Neuroanatomical basis for facilitation of hypothalamic-pituitary-adrenal responses to a novel stressor after chronic stress

doi:10.1016/S0306-4522(97)00577-0

Neuroscience

Volume 84, Issue 4, June 1998, Pages 1025-1039

https://doi.org/10.1016/S0306-4522(97)00577-0 Get rights and content

Abstract

Animals exposed to chronic stress exhibit normal or enhanced hypothalamic-pituitary-adrenal responses to novel, acute stimuli despite the inhibitory endogenous corticosterond response to the chronic stressor. Prior stress is thought to induce a central facilitatory trace that, upon exposure to a novel stimulus, balances or overcomes the inhibitory effects of corticosterone. The neuroanatomical basis for this facilitation of hypothalamic-pituitary-adrenal responses is unknown. In this study, we first show increased adrenocorticotropin and corticosterone responses to the novel stressor of restraint in rats exposed to intermittent cold for seven days. We then compared numbers of Fos-immunoreactive cells in 26 sites in control and chronically stressed rats at various times after onset of a 30 min restraint. At 60 min, density of Fos-stained cells was significantly higher in chronically stressed than in control rats in the parabrachial/Kölliker-Fuse area, posterior paraventricular thalamus, central, basolateral and basomedial nuclei of the amygdala and parvocellular paraventricular hypothalamus. The posterior paraventricular nucleus of the thalamus receives projections from the parabrachial nucleus and projects heavily to the differentially stained subnuclei of the amygdala, which in turn project to the parvocellular paraventricular nucleus of the hypothalamus.

We propose that increased activity in the parabrachial-posterior paraventricular thalamus-amygdala-parvocellular paraventricular hypothalamus underlies facilitation of the hypothalamic-pituitary-adrenal axis to novel stress in chronically stressed rats. We confirmed part of this proposal by showing that lesions of the posterior paraventricular nucleus of the thalamus increase adrenocorticotropin responses to restraint only in previously chronically stressed animals. This potential circuit provides a basis for further examination of the functional roles of these regions in stress-induced facilitation of hypothalamic-pituitary-adrenal activity.

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Neuroanatomical basis for facilitation of hypothalamic-pituitary-adrenal responses to a novel stressor after chronic stress

Abstract

Front. Neuroendocrinol.

Neuroscience

Brain Res.

Neuroscience

Neuroscience

Rec. Prog. Hormone Res.

Trends Neurosci.

J. Neurosci. Meth.

Brain Res.

Brain Res. Rev.

Brain Res.

Brain Res.

Brain Res.

Brain Res.

Brain Res.

Physiol. Behav.

Brain Res.

Brain Res.

Prog. Neurobiol.

Brain Res.

Feedback and facilitation in the adrenocortical system: unmasking facilitation by partial inhibition of the glucocorticoid response to prior stress

Endocrinology

Clamped corticosterone (B) reveals the effect of endogenous corticosterone on both facilitated responsivity to acute restraint and metabolic responses to chronic stress

Stress

Resetting of the circadian clock by a conditioned stimulus

Nature

Control of ACTH secretion by the central nucleus of the amygdala: implications of the serotonergic system and its relevance to the glucocorticoid delayed negative feedback mechanism

Neuroendocrinology

Regulation of the messenger ribonucleic acid for corticotropinreleasing factor in the paraventricular nucleus and other brain sites of the rat

Endocrinology

Hypothalamic-pituitary-adrenal function in chronic intermittently cold stressed neonatally handled and non-handled rats

J. Neuroendocrinol.

Evidence that corticotropinreleasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in rats

Brain Res.

Expression of c-Fos immunoreactivity in transmittercharacterized neurons after stress