Footshock-induced changes in brain catecholamines and indoleamines are not mediated by CRF or ACTH

Footshock-induced changes in brain catecholamines and indoleamines are not mediated by CRF or ACTH Stressful treatments have long been associated with increased activity of brain catecholaminergic and serotonergic neurons. An intracerebroventricular (icv) injection of the corticotropin-releasing factor (CRF) also activates brain catecholaminergic neurons. Because brain CRF-containing neurons appear to be activated during stress, it is possible that CRF mediates the catecholaminergic activation. This hypothesis has been tested by assessing the responses in brain catecholamines and indoleamines to footshock in mice pretreated icv with a CRF receptor antagonist, and in mice lacking the gene for CRF (CRFko mice). Consistent with earlier results, icv administration of CRF increased catabolites of dopamine and norepinephrine, but failed to alter tryptophan concentrations or serotonin catabolism. A brief period of footshock increased plasma corticosterone and the concentrations of tryptophan and the catabolites of dopamine, norepinephrine and serotonin in several brain regions. Mice injected icv with 25 μg alpha-helical CRF 9–41 prior to footshock had neurochemical responses that were indistinguishable from controls injected with vehicle, while the increase in plasma corticosterone was slightly attenuated in some experiments. CRFko mice exhibited neurochemical responses to footshock that were indistinguishable from wild-type mice. However, whereas wild-type mice showed the expected increase in plasma corticosterone, there was no such increase in CRFko mice. Similarly, hypophysectomized mice also showed normal neurochemical responses to footshock, but no increase in plasma corticosterone. Hypophysectomy itself elevated brain tryptophan and catecholamine and serotonin metabolism. Treatment with ACTH icv or peripherally failed to induce any changes in cerebral catecholamines and indoleamines. These results suggest that CRF and its receptors, and ACTH and other pituitary hormones, are not involved in the catecholamine and serotonin responses to a brief period of footshock. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurochemistry International Elsevier

Footshock-induced changes in brain catecholamines and indoleamines are not mediated by CRF or ACTH

Neurochemistry International, Volume 37 (1) – Jul 1, 2000

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Publisher
Elsevier
Copyright
Copyright © 2000 Elsevier Science Ltd
ISSN
0197-0186
DOI
10.1016/S0197-0186(99)00163-1
Publisher site
See Article on Publisher Site

Abstract

Stressful treatments have long been associated with increased activity of brain catecholaminergic and serotonergic neurons. An intracerebroventricular (icv) injection of the corticotropin-releasing factor (CRF) also activates brain catecholaminergic neurons. Because brain CRF-containing neurons appear to be activated during stress, it is possible that CRF mediates the catecholaminergic activation. This hypothesis has been tested by assessing the responses in brain catecholamines and indoleamines to footshock in mice pretreated icv with a CRF receptor antagonist, and in mice lacking the gene for CRF (CRFko mice). Consistent with earlier results, icv administration of CRF increased catabolites of dopamine and norepinephrine, but failed to alter tryptophan concentrations or serotonin catabolism. A brief period of footshock increased plasma corticosterone and the concentrations of tryptophan and the catabolites of dopamine, norepinephrine and serotonin in several brain regions. Mice injected icv with 25 μg alpha-helical CRF 9–41 prior to footshock had neurochemical responses that were indistinguishable from controls injected with vehicle, while the increase in plasma corticosterone was slightly attenuated in some experiments. CRFko mice exhibited neurochemical responses to footshock that were indistinguishable from wild-type mice. However, whereas wild-type mice showed the expected increase in plasma corticosterone, there was no such increase in CRFko mice. Similarly, hypophysectomized mice also showed normal neurochemical responses to footshock, but no increase in plasma corticosterone. Hypophysectomy itself elevated brain tryptophan and catecholamine and serotonin metabolism. Treatment with ACTH icv or peripherally failed to induce any changes in cerebral catecholamines and indoleamines. These results suggest that CRF and its receptors, and ACTH and other pituitary hormones, are not involved in the catecholamine and serotonin responses to a brief period of footshock.

Journal

Neurochemistry InternationalElsevier

Published: Jul 1, 2000

References

  • Influence of corticotropin-releasing hormone on electrophysiological activity of locus coeruleus neurons
    Borsody, M.K; Weiss, J.M
  • Stress-related changes in cerebral catecholamine and indoleamine metabolism: lack of effect of adrenalectomy and corticosterone
    Dunn, A.J
  • Stress- and endotoxin-induced increases in brain tryptophan and serotonin metabolism depend on sympathetic nervous system activity
    Dunn, A.J; Welch, J
  • Nucleus locus ceruleus: new evidence of anatomical and physiological specificity
    Foote, S.L; Bloom, F.E; Aston-Jones, G
  • Exogenous tryptophan increases synthesis, storage, and intraneuronal metabolism of 5-hydroxytryptamine in the rat hypothalamus
    Lookingland, K.J; Shannon, N.J; Chapin, D.S; Moore, K.E
  • CRF receptor antagonist attenuates immobilization stress-induced norepinephrine release in the prefrontal cortex in rats
    Smagin, G.M; Zhou, J; Harris, R.B; Ryan, D.H
  • Corticotropin-releasing factor administered into the locus coeruleus, but not the parabrachial nucleus, stimulates norepinephrine release in the prefrontal cortex
    Smagin, G.N; Swiergiel, A.H; Dunn, A.J

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