Hormonal Status and the Neuroendocrine Response to a Novel Heterotypic Stressor Involving Subchronic Noise Exposure

Abstract

Despite a number of studies on noise-induced health effects, it is still unclear to what extent different neuroendocrine pathways are affected by noise exposure. Male Wistar rats were housed in sound-attenuated rooms isolated for noise from outside. Three groups of chronically cannulated rats were exposed to either background noise (±64 dB) only or irregular experimental white noise (90 dB, 2-22 kHz). Two protocols, with approximately the same total amount of noise but with different densities, were used: protocol N1 (180 min random noise per day for 18 days) or protocol N2 (540 min random noise per day for 8 days). Basal levels of circulating hormones (ACTH, corticosterone, prolactin and catecholamines) and plasma glucose were measured. In control animals, no significant changes in any of these parameters were observed over 18 days. Except for plasma prolactin, N1 did not induce a significant elevation in basal hormonal levels. N2 however induced significant elevation in basal prolactin, corticosterone and noradrenaline levels. At the end of the exposure period, all animals were subjected to a novel heterotypic stressor (restraint stress) to monitor differences in neuroendocrine activation (ACTH, corticosterone and prolactin). Compared to nonexposed control animals, N1 animals showed a normal ACTH and an enhanced corticosterone response, whereas N2 animals showed an increased ACTH but a normal corticosterone response. The prolactin response of both Nl and N2 animals was significantly decreased. Adrenal cell suspension experiments revealed that in noise-exposed rats both basal- and ACTH-stimulated corticosterone production were significantly increased as compared to control animals. These results indicate that chronic noise exposure at mild intensities induces subtle but significant changes in hormonal regulation.

An Initial, Three-Day-Long Treatment with Alcohol Induces a Long-Lasting Phenomenon of Selective Tolerance in the Activity of the Rat Hypothalamic–Pituitary–Adrenal Axis

“…Most studies have focused on animals that were exposed to a particular stressor immediately after a period of repeated or continuous exposure to this same or another signal (Kant et al, 1985;Akana et al, 1992;Ottenweller et al, 1992;vanRaaij et al, 1997), including work showing adaptation of the HPA axis of rats chronically exposed to alcohol and to the drug itself but not to other stresses (Spencer and McEwen, 1990). To our knowledge, the only report of a long-lasting change in the activity of the HPA axis that persisted once the initial stressor had been removed indicated a prolongation, not a blunting, of the AC TH and corticosterone response to a single injection of the proinflammatory cytokine interleukin-1 (IL-1) (Schmidt et al, 1995).…”

Prenatal Dexamethasone Impairs Behavior and the Activation of the BDNF Exon IV Promoter in the Paraventricular Nucleus in Adult Offspring

“…Recently, it has been shown that acoustic trauma results in elevated hearing thresholds and reductions in BDNF protein levels (31) and alters the activation of the HPA axis (32). Moreover, acoustic trauma was shown to increase c-fos expression in the PVN and central auditory areas but not in the hippocampus or amygdala (33)(34)(35)(36). Even though direct anatomical connections between the auditory system and the hypothalamus have not been demonstrated, there is ample evidence demonstrating that acoustic challenge activates stress responses relating the PVN and the auditory pathway.…”

Plasma Concentration of Adrenocorticotropic Hormone in Traffic Policemen

“…In human subjects, acute carbon monoxide intoxication (CO) induces a marked increase in ACTH(P) levels, with values of 59 pg/ml in subjects with carboxyhemoglobin (COHb) <15% and 130 pg/ml in subjects with COHb>15% 1) . Aural stress has been observed to alter catecholamines, pituitary gland hormones and adrenal corticosteroids 6) both in animals and human subjects [6][7][8] . Animals exposed to 540 min of random noise per day for 8 d showed an increase in circulating ACTH levels 6) .…”

“…Aural stress has been observed to alter catecholamines, pituitary gland hormones and adrenal corticosteroids 6) both in animals and human subjects [6][7][8] . Animals exposed to 540 min of random noise per day for 8 d showed an increase in circulating ACTH levels 6) . A study on twelve paid male volunteers 8) exposed to industrial noise of 85 dB (A) from 09.00 to 21.00 h, showed temporarily increased levels of ACTH(P).…”

“…On the other hand, cadmium [3][4][5] , mercury and copper 5) cause a decrease in ACTH(P) levels. Physical agents such as noise [6][7][8] and psycho-social stressors [9][10][11][12][13][14] also increase concentrations of ACTH(P).…”