Vigorous intake of oil emulsion caused by chronic food deprivation remains after recovery in rats.

Oil emulsion intake over a 30-min period was compared under different dietary conditions (ad libitum feeding and chronic food deprivation) and at various concentrations of oil in rats. The pattern of intake for each dietary condition was extremely different. Food-deprived rats ingested more emulsion when the solution was thicker but intake amount became less at too high a concentration. Ad libitum feeding rats ingested less emulsion than deprived rats with no difference among the concentrations. Rats on a restricted diet clearly differentiated between concentrations, selecting the thicker emulsion when provided two-bottle selection between 10% oil and some other concentration. On the other hand, rats fed ad libitum differentiated between only extremely weak solutions. The vigorous intake of oil emulsion induced by chronic food deprivation was maintained after 2 weeks of normal feeding. Significant difference between prior dietary conditions was maintained at lower concentrations. Dietary timing for food-deprived rats affected little on emulsion intake. These results indicate that response to oil emulsion intake differs by concentration in rats.

Bisphenol A increases progesterone receptor immunoreactivity in the hypothalamus in a dose-dependent manner and affects sexual behaviour in adult ovariectomized rats.

Recently, we reported that bisphenol A (BPA), an endocrine disrupter, increased progesterone receptor (PR) mRNA in the preoptic area (POA) in adult ovariectomized rats. In the present study, we examined whether BPA also induced expression of PR proteins in both the POA and the ventromedial hypothalamic nucleus (VMH), and whether those proteins were involved in the induction of sexual behaviour. Two weeks after ovariectomy, rats received a subcutaneous (s.c.) injection of BPA, 17 beta-oestradiol or vehicle. Twenty-four hours after the injection, the rats were killed and their tissues were examined by immunocytochemistry. Some rats that received a s.c. injection of BPA, E2 or vehicle alone on the day before were injected with progesterone at 15.00 h and examined for sexual behaviour 5-7 h later. As expected, injection of 10 microg E2 significantly increased the number of PR immunoreactive cells in both the POA and the VMH compared to the number after injection of vehicle alone. In both the POA and the VMH, injection of BPA at a dose of 10 mg also significantly increased the number of PR immunoreactive cells compared to the number after injection of sesame oil alone. Furthermore, BPA induced a dose-dependent increase in the number of PR immunoreactive cells in both the POA and the VMH, demonstrating that the number of PR cells was significantly increased by as little as 100 microg of BPA. Ovariectomized (OVX) rats that were primed with 10 mg of BPA, followed by 1 mg of progesterone, displayed mainly rejection behaviour, but not lordosis as typically observed in OVX rats primed with E2 followed by progesterone. The present study suggests that BPA influences reproductive functions, including sexual behaviour even in adulthood, by altering the PR system in the hypothalamus.

t(11;14)(q23;q24) generates an MLL-human gephyrin fusion gene along with a de facto truncated MLL in acute monoblastic leukemia.

More than 20 different partner genes with MLL have been cloned from leukemia cells with translocations involving chromosome 11 band q23 (11q23). All reported partner genes fused in-frame to MLL and the fusion cDNA encode chimeric MLL proteins with a significant portion derived from the partner genes. We analyzed one patient with de novo acute monoblastic leukemia with t(11;14)(q23;q24) and identified that a human homologue of gephyrin (human gephyrin) fused with MLL. Gephyrin is a rat glycine receptor-associated protein, which forms submembranous complexes and anchor glycine or gamma-aminobutyric acidA receptors to microtubules. Alternative splicing of human gephyrin gene created two different forms of fusion cDNA. In one form, human gephyrin gene fused in-frame to MLL exon 9, and the chimeric product had COOH terminus of human gephyrin protein, including the tubulin binding site. In the other, the reading frame terminated shortly after the fusion point. As a result, only seven amino acids with no known function were attached to the NH2 terminus of MLL protein. The functional significance of this de facto truncated MLL gene product is not clear.

Changes in estrogenic regulation of estrogen receptor alpha mRNA and progesterone receptor mRNA in the female rat hypothalamus during aging: an in situ hybridization study.

We examined two molecular responses to estrogen, reduction in estrogen receptor alpha (ER alpha) mRNA and increase in progesterone receptor (PR) mRNA, in the hypothalamus of 3- (young) and 10-month-old (middle-aged) cycling, and 15-month-old (old) acyclic, Fischer 344 female rats. The rats were ovariectomized and then given silastic capsules containing 5% 17beta-estradiol. or empty implants, and killed 4 days after implantation. By means of in situ hybridization, we found that, in young rats, estrogen reduced ER alpha mRNA in both the ventromedial hypothalamus (VMH) and arcuate nucleus (ARC) but not in the preoptic area (POA). In contrast, the effect of estrogen on ER alpha mRNA in the VMH and ARC of middle-aged and old rats was not statistically significant. On the other hand in all regions the induction of PR mRNA by estrogen was at least as strong in middle-aged and old as in young rats. The present study revealed that the induction of PR mRNA by estrogen in the hypothalamus was not impaired with age but ER alpha mRNA in the VMH and ARC was significantly impaired with age, but not in the POA.

Pentobarbital stimulates the activity of the GnRH pulse generator interacting with opioid neurons in rats in proestrus.

In order to investigate the possibility that i.p. injection of pentobarbital sodium (PB, 32 mg/kg bw) potentiates the GnRH pulse generator activity, effects of i.v. infusions of an opiate receptor antagonist naloxone (NAL, 2 mg/h) on the pulsatile LH secretion were compared in saline (SAL)- and PB-injected rats in proestrus and diestrus 1. In SAL-injected rats in proestrus, NAL infusions significantly increased both the frequency and amplitude of LH pulses, and also the overall mean LH concentration. In PB-injected rats in proestrus, all the parameters of the pulsatile LH secretion were similar to those in SAL-injected rats in proestrus. The NAL infusion in PB-injected rats caused an increase in the frequency, but it was similar to that in SAL-injected rats. But, increases in the amplitude and the overall mean LH observed during NAL infusions in PB-injected rats were greater than in SAL-injected rats. In SAL-injected rats in diestrus 1, NAL infusions increased all the parameters, as in rats in proestrus. In PB-injected rats in diestrus 1, LH secretion was severely suppressed. NAL infusions recovered the pulsatile LH secretion, but the frequency and the overall mean LH of the secretion were smaller than those obtained during NAL infusions in SAL-injected rats. In addition, characteristic increases in the MUA (volleys), which occur in association with the initiation of an LH pulse and thus are considered to represent an increased activity of the GnRH pulse generator, appeared more frequently during NAL infusions in PB-injected rats in proestrus than in SAL-injected rats. These results suggest that the GnRH pulse generator in rats in proestrus, but not in rats in diestrus 1, is refractory to PB and further is potentiated by PB in the response to NAL. Together with the fact that this dosage of PB blocks the surge of LH secretion in rats in proestrus, the concept of the existence of separate neuronal mechanisms responsible for the surge and pulsatile secretion of LH are supported.

Effects of naloxone on the serum luteinizing hormone level and the number of Fos-positive gonadotropin-releasing hormone neurons in immature female rats.

To examine developmental changes in the number of gonadotropin-releasing hormone (GnRH) neurons activated by an opioid receptor antagonist in female rats, blood sampling and double-labeled immunocytochemistry for Fos and GnRH were performed after the injection of naloxone (NAL) in immature (postnatal d16 and d30) and mature female rats. Three age groups of rats were perfused with 4% paraformaldehyde-PB 90 min after the subcutaneous injection of NAL (2.5 mg/kg) or saline. All tissue incubation and staining for double-labeled immunocytochemistry were simultaneously performed. Although no significant developmental change was observed in the total number of GnRH neurons (p0.05), NAL-induced increases in serum luteinizing hormone (LH) concentrations were much greater in the d16 group than those in the d30 and mature groups (p<0.01). Conversely, Fos-positive GnRH neurons were rarely observed in d16, and some Fos-positive GnRH neurons were observed in the d30 group (p<0.05 vs. saline) and the mature group (p<0.01 vs. saline). These results suggest that opiatergic inhibitory system on GnRH neuron in immature female rats is different from that in mature female rats.

Acetylcholine suppresses the spread of excitation in the visual cortex revealed by optical recording: possible differential effect depending on the source of input.

Optical recording with a voltage-sensitive dye was performed in visual cortical slices of the rat to determine the effect of acetylcholine (ACh) on the spread of excitation. In the presence of ACh, the spread of excitation initiated by stimulation at the white matter/layer VI (WM/VI) was greatly suppressed throughout the cortex, with less suppression in the middle layers. By comparing the effect of ACh with that of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the fraction of the synaptic component that was sensitive to ACh was evaluated. ACh suppressed approximately 40-50% (maximum 55.8%, n = 11) of the initial synaptic component in the superficial and deep layers. In the middle, however, the effect was weakest and only approximately 20-30% (minimum 20.9%, n = 11) of the initial synaptic component was suppressed. On the basis of histological analysis, the region with the weakest ACh effect extended from upper V to lower II/III. To identify the site of ACh action in terms of pre- versus postsynaptic localization, exogenous glutamate was applied. Because ACh did not suppress the excitation induced by glutamate, the site of the ACh action was indicated to be presynaptic. When layer II/III was stimulated instead of WM/VI, the suppression was uniform throughout the cortex. A muscarinic receptor antagonist, atropine, blocked the suppression by ACh. In conclusion, our results indicate the following two points. First, ACh strongly suppresses intracortical connectivity through presynaptic muscarinic receptors. Secondly, in contrast to the intracortical connection, some group(s) of fibres, possibly thalamocortical afferents that arise from white matter and terminate in the middle cortical layers are suppressed much less by ACh. While ACh has been reported to have confusingly diverse effects, e.g. direct depolarization and hyperpolarization as well as synaptic facilitation and suppression, its effect on the propagation of excitation is very clear; suppression on intracortical connection, leaving thalamocortical inputs rather intact. We postulate that cholinergic innervation enables the afferent input to have a relatively dominant effect in the cortex.

[Estimation of antibacterial activity of various antibiotics against Pseudomonas aeruginosa by score method].

Antibacterial activity of various antibiotics against Pseudomonas aeruginosa isolated from each hospitals depends on the variety or amount of antibiotics used in each hospital. The antibiotic, which is effective to P. aeruginosa in a certain hospital is not always effective to that in other hospital. The excellent antibiotics in antibacterial activity have low MIC and hard to progress in resistance, and such antibiotics may be effective against P. aeruginosa isolated from any hospitals. Therefore we thought that the antibiotic, which was progress to resistance, would show a great difference in MIC among hospitals, and we investigated MIC and difference of MIC of various antibiotics against P. aeruginosa isolated from six hospitals. Furthermore, we converted the data of MICs and difference of MIC among six hospitals into the score, and tried to estimate antibacterial activity of various antibiotics by using those scores. From the results of analysis in this report, we think the antibiotics actually surpass in antibacterial activity may be imipenem, cefozopran, cefsulodin and amikacin. New analytical method proposed in this report will become one of potential methods to estimate antibacterial activity of antibiotics against bacteria isolated from inpatient with bacterial infections.

Effects of noradrenaline on GnRH-secreting immortalized hypothalamic (GT1-7) neurons.

Noradrenaline (NA) is one of the most important neurotransmitters involved in the regulation of gonadotropin-releasing hormone (GnRH) secretion. In this study, the effects of NA on GnRH secretion, intracellular Ca2+ concentrations ([Ca2+]i), and membrane potentials were investigated in immortalized hypothalamic neurons (GT1-7) to determine the direct effects of NA on GnRH cells. Cells were perfused in a plastic minicolumn, and GnRH concentrations of the effluents were measured. NA increased the release of GnRH in a dose-dependent manner. Cells were loaded with a 4 microM Fura 2-AM, and the ratio of the intensities of fluorescent emission at 510 nm with excitation at 340 and 380 nm was calculated at 100-ms intervals. NA increased the [Ca2+]i responses of single GnRH cells dose-dependently. The NA-induced [Ca2+]i increase was attenuated in the absence of extracellular calcium and was blocked by the beta-adrenergic antagonist propranolol, but not by the alpha-adrenergic antagonist phentolamine. The cell membrane potential was recorded with a whole-cell patch clamp amplifier with glass-electrodes. NA induced membrane depolarization under current-clamp conditions. The depolarization was also inhibited by propranolol, but not by phentolamine. The results show that NA directly affects the membrane potential of GT1-7 cells via beta-adrenergic receptors and induces Ca2+ mobilization; these effects stimulate GnRH secretion.

Neuronal synchronization and ionic mechanisms for propagation of excitation in the functional network of immortalized GT1-7 neurons: optical imaging with a voltage-sensitive dye.

Immortalized gonadotropin releasing hormone (GnRH) neurons (GT1 cell line) in culture release GnRH in a pulsatile manner, suggesting that GT1 cells form a functional neuronal network. Optical imaging techniques and a voltage-sensitive fluorescent dye (RH795) were used to study the mechanism of neuronal synchronization and intercellular communication in cultured GT1-7 cells (one of the subclones of the GT1 cell line). The majority (79%) of GT1-7 cells in contact with one another revealed synchronized fluctuations in spontaneous neuronal activity. When a cell in contact with other cells was electrically stimulated, the evoked excitation was propagated to neighbouring cells. The ionic mechanisms involved in the propagation of electrical signals between interconnected GT1-7 cells were investigated using various blockers of Na+, Ca2+ and K+ channels. The propagation of stimulus-evoked excitation was prevented by the voltage-dependent Na+ channel blocker tetrodotoxin. It was also prevented by the voltage-dependent Ca2+ channel blockers, Ni+ (nonselective), nimodipine (L-type) and flunarizine (T-type > L-type), but not apparently affected by omega-agatoxin IVA (P- and Q-type) and omega-conotoxin MVIIA (N-type). The propagation was not influenced by the K+ channel blockers, quinine, tetraethylammonium and Ba2+, but in some cases, it was enhanced by 4-aminopyridine (4-AP) and prevented by apamin. These results suggest that voltage-dependent Na+ channels and L- and T-type Ca2+ channels are involved in the propagation of electrical signals in the GT1-7 neuronal network. Ionic mechanisms, through 4-AP- or apamin-sensitive K+ channels, also seem to be involved in the regulation of signal propagation. These mechanisms may underlie the functioning of the neuronal network formed by immortalized GnRH neurons.

Inhibitory effect of a traditional Chinese medicine, Juzen-taiho-to, on progressive growth of weakly malignant clone cells derived from murine fibrosarcoma.

We have investigated the inhibitory effect of oral administration of Juzen-taiho-to, a Kampo (Chinese herbal) medicine, on progressive growth of a mouse fibrosarcoma. Spontaneously regressive QR-32 tumor cells were able to grow progressively in vivo when coimplanted s.c. with a foreign body, gelatin sponge, whereas QR-32 cells alone gradually grew for over 15 days after inoculation and thereafter regressed for up to 25 days. Oral administration of Juzen-taiho-to (40 mg/day/mouse) for 7 days after inoculation of QR-32 cells with gelatin sponge resulted in significant inhibition of tumor growth and prolongation of the survival of the tumor-bearing mice. This growth-inhibitory effect of Juzen-taiho-to observed on day 25 was dose-dependent over the dose range from 4 to 40 mg/day. Treatment with Juzen-taiho-to for 7 days before tumor inoculation with gelatin sponge also significantly suppressed tumor growth examined on day 25, as did the administration of bismuth subnitrate, which is well known to induce metallothionein, an antioxidant. On the other hand, inoculation of progressed tumor cells (QRsP) resulted in growth without gelatin sponge, leading to death in syngeneic mice. Administration of Juzen-taiho-to for 7 days after inoculation of QRsP cells resulted in a decrease of the tumor growth and prolongation of the survival of mice, but the effect was less than that on the growth of QR-32 regressor tumor after coimplantation with gelatin sponge. These results suggest that the inhibitory effect of Juzen-taiho-to is partly associated with prevention of gelatin sponge-elicited progressive growth, probably mediated by endogenous factors including antioxidant substances, in addition to the augmentation of host-mediated antitumor activity.

[A long-survival case of unresectable liver metastasis of colon cancer by hepatic arterial intermittent multidrug infusion chemotherapy].

We experienced a long-survival case with unresectable liver metastasis of sigmoid cancer by hepatic arterial intermittent multidrug infusion chemotherapy. The patient was a 65-year-old man. A movable tumor was palpable at the left lower abdomen. The serum CEA value was 15.6 ng/ml. Abdominal CT scan showed a 3 cm-sized low-density area near the root of the right and middle hepatic vein in segment 4. He had undergone sigmoidectomy, cholecystectomy and cannulation into the proper hepatic artery. Chemotherapy was performed by using 5-FU (250 mg), Adriacin (5 mg) and mitomycin C (4 mg) every second week from 4 months after surgery as an outpatient. In the CT scan image, the low-density area completely disappeared at 10 months after treatment, and the CR interval was 14 months. The patient has been alive for 5 years after surgery.

Cessation of the electrical activity of gonadotropin-releasing hormone pulse generator during the steroid-induced surge of luteinizing hormone in the rat.

Neuronal activity in the mediobasal hypothalamus was recorded during the steroid-induced surge of luteinizing hormone (LH) in ovariectomized female rats by means of multiunit activity (MUA) recording techniques. The day of subcutaneous implantation of estradiol-containing silastic tubing, which was done at 12.00 h, was designated as day 1, and progesterone (1 mg) dissolved in sesame oil was injected at 12.00 h on day 5. The hypothalamic MUA and serum LH level were monitored between 10.00 and 20.00 h on days 1, 4 and 5. All 5 animals examined showed characteristic increases (volleys) in MUA associated with pulsatile LH secretion. After implantation of estradiol on day 1, gradual and significant decreases in the serum LH level and in MUA volley frequency were observed. In the afternoon of both days 4 and 5, an LH surge occurred, though it was much greater on day 5 than day 4 due to progesterone injection on day 5. However, neither MUA volleys nor considerable changes in baseline MUA were discernible throughout the recording period on days 4 and 5. More than 5 days after the removal of estradiol-containing tubing, MUA volleys were found to reappear in all the animals. These results suggest that estradiol has an inhibitory effect on gonadotropin-releasing hormone (GnRH) pulse generator activity, and that the GnRH pulse generator is not involved in inducing the LH surge in the rat.

Acute estradiol modulation of electrical activity of the LHRH pulse generator in the ovariectomized rat: restoration by naloxone.

Whether estrogen has the brain as a site of its negative feedback action was investigated by checking the acute effect of estradiol-17 beta (E2) on the electrical activity of the luteinizing hormone-releasing hormone (LHRH) pulse generator in ovariectomized rats fitted with chronically implanted electrode arrays in the medial basal hypothalamus. Before subcutaneous E2 implantation, the hypothalamic multiunit activity (MUA) exhibited, at an average frequency of 2.43/h, characteristic increases (volleys), each of which was associated with the initiation of an LH pulse. Within 2 h after E2 implantation, the frequency of MUA volleys was reduced significantly, probably associated with decreases in the frequency of LH pulses. The decrease in the amplitude of LH pulses occurred later than 2 h, but this effect was considered not to be mediated by the brain since the duration of MUA volleys was not changed. Since the mean serum LH concentration started to decrease within 2 h after E2 implantation, it was concluded that the acute inhibitory E2 effect on LH release is mediated by the brain. On the day after E2 implantation, intravenous infusion of naloxone (2 mg/kg/h) promptly elicited intermittent MUA volleys each of which was associated with an LH pulse. This suggests that operation of the LHRH pulse generator in the ovariectomized condition is restrained by the action of E2 with the mediation of endogenous opioid peptide neurons.

Injection of bicuculline elicits firing of luteinizing hormone releasing hormone pulse generator in muscimol-treated ovariectomized rats.

We have already demonstrated that, although exogenous gamma-aminobutyric acidA (GABAA) receptor agonist is capable of inhibiting the activity of luteinizing hormone releasing hormone (LHRH) pulse generator, the reduction in the endogenous GABAA receptor activity does not have a significant effect in ovariectomized rats, suggesting a minor role of inhibitory GABA neurons in the control of pulsatile release of LHRH. In this study, we further analyzed the role of the GABAA receptor system in the regulation of LHRH pulse generator activity observed by recording the multiunit activity (MUA) in the hypothalamus of ovariectomized rats. An abrupt increase (volley) in the MUA in the arcuate nucleus (ARC)-median eminence region (ME) was accompanied by the initiation of a luteinizing hormone (LH) pulse, determined by measuring LH concentrations in blood sampled simultaneously. The injection of 1-3 mg/kg muscimol (MUS), a GABAA receptor agonist, decreased the basal MUA and delayed the occurrence of the next MUA volley, but it did not change the LH pulse amplitude. I.v. injection of 5 mg/kg bicuculline (BIC), a GABAA receptor antagonist, during continuous infusion of MUS (5 mg/kg/h) which decreased the basal MUA and prevented the MUA volley from occurring, evoked MUA volleys and LH pulses whose amplitudes were similar to those found before the MUS infusion. Injection of the same dose of BIC during the infusion of saline increased the MUA transiently, but this increase was not accompanied by an LH pulse and afterwards there occurred MUA volleys at ordinary intervals accompanied by LH pulses with unchanged pulse amplitudes.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of gamma-aminobutyric acid-A receptor antagonist, bicuculline, on the electrical activity of luteinizing hormone-releasing hormone pulse generator in the ovariectomized rat.

The role of GABA neurons in the control of pulsatile release of LHRH was investigated by checking the effect of the GABAA receptor agonist, muscimol, and antagonist, bicuculline, on the electrical activity of the luteinizing hormone-releasing hormone (LHRH) pulse generator in the ovariectomized rat fitted with chronically implanted electrode arrays in the medial basal hypothalamus. In untreated control animals, the hypothalamic multiunit activity (MUA) exhibited, at an average of 20.5-min intervals, characteristic increases (volleys), each of which was associated with the initiation of an LH pulse. A bolus i.v. injection of muscimol (2 mg/kg) significantly increased the interval between MUA volleys and LH pulses without affecting the pulse amplitude. Continuous i.v. infusion of saline increased the interval between MUA volleys to an average of 24.1 min without affecting the LH pulse amplitudes. Bicuculline infusion (10 mg/kg/h) altered neither the interval between MUA volleys nor the pulsatile release of LH. This was further checked in the condition where presynaptic inhibition by opioid peptides on the noradrenergic system was presumably decreased by naloxone. Naloxone infusion (0.5 or 0.7 mg/kg/h) caused the MUA volleys to occur markedly frequently, an average of 13.8-min intervals. The interval during combined infusion of bicuculline with naloxone was an average of 16.2 min, suggesting that bicuculline could not decrease the interval that was set by naloxone. The results show that, although exogenous GABAA receptor agonist is capable of inhibiting the activity of LHRH pulse generator, the reduction in the endogenous GABAA receptor activity does not cause a significant effect, suggesting a minor role of inhibitory GABA neurons in the control of pulsatile release of LHRH. Further, together with the well-known fact that activation of GABAA receptor hyperpolarizes neurons postsynaptically, it is assumed that the GABAergic system, unlike the opioidergic one, is not involved in the presynaptic inhibition of the adrenergic receptor system which is probably implicated in the frequency control of LHRH pulse generator.

Hypothalamic electrical activity that relates to the pulsatile release of luteinizing hormone exhibits diurnal variation in ovariectomized rats.

The multiunit activity (MUA) was recorded in the arcuate nucleus-median eminence region in freely moving ovariectomized rats maintained under controlled lighting conditions (lights on 05.00-19.00 h) over a period of 24 h. The MUA of each rat had been confirmed to exhibit characteristic increases (volleys) in association with pulses of luteinizing hormone. In 6 MUAs examined, the frequency of MUA volleys was significantly greater in the dark period than in the light period, suggesting a diurnal variation in the release of luteinizing hormone-releasing hormone in the ovariectomized rat.

The role of limbic-hypothalamic systems in metabolic responses of phenylalanine to repeated cold exposures in rabbits.

In this study we examine the effects of lesions to limbic or hypothalamic structures on the metabolic responses of phenylalanine in liver slices prepared from rabbits exposed to cold stress (-20 degrees C) for 12 hours at a fixed time once a day. The results were as follows: 1. The 1st cold exposure (cold exposure on the 1st day) had marked and various effects on phenylalanine metabolism, and the metabolic responses of phenylalanine to cold exposure gradually decreased and then completely disappeared with repetitions of exposure in intact rabbits. 2. The metabolic patterns and responses of phenylalanine to the 1st cold exposure were altered by lesioning the periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) or dorsal fornix (FX). 3. The complete abolishment of the metabolic responses to cold exposure by its repetition was observed in rabbits with lesions in the ARC or VMH as well. 4. In contrast, metabolic responses of phenylalanine to cold exposure in rabbits with lesions in the ST or FX remained even after six exposures. These results suggest that the ARC, VMH, amygdala (AMYG)-ST system and dorsal hippocampus (HPC)-FX system played a role in the metabolic regulation of phenylalanine and in the metabolic responses of phenylalanine to the 1st cold exposure and that the AMYG-ST and HPC-FX systems, but not the ARC or VMH, participated in the process of the metabolic adaptation of phenylalanine to cold exposure.

Influence of the electrical stimulation of the hypothalamus on adrenocortical steroidogenesis in hypophysectomized rats.

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.