among strains were not observed at central levels. Thus, chronic IMO increased the CRF mRNA content in the PVN, analyzed by in situ hybridization, similarly in all strains. In addition, after chronic IMO no differences were found among strains in hippocampal GR mRNA and RM mRNA contents. Considering data from all strains together, chronic IMO reduced the GR mRNA (50-60%) content in the hippocampal CA1, CA3 and DG areas, and slightly diminished (11–13%) MR mRNA levels in CA1 and CA3 areas. The present results indicate that: (i) chronic IMO down-regulates GR mRNA in the hippocampus and slightly up-regulates CRF mRNA in the hypothalamic PVN similarly in all strains; (ii) after chronic IMO interstrain differences were observed in serum ACTH and B levels as well as adrenal hypertrophy; (iii) some changes are probably located at the adrenal level since changes in serum B level and adrenal weight were not related to changes in ACTH; (iv) in LEW and WKY rats, B hyporesponsiveness to chronic IMO might be linked to low adrenal sensitivity to ACTH, and (v) HPA axis changes induced by the chronic IMO procedure are not related to previously reported data on depressive-like behavior of BN and WKY in the forced swimming test.

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“…On the contrary, the changes in central DA activity provoked by stress are considerably less pronounced than those of NA [3]. Brain DA appears to be more resistant to change after acute stress [34], and inconsistent results are available with respect to DA alterations following stress [3,16]. A recent report from this laboratory indicates that, unlike central NA, DA has no role in stress-induced release of the adrenocorticotrophic hormone in rats [2].…”

Section: Discussionmentioning

confidence: 96%

Inhibition of carrageenin-induced pedal oedema in rats by immobilisation stress

1987

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The effect of immobilisation stress on acute pedal inflammation induced by carrageenin, and the mechanism of stress-induced anti-inflammatory effect, were investigated in male Wistar strain albino rats. Carrageenin-induced pedal inflammation oedema was attenuated by immobilisation stress in a time-dependent manner, when the rats were restrained for 30 min, 1 h, and 2 h immediately after the induction of the inflammation. Pentobarbitone exhibited significant anti-inflammatory effect of its own in an anaesthetic dose and also inhibited stress (1 h)-induced attenuation of the inflammation. Likewise, lignocaine, injected behind the knee joint of the inflamed limb, attenuated the inflammation and also inhibited the stress-induced anti-inflammatory effect. These findings indicate the importance of the central nervous system (CNS) and the afferent/efferent neural pathways from and to the inflammatory site, in inflammation and in stress-induced anti-inflammatory effect. Earlier studies from this laboratory have shown that the central noradrenergic, histaminergic, serotonergic and GABA-ergic neurotransmitter systems have a modulatory anti-inflammatory effect on carrageenin-induced pedal oedema. Since all these neurotransmitter systems have been reported to be activated by stress, their role was assessed in the inflammation-attenuation effect of immobilisation stress. The present studies indicate that, of these neurotransmitters, only the central noradrenergic system is involved in the anti-oedema effect of stress. Endogenous opioid peptides may also be involved in the stress-inflammation interaction, since naloxone inhibited the stress effect. Bilateral adrenalectomy and peripheral chemical sympathectomy, induced by i.p. administration of 6-hydroxydopamine, augmented carrageenin oedema and antagonised the stress-induced anti-inflammatory effect. However, metyrapone, an inhibitor of endogenous corticoid synthesis, failed to inhibit the stress effect. These findings indicate that the sympatho-medullary system, which is known to be activated during stress, is responsible for the observed anti-inflammatory effect of immobilisation stress, rather than augmented release of adrenal corticoids. It is suggested that the observed inflammation reducing effect of immobilisation stress is a consequence of increased central noradrenergic and peripheral sympatho-medullary activity.

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Brain Adrenergic receptors and resistance to stress

Cited by 186 publications

References 13 publications

Discovery of antidepressant activity by forced swimming test may depend on pre-exposure of rats to a stressful situation

Discovery of antidepressant activity by forced swimming test may depend on pre-exposure of rats to a stressful situation

Hypothalamic-Pituitary-Adrenal Response to Chronic Stress in Five Inbred Rat Strains: Differential Responses Are Mainly Located at the Adrenocortical Level

Inhibition of carrageenin-induced pedal oedema in rats by immobilisation stress

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