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Since the pineal gland is an end organ of the sympathetic nervous system, stress might increase the synthesis of its hormone, melatonin. The stress of a 10 min swim, which elicits a marked rise in circulating catecholamines, causes a dramatic depression of high pineal melatonin levels at night within 15 min after swimming onset. N-acetyltransferase (NAT) activity is unaffected by the treatment at 15 or 30 min after swimming onset. Within 90 min after initiation of a 15 min swim, high nighttime pineal melatonin levels are restored while NAT values remain elevated. The swimming-induced reduction in high pineal melatonin levels is not influenced by either hypophysectomy, superior cervical ganglionectomy, prazosin (alpha 1-adrenergic receptor blocker) pretreatment, yohimbine (alpha 2-adrenergic receptor blocker) pretreatment, or reserpine (amine depletor) pretreatment. These results indicate that neither hormones secreted from the pituitary gland nor catecholamines secreted from the sympathetic nerves are involved in eliciting the dramatic reduction in elevated pineal melatonin levels in the rat.

Three subspecies of Peromyscus inhabiting the montane, foothill, and coastal plain regions of the Carolinas were trapped in midwinter and the occurrence of spontaneous and ration-induced daily torpor was monitored via biotelemetric determination of body temperature. All tests were undertaken with field-caught mice that were subjected to a minimum of laboratory acclimation (two days). The tendency to enter torpor in the presence of adequate food was highest in P. maniculatus nubiterrae, whose natural montane habitat presents it with the greatest seasonal stress in terms of ambient temperature and food availability. This species exhibited significantly (P<0.05) longer spontaneous torpor bouts than did the two lowland subspecies, P, gossypinus gossypinus and P. leucopus leucopus ( Table 1). Restriction of food to one-half the ad libitum level increased the frequency, duration, and depth (mean minimum body temperature) of torpor in all three species (Fig. 1). P. maniculatus, however, displayed significantly (P < 0.001) longer episodes of torpor induced by rationing than did either of the other two subspecies. The ability to compensate for a reduction in energy intake by adjusting levels of energy utilization may profoundly affect survival during short-term environmental stress in any of these three species.

The activity of N-acetyltransferase (NAT) and the content of melatonin (MEL) in the rat pineal have been shown to be sensitive to several types of stressors. This study was designed to assess the role of the adrenals in mediating the effect of one such stressor, insulin-induced hypoglycemia, on pineal synthetic activity. Intact and bilaterally adrenalectomized (ADX) adult male rats were kept under light:dark cycles of 14:10 (lights on 0600 h) and injected intraperitoneally with 10 IU insulin at 1300 h, and groups (n = 8) were killed 2, 3, or 4 h postinjection. Plasma catecholamines were assayed by means of high performance liquid chromatography and radioimmunoassay was used to assess pineal NAT activity and MEL content. All injected groups were rendered hypoglycemic by insulin administration. Compared to uninjected controls, plasma epinephrine in hypoglycemic intact rats rose after 2 h, whereas epinephrine did not change in hypoglycemic ADX animals. The increase in epinephrine in intact animals was correlated with a rise in NAT activity at 2 h. Moreover, pineal MEL content at 2, 3, and 4 h was significantly greater than control values. In contrast, no changes in pineal biosynthetic function were found in ADX rats. This differential response by intact and ADX rats suggests that an adrenal product (possibly epinephrine) is responsible for mediating the stimulatory effects of acute insulin-induced hypoglycemic stress on the rat pineal.