there are no studies at present in the literature investigating a possible BDNF circadian rhythm in humans, we studied the BDNF levels throughout 24 h in healthy men, in order to detect the possible relative changes in plasma BDNF protein. Additionally
Silvia Begliuomini, Elena Lenzi, Filippo Ninni, Elena Casarosa, Sara Merlini, Nicola Pluchino, Valeria Valentino, Stefano Luisi, Michele Luisi and Andrea R Genazzani
Y. C. PATEL, H. W. G. BAKER, H. G. BURGER, M. W. JOHNS and JOANNE E. LEDINEK
Pharmacological doses of glucocorticoids inhibit thyroid function in man and laboratory animals due to suppression of thyrotrophin (TSH) secretion (Wilber & Utiger, 1969). Administration of prednisolone or dexamethasone for 1–2 days results in a suppression of basal serum TSH levels in normal subjects and in patients with primary hypothyroidism, whilst the pituitary TSH reserve capacity, as assessed by the response to synthetic thyrotrophin releasing hormone (TRH), remains unaltered (Wilber & Utiger, 1969; Besser, Ratcliffe, Kilborn, Ormston & Hall, 1971; Haigler, Pittman & Hershman, 1971). However, impairment of serum TSH response to administered TRH does occur in patients treated with glucocorticoids for 1 or more months (Otsuki, Dakoda & Baba, 1973). These studies suggest that glucocorticoids may inhibit TSH secretion at both hypothalamic and pituitary levels but the main effect of the short-term treatment is suppression of TRH production.
Nicoloff, Fisher & Appleman (1970) found that the circadian rhythm of thyroidal
D. C. HOLLEY, D. A. BECKMAN and J. W. EVANS
Department of Animal Science, University of California, Davis, California 95616, U.S.A.
(Received 8 October 1974)
Few studies have dealt with diurnal cortisol rhythm in sheep (McNatty, Cashmore & Young, 1972; McNatty & Young, 1973). The present results elucidate further the circadian rhythm of ovine plasma cortisol and describe the effect of sudden and continuous cage restraint.
Experimental methods and conditions were reported in detail by Holley & Evans (1974). Six mature rams were sampled at 4 h intervals for 32 days. On day 17 the animals were placed singly in small cages. Throughout the experiment the sheep received lucerne pellets at 16.00 h and the lighting schedule was maintained at 14 h light: 10 h darkness. Plasma cortisol was determined in duplicate without correction for other steroids as described by Bassett & Hinks (1969) and adjusted for extraction efficiency.
Fig. 1. Daily percentage variations (means ± s.e.m.) in plasma cortisol
Roberto Dominguez, Laura Riboni, Domingo Zipitria and Rodolfo Revilla
Rats with a 4-day oestrous cycle were given a single dose of atropine (100, 300, 500 or 700 mg/kg body wt) at 13.00 h on the days of oestrus, dioestrus 1, dioestrus 2 or pro-oestrus and were autopsied on the next expected day of oestrus. The doses of atropine (in mg/kg body wt) necessary to block ovulation during the cycle were 300 at oestrus, 100 at dioestrus 1 or 2 and 700 at pro-oestrus. A single dose of atropine (100 mg/kg) at oestrus, dioestrus 1 or dioestrus 2 was given at 09.00, 13.00, 17.00 or 21.00 h, autopsy again being performed on the next expected day of oestrus. The ability of atropine to block ovulation appeared to have a circadian rhythm, with a maximum blockade at 13.00 h on dioestrus 1 and dioestrus 2 and a minimum at 21.00 h on the same days. Hormone replacement (human chorionic gonadotrophin at oestrus, dioestrus 1 or 2, oestradiol benzoate at dioestrus 2 or progesterone at pro-oestrus) re-established normal ovulation in rats whose ovulation was blocked with atropine (100 mg/kg) on dioestrus 1 at 13.00 h. When ovulation was blocked with atropine but no hormone replacement had been given, rats ovulated 24 h after the next expected day of oestrus.
Results obtained in these experiments suggest the existence of a circadian rhythm of gonadotrophin secretion thoughout the oestrous cycle and a close relationship between that rhythm and the cholinergic system.
A. M. McNicol, I. D. Penman and A. E. Duffy
Using a metaphase arrest technique, mitotic activity was quantified in the adrenal cortex over a 24-h period in 14-day-old male Sprague–Dawley rats before functional rhythmicity of the hypothalamic pituitary-adrenal (HPA) axis is established, and after its onset, in 6- to 7-week-old rats. At all times, proliferative activity was greater in the younger animals, as previously reported. A significant circadian rhythm was identified in both groups, but the timing of the peak differed, lying between 17.00 and 21.00 h at 14 days and 11.00 and 15.00 h at 6–7 weeks. These results raise the possibility that functional rhythmicity of the HPA axis may alter an inherent proliferative rhythm.
Journal of Endocrinology (1989) 120, 307–310
J. F. Cockrem and B. K. Follett
Melatonin was measured by radioimmunoassay in homogenates of pineal glands from quail (Coturnix coturnix japonica) kept under different photoperiods and in darkness. Under 8-, 12- and 16-h daylengths melatonin levels were increased during the dark period, the duration of the increase depending on the duration of the dark period. As the daylength was increased the peak occurred closer to lights-off, reflecting the more rapid melatonin rise under the longer photoperiods. The pineal melatonin rhythm continued in darkness with an amplitude relative to that seen under a light/dark cycle of slightly less than one-half after 2 days in darkness and one-third after 6 days in darkness. The corresponding average periods of the rhythm were 25·5 h and 25·7 h. These results show that there is a circadian rhythm of melatonin in the pineal gland of the quail which is entrained by light/dark cycles and which continues in darkness.
J. Endocr. (1985) 107, 317–324
R. SRIDARAN and C. E. McCORMACK
Continuous monitoring of wheel-running activity and determination of the time of ovulation in rats by serial laparotomies revealed that ovulation followed the onset of running at prooestrus by approximately 9 h (range 7–11 h). This temporal relationship held in rats in which the period of the circadian rhythm had been modified (entrained) by daily exposure to 14 h photoperiods, and in rats in dim continuous light whose rhythms were non-entrained (freerunning). Knowledge of this temporal relationship between the two rhythms made it possible to give bright light signals at known points in the circadian cycle of the rat and to observe the effects on the timing of running and ovulation in subsequent cycles. Giving daily light signals near the onset of running (i.e. at subjective dusk) delayed, whereas giving signals near the end of running (i.e. at subjective dawn) advanced, the time of running and ovulation in subsequent cycles. These results indicate that in rats exposed to the usual laboratory photoperiod the delaying effect of dusk light and the advancing effect of dawn light balance one another; thus the preovulatory surge of LH occurs at a relatively consistent time at prooestrus.
IRVING ZUCKER, CATHERINE P. CRAMER and E. L. BITTMAN
Locomotor activity of male hamsters was recorded during long-term exposure to constant light (LL), constant darkness (DD) and during entrainment (modification of a circadian rhythm) to a 14 h light: 10 h darkness photoperiod (14L: 10D). In LL the period of the activity cycle was substantially longer in hypophysectomized than in control animals. This difference persisted during tests in DD. Although hypophysectomy reduced the duration of the active phase in some hamsters, overall the difference between the groups was not significant. The phase angle of onset of activity in 14L: 10D was not affected by hypophysectomy. Hypophysectomized female hamsters tested in DD had activity rhythms whose periods were longer than those of control animals; they were also significantly less active than corresponding controls during the first 4 h of the subjective night but the duration of the active phase did not differ significantly between the groups. These results suggest that hormones of the pituitary-gonadal axis modulate the period of circadian oscillation.
G. CHAZAL, M. FAUDON, F. GOGAN, M. HERY, C. KORDON and E. LAPLANTE
Implantation of a solid source of oestradiol into ovariectomized rats produced constant plasma concentrations of the hormone over a long period of time. Under these conditions, LH is released in a circadian pattern with a very marked peak in the afternoon. This circadian rhythm is synchronized to the light–darkness cycle, since it follows exactly a shift in the nycthemeral cycle. The first peak appeared on day 3 after placement of the oestrogen implant; its amplitude was constant from days 3 to 9 after implantation, and decreased gradually during prolonged implantation. The afternoon peak was not correlated with changes in the pituitary sensitivity to exogenous LH releasing hormone (LH-RH), since the LH response to increasing doses of the peptide could be superimposed in the morning and in the afternoon. However, the decreased amplitude of the rhythm observed after more than 9 days of implantation seemed to depend upon a progressive desensitization of the pituitary gland to LH-RH. Pituitary LH content also decreased as a function of implantation time. It is concluded that, under conditions of constant plasma oestradiol concentrations and of constant pituitary sensitivity to LH-RH, a daily activation of the neural trigger releasing pituitary gonadotrophins occurs.
A. H. Cincotta and A. H. Meier
Lipogenesis and blood glucose concentrations were determined at 4-hourly intervals in control and insulin-treated golden hamsters maintained on 14-h daily photoperiods (08·00–22·00 h). Lipogenesis was studied by measuring the incorporation of label into liver and fat pad lipids in animals killed 30 min after i.p. [3H]acetate injection and 2 h after insulin or saline (control) injections. Circadian rhythms of lipogenesis and plasma glucose concentration were present in both control and insulin-treated hamsters. In control animals most lipogenic activity occurred during the dark period and early during the daily photoperiod (14 h light: 10 h darkness). There were dramatic differences in the lipogenic (fat pad) and hypoglycaemic responses to insulin which varied as a function of the time of day at which insulin was injected. Insulin stimulated fivefold increases in lipid deposition (fat pad incorporation) when injected late during the dark period but had little or no effect 4–8 h after the onset of light. Daily injections for 8 days also produced variable cumulative effects on body fat stores as a function of the time of day. Insulin injected late during the dark period stimulated a 40% increase in abdominal fat weight over controls, whereas insulin injected at 4 and 12 h after the onset of light had no effect on abdominal fat weight. Insulin decreased plasma glucose concentrations markedly at 8 and 20–24 h after the onset of light but had no apparent hypoglycaemic activity (120 min after its injection) at 4 h after the onset of light. These response rhythms coupled with rhythms of insulin secretion provide a basis for temporal synergisms which could produce a spectrum of physiological conditions as a function of the phase relations between the rhythms.
J. Endocr. (1984) 103, 141–146