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T Hiroshige

Publications and source records attributed to T Hiroshige.

At least 37 records · Page 2Linked to original sources

Effects of elimination of maternal circadian rhythms during pregnancy on the postnatal development of circadian corticosterone rhythm in blinded infantile rats.

The influence of maternal circadian rhythms on fetal circadian oscillations during pregnancy was examined. Circadian rhythms of spontaneous locomotor activity and plasma corticosterone level in pregnant rats were eliminated by bilateral lesions of the suprachiasmatic nuclei (SCN) at different stages of gestation and the postnatal manifestation of the circadian corticosterone rhythm was examined in individual pups. Effective lesions of SCN at day 3 of gestation resulted in an abortion in all rats examined. Rats whose SCN were lesioned at day 10 or 17 of gestation maintained their pregnancies. At term, pups were removed by Cesarean operation and immediately blinded by bilateral ocular enucleation; they were reared by unoperated foster mother afterwards. All pups from SCN lesioned mothers showed a clear free running circadian rhythm of plasma corticosterone levels after the 4th week of postnatal life. Furthermore, the circadian rhythm that developed in pups from SCN-lesioned mother at day 10 of gestation (G10 pups) was always phase-delayed about 4 h as compared with that in pups from mothers whose SCN were lesioned at day 17 of gestation (G17 pups) and in pups from sham-operated mothers (S pups). It is concluded that the circadian hormone rhythmicity develops in normal fashion postnatally when the maternal SCN are effectively lesioned after day 10 of gestation. The phase-angle difference in the circadian rhythm between G10 pups and G17 or S pups suggests that fetal circadian oscillation is entrainable at least after day 10 of gestation.

Animals↗

Maternal phase setting of fetal circadian oscillation underlying the plasma corticosterone rhythm in rats.

We examined the entraining effect of the maternal circadian system on the fetal circadian oscillation during pregnancy. The circadian rhythm of locomotor activity and plasma corticosterone of pregnant rats was abolished by bilateral ablation of the suprachiasmatic nuclei at day 10 of gestation. At term, pups were removed by Cesarean section and were blinded immediately. To avoid possible rhythmic influences of a nursing mother on the pups' circadian rhythms, alternating nursing was imposed on blinded infants. Thus, pups were exchanged every 12 h between two foster mothers, one entrained to a light-dark cycle and the other to dark-light, so that one group of pups were always nursed in the light period and the other in the dark. Both groups of pups showed free-running circadian hormone rhythms with similar phase angles. However, the circadian rhythm of these pups was always phase delayed by about 8 h to that of blinded control pups which were born to unoperated mothers. Furthermore, blinded pups born to and nursed by a suprachiasmatic nuclei lesioned mother developed a circadian hormone rhythm which was phase delayed by 4 h to that of the control. It is concluded that the circadian oscillation underlying the rhythm of corticosterone release in rats has entrained to the maternal circadian system during fetal life. It is further suggested that the entrainment starts before day 10 of gestation.

Animals↗

Ontogeny of an oscillation underlying the circadian rhythm of plasma corticosterone in rats.

In previous reports (J. Physiol. 325, 493, 507, 521, 1982) we have suggested a prenatal onset of the circadian oscillation in rats. This was based mainly on the findings obtained in pups which were reared by an alternating nursing. In the present study we have applied this technique to experiments which were designed to determine the stage of gestation in the original mother that decided the phase angle of pup's hormone rhythm which was to develop later in the postnatal life. In this experiment we observed, though preliminarily, that reversal of the light-dark cycle of the pregnant mother at day 10 of pregnancy resulted in an effective reversal of pup's hormone rhythm, whereas the reversal at day 17 of pregnancy failed to affect it. From these results it is surmised that the original mother primarily determined the phase angle of the circadian oscillation in the fetus prior to the 17th day of gestation.

Aging↗

Critical role of food amount for prefeeding corticosterone peak in rats.

The effects of food on plasma corticosterone levels were examined in rats under restricted daily feeding or prolonged food deprivation. High hormone levels before feeding were observed when the daily meal was restricted to 2 h at a fixed time of day, but it was not detected when food availability was extended to 6 h. The amount of food intake under the latter condition was comparable to that in 24 h of ad libitum feeding. After the termination of restricted feeding, the prefeeding hormone peak was maintained in rats fasted subsequently but disappeared when rats were returned to ad libitum feeding. Food deprivation for 10 days increased plasma corticosterone levels in the light period, resulting in abolition of the circadian rhythm. A subsequent meal decreased the hormone level such that the 24-h mean hormone level after food ingestion was inversely related to the amount of food intake. When rats were allowed to feed for 6 h after prolonged food deprivation, the prefeeding hormone peak observed at the second meal disappeared at the fourth meal. The amount of food consumption in these rats increased and reached a level comparable to that with ad libitum feeding at the third meal. It is concluded that the amount of food intake is critical for the development and maintenance of the prefeeding hormone peak under restricted feeding; prolonged fasting.

Animals↗

Ontogeny of the circadian rhythm of plasma corticosterone in blind infantile rats.

1. Post-natal manifestation of plasma corticosterone rhythm was followed by individual pups until the end of 12 weeks of life. Results obtained were analysed by both visual inspection and a least squares spectrum method. The validity of the approaches used was evaluated. 2. Circadian rhythm of plasma corticosterone in sighted pups under light-dark cycle (LD) first appeared at around the third post-natal week, accompanied often with a bimodal pattern: a second peak being counterphased to the first main peak. The second peak became obscure at the fourth week, disappearing as pups matured. 3. The hormone rhythm in blinded pups whose eyes were removed within 16 h of birth was free-running under LD with a period of 24.40 +/- 0.02 h (mean +/- S.E.M.). The free-running period was stable until at least the end of the twelfth week of life. 4. The acrophase of the circadian rhythm in blind pups born and reared under LD was 180 degrees out of phase to that born and reared under DL, a reversed light-dark condition. In each case, the acrophase shifted about 8 h from that of sighted pups at the fourth week of life. 5. It is suggested that an underlying oscillator for the hormone rhythm starts to oscillate earlier than the fourth week of life and the environmental light-dark cycle prior to the fourth week determines the phase angle of the circadian rhythm in blind pups.

Aging↗

Possible zeitgebers for external entrainment of the circadian rhythm of plasma corticosterone in blind infantile rats.

1. The phase angle of circadian rhythm of plasma corticosterone in individual blind pups was followed in order to find out an effective zeitgeber(s) during the post-natal development. 2. The retinal light pathway before the opening of eyes was not essential for the entrainment of pups' rhythm to the environmental light-dark (LD) cycle. 3. In blinded pups whose eyes were enucleated on the day of birth, no evidence was obtained for effective extra-retinal pathways for photic inputs. 4. Free-running circadian hormone rhythm of blind pups was not entrained by 'social contact' with other sighted pups in the same cage. 5. Even when the duration of nursing was varied from 2 to 4 weeks, the phase angle of pups' rhythm at the fourth week was not affected. 6. In mother-pups exchange experiments in which pups born from LD mother were reared by DL mother (LD-DL pups) and conversely, pups from DL original mother were reared by LD foster mother (DL-LD pups), about one half of the pups at the fourth post-natal week of both groups exhibited phase angles belonging to their original mothers and the other half showed phase angles of their foster mothers. 7. It is suggested that blind pups may retain the phase angle of circadian rhythm of the original mother and the overt hormone rhythm may be modifiable by the foster mother during the early phase of post-natal life.

Aging↗

Prenatal onset and maternal modifications of the circadian rhythm of plasma corticosterone in blind infantile rats.

1. In order to clarify the manner in which maternal nursing modifies the circadian rhythm of plasma corticosterone in blind pups, specified schedules of maternal nursing were imposed on blind pups and the hormone rhythm was followed individually. 2. Two groups of blinded pups were continuously nursed, alternately by two mother rats having different circadian phases of lactating period. In both groups, phase angles of the original mother were predominantly reflected in the phase of the pups' hormone rhythm. 3. When the maternal nursing was limited only during the light period (L nursing), it caused no detectable effect on the pups' hormone rhythm. 4. In contrast, when the maternal nursing was limited only during the dark period (D nursing), approximately one half of the pups at the fourth post-natal week showed a bimodal pattern of hormone rhythm. A second peak appearing 180 degrees out of phase to the first peak disappeared by the sixth or eight post-natal week. 5. It is concluded that the circadian oscillation underlying the plasma corticosterone rhythm starts to function prenatally and the original mother (probably, a prenatal LD cycle) primarily determines the phase angle of the circadian oscillation in blind pups. The maternal nursing does not entrain the pups' circadian oscillation, but does modify transiently the overt hormone rhythm, probably through a discord between maternal nursing and pups' feeding phases.

Animals↗

Phase relation between episodic fluctuations of spontaneous locomotor activity and plasma corticosterone in rats with suprachiasmatic nuclei lesions.

Phase relation between plasma corticosterone and locomotor activity rhythms was analyzed in individual rats with selective lesions of suprachiasmatic nuclei (SCN). SCN in Wistar male rats were selectively coagulated electrically and the extent of SCN destruction was examined histologically. Spontaneous locomotor activity was monitored on an Animex and blood samples were simultaneously taken from the cut end of the tail vein or through a catheter which had been implanted into the right jugular vein. Plasma corticosterone was determined by a competitive protein binding assay. After the SCN lesion, both locomotor activity and plasma corticosterone lost a circadian rhythmicity and decomposed into ultradian components. Both least squares and periodogram analyses of the ultradian components of locomotor activity revealed the presence of a burst component of about 1-2 h duration. In addition, episodic fluctuations of plasma corticosterone were closely correlated with those of locomotor activity (r = 0.755, p less than 0.001). The findings suggest the existence of a phase-locking mechanism between ultradian components of both functions in the absence of SCN function.

Animals↗

Oxidation of plasma free fatty acids in nonshivering thermogenesis of rats treated chronically with norepinephrine and thyroxine.

In rats treated chronically with norepinephrine and thyroxine, enhanced nonshivering thermogenesis was observed, with a concomitant increase in the utilization of plasma free fatty acids (FFA). The increased utilization of plasma FFA was characterized by a more preferential increment in the oxidation of FFA in tissues rather than that in the uptake of FFA by tissues. These biochemical findings were accompanied by an increased mitochondrial mass in red fibers of skeletal muscle. Both biochemical and morphological changes of a similar nature were found in cold-acclimated rats.

Animals↗

Participation of brain catecholaminergic neurons in a self-sustained circadian oscillation of plasma corticosterone in the rat.

Circadian rhythms of locomotor activity and plasma corticosterone were determined simultaneously in individual rats which were injected intraventricularly with 6-hydroxydopamine (6-OHDA), a specific depletor of catecholamines. In light-dark cycles (LD), 6-OHDA-treated rats showed essentially normal circadian rhythms of both functions. In 200 lux continuous light (LL) the locomotor activity in the drug-treated rats ran freely with a period slightly longer than 24 h: free-running parameters (mesor, amplitude and period) of the locomotor activity were the same as those control rats. The circadian rhythm of plasma corticosterone in control rats also ran freely in LL, resulting in a reversal of their phase after 12 days exposure to LL. However, the rhythm disappeared in 6-OHDA-treated rats under LL: instead in these rats 3--4 episodes of secretion were obsered over a 24 h period. These results suggest a difference in the biochemical background between the regulatory mechanism of circadian rhythm of locomotor actitivity and that of plasma corticosterone. It is also apparent that brain catecholaminergic components are indispensable for the circadian rhythm of plasma corticosterone to freerun normally in LL, but are dispensable in LD. A plausible model consisting of two oscillators is proposed to explain these findings.

Animals↗

Effects of parachlorophenylalanine and 5, 6-dihydroxytryptamine on the free-running rhythms of locomotor activity and plasma corticosterone in the rat exposed to continuous light.

Parachlorophenylalanine (PCPA) and 5,6-dihydroxytryptamine (5,6-DHT), depletors of brain serotonin, were administered to the rat and circadian rhythms of locomotor activity and plasma corticosterone were determined simultaneously in individual rats in light-dark cycles (LD) and in 200 lux continuous light (LL). Free-running periods and acrophases on the 12th day in LL (LL12) were calculated by a least squares spectrum method. In PCPA-treated rats which showed 70% depletion of brain serotonin, circadian rhythms of locomotor activity in LL and of plasma corticosterone and ACTH in LD disappeared for several days after the drug injection. Circadian rhythms of locomotor activity reappeared after the LL7 day and free-ran with a phase shift. Free-running periods of these rats did not differ significantly from that of control rats. However, the acrophase of PCPA-treated group on the LL11 day was 5 h advanced as compared to that of control. Circadian rhythm of plasma corticosterone in the PCPA-treated rats was detected on the LL12 day but their peak times were distributed around 24:00 h instead 08:00 h observed rats. The 5,6-DHT-treated rats which showed only 40% depletion of brain serotonin exhibited normal free-running rhythms in both locomotor activity and plasma corticosterone in LL and no difference in the acrophases of these functions on the LL12 day as compared to controls. These results suggest that PCPA affects the circadian clock (or clocks) itself in such a way that it blocks the clock to free-run or at least it effectively shortens the free-running periods of locomotor activity and plasma corticosterone in the rat.

5,6-Dihydroxytryptamine↗

A phase response curve for the locomotor activity rhythm of the rat.

A phase response curve was obtained for the locomotor activity rhythm of the rat. Mus norvegicus albicus, by interrupting a free-running rhythm with light signals of short duration. The response curve obtained was continuous and had the switch-over point at the position of 2 h before the acrophase, followed by the portion of advancing phase shift. The pattern of the curve was typical for the nocturnal rodent.

Adaptation, Physiological↗

Fast, rate-sensitive corticosteroid negative feedback during stress.

Characteristics of the fast, rate-sensitive, negative-feedback regulation of adrenocorticotropin secretion during stress was quantitatively analyzed using rats anesthetized with pentobarbital sodium. Various levels of plasma corticosterone were achieved during morning hours by infusing corticosterone solutions of different concentrations. Blood was sampled serially from the carotid artery. An increase in plasma corticosterone concentration 15 min after intravenous, pulsed injection of histamine (230 microgram) during saline intravenous infusion was defined as the "control response". When plasma corticosterone was rising during corticosterone infusion, the response to histamine stimulus was distinctly inhibited (fast, rate-sensitive feedback inhibition), whereas such an inhibition was not observed when plasma corticosterone levels were not rising, regardless of the absolute level. The critical rate of rise of plasma corticosterone, at or above which the fast rate-sensitive feedback was manifested, was 4-6 microgram/100 ml per min. When three graded doses of histamine were injected while plasma corticosterone levels were increasing at a rate of 6 microgram/100 ml per min, the absolute value of the inhibition observed was independent of the administered dose of the stressor. A hypothetical model for the mechanism of this feedback inhibition, based on the assumption that the hormone effect was proportional to the rate of formation of hormone-receptor complex, satisfied the quantitative characteristics of the inhibition experimentally observed in this study.

Adrenocorticotropic Hormone↗