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The effects of electrical stimulation of medial amygdala on the adrenocortical sensitivity to adrenocorticotrophin (ACTH) were investigated in hypophysectomized rats. The intravenous injection of ACTH increased the rates of 14C transfer from 14C-l-acetate into corticosterone and cortisol in the adrenal slices of hypophysectomized rats. The electrical stimulation of the medial amygdala produced a further increase in the rates of 14C transfer from 14C-l-acetate into corticosterone and cortisol. From these results, it might be suggested that the medial amygdala was capable of enhancing the adrenocortical steroidogenesis in response to ACTH.

The electrical stimulation of the ventromedial hypothalamus (VMH), lateral hypothalamic area (LHA), periventricular arcuate nucleus (ARC), and posterior hypothalamus (PHY), on 14C transfer rates from 14C-1-acetate into adrenocortical steroids in adrenal slices of hypophysectomized rats were investigated. The 14C transfer rates into corticosterone and cortisol were increased by the stimulation of the VMH, ARC, and PHY, but decreased by the stimulation of the LHA. From these results, it might be suggested that these hypothalamic structures were involved in the regulation of adrenocortical steroidogenesis without participation of the pituitary.

Injections of 50 microU insulin into the ventromedial hypothalamic nuclei (VMH) in intact sheep decreased the rates of 14C transfer from 14C-1-acetate into CO2, glucose, ketone bodies, and increased the rates into triglyceride and phospholipids in rumen epithelium of sheep. Insulin injections into the parietal cortex of intact sheep or into the VMH of sheep with VMH lesions had no effect on the acetate metabolism in rumen epithelium as compared with the control groups which received saline injections into the same brain regions. These results support the view that the VMH serves as an integral part of an insulin-sensitive brain regulatory system in the acetate metabolism of rumen epithelium.

We examined the effects of stimulation of the dorsal hippocampus and lesions of the dorsal fornix on glucose metabolism in liver slices of rabbits. Hippocampal stimulation decreased the 14C transfer rates from 14C-glucose into CO2, ketone bodies, cholesterol ester and free fatty acids, but increased the rates into triglyceride, phospholipids and glycogen. Fornix lesions had various effects on glucose metabolism, and the effects of hippocampal stimulation on glucose metabolism were abolished by fornix lesions. These observations support the hypothesis that the hippocampus is an integral part of the brain regulator system in the hepatic glucose metabolism.

The effects of electrical stimulation of the lateral hypothalamic area (LHA), periventricular arcuate nucleus (ARC) and ventromedial hypothalamic nucleus (VMH) on the rates of 14C transfer from 14C-1 acetate into ovarian steroids in ovarian slices of hypophysectomized and adrenalectomized (H-A) rats were investigated. The 14C transfer rates into estrogen and 20 alpha-hydroxypregn-4-en-3-one (20 alpha-OH-P) were decreased by LHA stimulation. The stimulation of the ARC and VMH increased the rates of 14C transfer into estrogen, progesterone and 20 alpha-OH-P. From these results, it might be suggested that these hypothalamic structures were involved in the regulation of ovarian steroidogenesis without participation of the pituitary and adrenal.

Amygdala (AMYG) stimulation caused marked increase in the circulating level of glucagon and these stimulatory effects were abolished by lesions of stria terminalis (ST). Stimulation of dorsal hippocampus (DHPC), on the other hand, greatly decreased the glucagon level and lesions of dorsal fornix (DFX) abolished these stimulatory effects. These results suggested that the reciprocal influence of AMYG and DHPC on plasma level of glucagon played some role in the regulation of glucagon release and these limbic structure had hypothalamic-mediated effects on glucagon release.

The plasma corticosterone concentration and incorporation of 14C-1-acetate into adrenocortical hormones were measured in male rats exposed to hypoxia (12.5% O2 in N2 balance) for periods of 30 min--14 days. Hypoxia significantly increased the weight of the adrenal and pituitary glands in early stages of exposure. However, weight returned to the control level on the 14th day of exposure. Hypoxia consistently decreased the weight of the thymus. Hypoxia elevated the plasma corticosterone concentration in the early stages of exposure. However, the elevated corticosterone level gradually decreased by the 7th day. The corticosterone level at this stage was lower than in the control. The corticosterone concentration returned to the control level on the 14th day. Hypoxia significantly facilitated incorporation of 14C-1-acetate into corticosterone and cortisol in the adrenal homogenate. The elevated incorporation was maintained until the 7th day and gradually decreased to the control level there after. Body weight was decreased by hypoxia (12 gram in 24 hours). On the 5th day, the weight returned to the control level. Hematocrit increased gradually during 14 days of hypoxia exposure. These results suggest that pituitary-adrenal function is greatly facilitated by 1-6 hours of hypoxia exposure, and hypoxia acclimatization is accomplished humorally within 14 days of exposure in rats.

Insulin was injected directly into the medial amygdala (AMYG) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 50 microU insulin into the AMYG decreased the rates of 14C transfer from 14C-1-acetate into CO2 and cholesterol ester, and increased those into free cholesterol and phospholipids. But after insulin injection into parietal cortex of intact rabbits and into the AMYG of rabbits with lesions of stria terminalis (ST), hepatic acetate metabolism did not differ from that of the control rabbits, which received saline injection into the same brain regions. These observations support the hypothesis that the AMYG is a part of insulin-sensitive brain regulator system in the hepatic acetate metabolism.

Glucagon was injected directly into the medial amygdala (AMYG) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 3 ng glucagon into the AMYG of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose, ketone bodies, cholesterol ester, free fatty acids and phospholipids but decreased those of 14C transfer into triglyceride. However, the glucagon injection into the AMYG of rabbits with lesions of stria terminals or into the parietal cortex of intact rabbits had no effects on the hepatic acetate metabolism. These observations support the hypothesis that the AMYG is a part of the glucagon-sensitive brain regulator system in the hepatic acetate metabolism.

Insulin was injected directly into the dorsal hippocampus (DHPC) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 50 microU insulin into the DHPC decreased the rates of 14C transfer from 14C-1-acetate into glucose and ketone bodies, and increased 14C transfer into cholesterol ester, triglyceride, free cholesterol and free fatty acids. But after insulin injection into the DHPC of rabbits with lesions of dorsal fornix (DFX), hepatic acetate metabolism did not differ from that of control rabbits, which received saline injection into the same brain region. From these results it might be suggested that the DHPC are parts of insulin-sensitive brain regulator system in the hepatic acetate metabolism.

Extracellular single-unit recordings were made from medial preoptic/anterior hypothalamic (MPOAH) neurones in urethane-anaesthetized female rats, and the responses of these neurones to electrical stimulation of the ventrolateral medulla (VLM) were investigated. Of 189 neurones tested, 20% were excited and 21% were inhibited following VLM stimulation. The latency of inhibitory responses showed a normal distribution and the mean latency was 47 ms, whereas the latency of excitatory responses showed a bimodal distribution with peaks in the ranges of 0-10 ms and 40-50 ms, respectively. Excitatory responses with latencies greater than 15 ms and inhibitory responses were significantly attenuated by intravenous injections of the alpha-adrenoceptor antagonist phenoxybenzamine but not the beta-adrenoceptor antagonist propranolol. In the light of these observations and the known anatomical and electrophysiological findings, it is suggested that A1 noradrenergic and/or C1 adrenergic inputs from the VLM to MPOAH neurones are, at least in part, mediated by alpha-adrenoceptors.

The plasma corticosterone levels and incorporation of 14C-l-acetate into corticosterone and cortisol were measured in dehydroepiandrosterone (DHA)-treated persistent estrous rats and control estrous cyclic rats exposed to cold (-5 degrees C) for 12 hrs. Cold exposure significantly facilitated incorporation of 14C-l-acetate into corticosterone and cortisol in both DHA-treated and control rats. However, the rates of increase of plasma corticosterone level and 14C-incorporation into corticosterone are 61% and 77% in controls, and 19% and 44% in DHA-treated rats, respectively. The activity of stress-induced pituitary-adrenal function showed masculine patterns in DHA-treated rats. The diurnal patterns of plasma corticosterone in DHA-treated rats are similar in controls. Plasma corticosterone levels in DHA-treated rats are evidently greater than those in controls. It is suggested that neonatal administration of DHA caused the changes not only in pituitary-gonadal system but also in pituitary-adrenal system.

The effects of electrical stimulation of the medial amygdala (AMYG) and dorsal hippocampus (DHPC) on the rates of 14C transfer from 14C-1-acetate into adrenocortical steroids in adrenal slices of hypophysectomized rats were investigated. The 14C transfer rates into corticosterone were increased by stimulation of the AMYG and DHPC. The 14C transfer rates into cortisol were increased by the AMYG stimulation but were not altered by the DHPC stimulation. From these results, it might be suggested that these limbic structures were involved in the regulation of adrenocortical steroidogenesis without participation of the pituitary.

The effects of lesions in the basal medial hypothalamus and limbic structures on the responses in plasma levels of insulin and glucose to daily repeated cold exposure in rabbits have been investigated. The results obtained were summarized as follows: (1) The 1st cold exposure (cold exposure on the 1st day) decreased insulin levels and increased glucose levels, and these responses of insulin and glucose to cold exposure gradually decreased and then completely abolished by daily repetition of exposures in intact rabbits and each sham-operated group. (2) The lesions of periventricular arcuate nucleus (ARC), stria terminalis (ST) and dorsal fornix (FX) had no effects on the insulin responses to the 1st cold exposure, but the rates of insulin responses to the 1st cold exposure were decreased by the lesions of ventromedial hypothalamus (VMH). (3) The ARC lesions had no effects on the glucose responses to the 1st cold exposure, but the glucose responses to the 1st cold exposure were abolished by VMH lesions and were altered by lesions of ST and FX. (4) The insulin responses to cold exposure were abolished by daily repetition of exposures in rabbits with ARC lesions as same in the cases of sham-operated animals, but the insulin responses to cold exposure persisted even after daily repetition of exposures in rabbits with lesions of VMH, ST and FX different from sham-operated animals. (5) The glucose responses to cold exposure were abolished by daily repetition of exposures in rabbits with lesions of ARC and ST as same as in the cases of sham-operated animals, but the glucose responses to cold exposure persisted even after daily repetition of exposures in rabbits with FX lesions different from sham-operated animals.

The effects of lesions of the limbic-hypothalamic structures on the pyruvate metabolic responses to daily repeated heat exposures in the liver of rabbits have been investigated. The experimental results were as follows: 1. The pyruvate metabolic responses to the 1st heat exposure (heat exposure on the 1st day) were altered by lesions of periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). 2. The pyruvate metabolic responses to heat exposure were completely abolished by the ten times repetition of daily heat exposures in rabbits with lesions of ARC, VMH and ST, as same as in each sham-operated group. 3. In rabbits with FX lesions, the pyruvate metabolic responses to heat exposure remained even after the ten times repetition of daily heat exposures. 4. From these results, it might be suggested that ARC, VMH, amygdala (AMYG)-ST system and dorsal hippocampus (HPC)-FX system played a certain role in the mechanisms of pyruvate metabolic responses to the 1st heat exposure, but only the HPC-FX system participated in the process of pyruvate metabolic adaptation to daily repeated heat exposures.

The effects of lesions of the limbic-hypothalamic structures on the pyruvate metabolic responses to daily repeated cold exposures in the liver of rabbits have been investigated. The experimental results were as follows: The metabolic pattern of pyruvate and the pyruvate metabolic responses to the 1st cold exposure (cold exposure on the 1st day) were altered by lesions of periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). The pyruvate metabolic responses to cold exposure were completely abolished by seven times repetition of daily cold exposures in rabbits with lesions of ARC, VMH and FX, as well as in each sham-operated group. In rabbits with ST lesions, the pyruvate metabolic responses to cold exposure remained even after the seven times repetition of daily cold exposures. From these results, it might be suggested that the ARC, VMH, amygdala (AMYG)-ST system and dorsal hippocampus (HPC)-FX system played a certain role in the metabolic regulation of pyruvate and in the mechanisms of pyruvate metabolic responses to the 1st cold exposure, but that only the AMYG-ST system participated in the process of pyruvate metabolic adaptation to daily repeated cold exposures.

Corticosterone was injected directly into the hippocampus of rabbits, and changes in hepatic acetate metabolism were studied. The microinjection of corticosterone with seasame oil into hippocampus decreased the rates of 14C transfer from 14C-1-acetate into CO2 and free cholesterol, and increased 14C transfer into glucose, ketone bodies, triglyceride, free fatty acids and phospholipids. But after microinjection of corticosterone into the hippocampus of rabbits with lesions of dorsal fornix, hepatic acetate metabolism did not differ from that of control rabbits, which received injection of seasame oil into the same brain region. From these results it might be suggested that the hippocampus is a part of corticosterone-sensitive brain regulator system in the hepatic acetate metabolism.

The effects of lesions in the basal medial hypothalamus and limbic structure upon the responses of adrenocorticoids formation in adrenal slices of rabbits to daily repeated heat exposures has been investigated. (1) The adrenocortical responses to heat exposure on the 1st day were decreased by lesions in the periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). (2) There were no effects of heat exposure on the 10th day upon the adrenocorticoid formation in either the sham-lesioned rabbits or the rabbits with the lesions of ARC, VMH and ST. (3) In rabbits with the FX lesions, the adrenocorticoids formation was significantly increased by heat exposure on the 10th day. (4) These results suggested that the basal medial hypothalamus, amygdala (AMYG)-ST system and dorsal hippocampus (HPC)-FX system participated in the mechanisms of adrenocortical responses to heat exposure on the 1st day, but only the HPC-FX system played some roles in complete disappearance process of adrenocortical responses to heat exposure by repetition of exposures.

The pyruvate metabolic response to the 1st exposure (exposure on the 1st day) to immobilization stress (IMO) were considerably altered by lesions of the periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). The pyruvate metabolic responses to IMO were completely abolished by seven times repetition of exposure to IMO in the rabbits with lesions of ARC and VMH; they were similar to sham-operated groups. In rabbits with lesions of ST and FX, the pyruvate metabolic responses to the 7th exposure (exposure on the 7th day) to IMO were almost the same as those after the 1st exposure to IMO, but these metabolic responses were completely abolished by the seven times repetition of exposure to IMO in the sham-operated animals. These results suggest that firstly the ARC, VMH, amygdala (AMYG)-ST system and dorsal hippocampus (HPC)-FX system are involved in the pyruvate metabolic responses to the 1st exposure to IMO, and secondly, that the AMYG-ST system and the HPC-FX system are involved in the disappearance process of pyruvate metabolic responses to IMO by the daily repetition of exposure to IMO.

The effects of lesions in the basal medial hypothalamus and limbic structure on the acetate metabolic responses to daily repeated heat exposure in the liver of rabbits have been investigated. The results obtained were summarized as follows: (1) THe acetate metabolic responses to the 1st heat exposure (heat exposure on the 1st day) were altered by the lesions in the periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). (2) The acetate metabolic responses to heat exposure were completely abolished by the ten times repetition of heat exposure in the rabbits with lesions in ARC or VMH. They were similar to sham-operated animals. (3) The acetate metabolic responses to heat exposure remained even after the ten times repetition of heat exposure in the rabbits with lesions in ST and FX indicating the differences from sham-operated animals. (4) From these results, it might be suggested that the basal medial hypothalamus and limbic structure participated in the mechanism of acetate metabolic response to the 1st heat exposure, but only these limbic structure played some roles in the complete disappearance process of acetate metabolic responses to heat exposure by the ten times repetition of heat exposure.

Corticosterone was injected into the ventromedial hypothalamus (VMH) of rabbits, and changes in hepatic acetate metabolism were studied. The microinjection of corticosterone with seasame oil into the VMH of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose, ketone bodies, triglyceride, free cholesterol, free fatty acids and phospholipids but decreased those of 14C transfer into cholesterol ester. However, corticosterone injected into the VMH of rabbits with VMH lesions or the parietal cortex of intact rabbits was without effect on the hepatic acetate metabolism. From these results it might be suggested that the VMH is an integral part of the corticosterone-sensitive brain regulator system in the hepatic acetate metabolism.

Glucagon was injected directly into the ventromedial hypothalamic nuclei (VMH) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 3 ng glucagon into the VMH of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose and ketone bodies but decreased those into cholesterol ester, triglyceride, free cholesterol, free fatty acids and phospholipids. However, after glucagon injection into the VMH of rabbits with VMH lesions and the parietal cortex of intact rabbits, hepatic acetate metabolism did not differ from that of the control rabbits, which received saline injection into the same brain regions. These observations support the hypothesis that the VMH are parts of a glucagon-sensitive brain regulator system in the hepatic acetate metabolism.

In order to elucidate the role of the limbic-hypothalamic system in the adrenocortical responses to repeated immobilization stress, the influences of daily repeated exposures of immobilization stress on the adrenocorticoid formation in adrenal slices of rabbits with lesions of various sites of the hypothalamus and limbic structures had been investigated. The experimental results obtained were as follows: (1) Lesions in periventricular arcuate nucleus (ARC) and ventromedial hypothalamus (VMH) decreased the rates of adrenocortical responses to the 1st immobilization exposure (exposure on the 1st day), but did not alter the rates of adrenocortical responses to the 4th immobilization exposure (exposure on the 4th day). (2) Lesions in stria-terminalis (ST) and dorsal fornix (FX) did not alter the rates of adrenocortical responses to the 1st immobilization exposure, but increased the rates of adrenocortical responses to the 4th immobilization exposure. (3) The adrenocortical responses to immobilization stress were completely abolished by the seven times repetition of exposures in each sham-operated group and in the animals with lesions of ARC and VMH, but in the rabbits with lesions of ST and FX the adrenocortical responses to immobilization stress were not abolished by the seven times repetition of exposures. (4) These results suggested that such basal medial hypothalamus participated in the mechanisms of adrenocortical responses to the 1st exposure of immobilization stress, but did not participate in the disappearance process of adrenocortical responses to immobilization stress by the seven times repetition of exposures. On the other hand, it might be supposed that the amygdala(AMYG)-ST system and dorsal hippocampus(HPC)-FX system do not participate in the mechanism of adrenocortical responses to the 1st immobilization exposure, but these limbic areas played some roles in the disappearance process of the adrenocortical responses to immobilization stress by the seven times repetition of exposures.

The amygdala (AMYG) stimulation caused a marked decrease in the circulating level of insulin coincident with a considerable rise in the glucose level in rabbits. The stimulation of dorsal hippocampus (DHPC), on the other hand, greatly increased the insulin level and decreased the glucose level. The results suggested that the reciprocal influence of AMYG and DHPC on plasma levels of insulin and glucose played some roles in the regulation of insulin release and the homeostasis glucose metabolism in rabbits.

The effects of lesions in the basal medial hypothalamus and limbic structure on the acetate metabolic responses to daily repeated exposure to immobilization stress in the liver of rabbits have been investigated. The experimental results were as follows: (1) The acetate metabolic response to the 1st exposure to immobilization stress (exposure on the 1st day) were considerably altered by lesions in the periventricular arcuate nucleus (ARC) ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). (2) The acetate metabolic responses to immobilization stress were completely abolished by seven times repetition of immobilization stress in the rabbits with lesions in ARC, VMH and FX; they were similar to sham-operated groups. (3) In rabbits with ST lesions, the acetate metabolic responses to the 7th exposure (exposure on the 7th day) to immobilization stress were exactly the same as those after the 1st exposure of immobilization stress, but these metabolic responses were completely abolished by the seven times repetition of exposure in the sham-operated animals. (4) These results suggest that firstly, the ARC, VMH, amygdala(AMYG)-ST system and dorsal hippocampus(HPC)-FX system are involved in the acetate metabolic responses to the 1st exposure of immobilization stress, and secondly, that only the AMYG-ST is involved in the disappearance process of acetate metabolic responses to immobilization stress by the daily repetition of immobilization stress.

The effects of the lesions of basal medial hypothalamus and limbic structure on the acetate metabolic responses to daily repeated cold exposures in rabbit's liver has been investigated. The results obtained were summarized as follows: (1) The lesions of periventricular arcuate nucleus (ARC) had no effects on the acetate metabolism and on the acetate metabolic responses to the 1st cold exposure (cold exposure on the 1st day). (2) The metabolic pattern of acetate and the acetate metabolic responses to the 1st cold exposure were altered by the lesions of ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). (3) The effects of cold exposure on the acetate metabolism were completely abolished by the seven times repetition of cold exposures in the rabbits with the lesions of ARC, VMH or ST, as the same as in each sham-operated group. (4) The acetate metabolic responses to cold exposure remained after the seven times repetition of cold exposure in the rabbits with the lesions of FX, but those disappeared completely in sham-operated animals. (5) From these results, it might be suggested that the VMH, amygdala(AMYG)-ST system, dorsal hippocampus(HPC)-FX system played some roles in the metabolic regulation of acetate and in the mechanisms of acetate metabolic responses to the 1st cold exposure, but the ARC did not participate in those mechanisms. And it was suggested that the HPC-FX system participated in the acetate metabolic adaptation to daily cold exposures, but the basal medial hypothalamus and AMYG-ST system did not participate in this process.

Insulin was injected directly into the ventromedial hypothalamic nuclei (VMH) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 50 microU insulin into the VMH of intact rabbits decreased the rates of 14C transfer from 14C-1-acetate into glucose and cholesterol ester in liver slices. But after insulin injection into the parietal cortex of intact rabbits and into the VMH of rabbits with VMH lesions, hepatic acetate metabolism did not differ from that of the control rabbits, which received saline injection into the same brain regions. These observations support the hypothesis that the VMH are parts of an insulin-sensitive brain regulator system in the hepatic acetate metabolism.

The effects of electrical stimulation of the medial amygdala (AMYG) and dorsal hippocampus (DHPC) on the rates of 14C transfer from 14C-1-acetate into ovarian steroids in hypophysectomized and adrenalectomized rats (H-A rats) were investigated. The 14C transfer rates into estrogen were increased by stimulation of AMYG and DHPC. The 14C transfer rates into progesterone and 20 alpha-hydroxy-pregn-4-en-3-one (20 alpha-OH-P) were increased by the AMYG stimulation but decreased by the DHPC stimulation. From these results, it might be suggested that these limbic structures were involved in the regulation of ovarian steroidogenesis without participation of pituitary and adrenal.