Volume 65, Issue 1 pp. 263-267
Full Access

Effect of Development of Habituation to Restraint Stress on Hypothalamic Noradrenaline Release and Adrenocorticotropin Secretion

S. Terrazzino

S. Terrazzino

Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy

Search for more papers by this author
C. Perego

C. Perego

Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy

Search for more papers by this author
M. G. De Simoni

Corresponding Author

M. G. De Simoni

Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy

Address correspondence and reprint requests to Dr. M. G. De Simoni at Istituto di Recherche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milan, Italy.Search for more papers by this author
First published: July 1995
Citations: 29

Abstract

Abstract: The effect of repeated stress has been studied on noradrenaline release in the hypothalamic paraventricular nucleus and on adrenocorticotropin levels. Rats were stressed by 20-min immobilization once a day for 5 days. On day 6 they were exposed to the same stress or to a different one (ether vapors for 2 min). Immobilization and ether stress increased noradrenaline release in naive rats (271 ± 43 and 197 ± 9%, respectively) and raised adrenocorticotropin levels, showing activation of the hypothalamus-pituitary axis. Repeated daily restraint did not modify basal noradrenaline or adrenocorticotropin levels. The further immobilization session on day 6 did not change noradrenaline levels at any observation time (20–120 min). The adrenocorticotropin response was still present, although significantly reduced. In repeatedly restrained rats, exposure to ether vapors induced a maximal increase in noradrenaline level similar to that observed in naive rats, although prolonged. In these rats the adrenocorticotropin response did not differ from that in acutely stressed rats. These results suggest that habituation may develop to a stressful stimulus leading to suppression of the hypothalamic noradrenergic response and that this phenomenon is stress specific. Moreover, modifications of noradrenaline release in the paraventricular nucleus are not solely responsible for the adrenocorticotropin response during stress, suggesting that other pathways and/or neurotransmitters are involved too.

Abbreviations used: ACTH, adrenocorticotropin; CA, catecholaminergic; CRF, corticotropin releasing factor; CURT, curve randomization test; HPA axis, hypothalamus-pituitary-adrenal axis; NA, noradrenaline; PVN, hypothalamic paraventricular nucleus.

    The full text of this article hosted at iucr.org is unavailable due to technical difficulties.