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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.

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.

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.

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.

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 electrical stimulation of the ventromedial hypothalamus (VMH), lateral hypothalamic area (LHA), periventricular arcuate nucleus (ARC), and posterior hypothalamus (PHY), on 14 C transfer rates from 14 C-1-acetate into adrenocortical steriods in adrenal slices of hypophysectomized rats were investigated. The 14 C 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

The exact nature of how nitric oxide (NO) acts in the regulation of milk ejection during lactation is not clearly understood at the moment. In this study, we have examined the effect of drugs which spontaneously release NO (sodium nitroprusside, SNP) or inhibit the NO synthase (NOS) enzyme (Nω-nitro- l -arginine, l -NA) on the activity of some hypothalamic and functionally associated nuclei using Fos expression as an index of neuronal activation. Lactating rats received intracerebroventricular injection of SNP, l -NA or vehicle (saline) just before they were reunited with their pups after a 12-h period of separation and allowed to suckle for 2 h. The difference in the total pup body weight before and after the period of suckling was used as a functional end-point of milk transfer. Central injection of SNP in conscious rats significantly inhibited Fos expression in the paraventricular nucleus (PVN), supraoptic nucleus (SON), periventricular and preoptic nuclei and also decreased pup body weight compared with saline- or l -NA-injected rats. Urethane-anesthetized animals, compared with their conscious counterparts, showed increased Fos expression in the PVN and SON. However, Fos expression in the PVN of the anesthetized animals was attenuated by l -NA injection compared with SNP and saline injection. Taken together with an earlier finding that SNP disrupts the milk ejection burst of oxytocinergic neurons, these observations suggest that NO may act within the neuron(s) possibly to alter the mechanism(s) regulating the periodic neuronal burst activity during lactation.

Human peripheral blood polymorphonuclear leukocytes were preincubated with water extracts from Rhizopus delemar. The water extracts significantly inhibited arachidonic acid induced superoxide generation, whereas enhanced superoxide generation induced by phorbol 12-myristate 13-acetate but not those induced by N-formyl-methionyl-leucyl-phenylalanine. Superoxide generation induced by water extracts was inhibited by staurosporine, an inhibitor of protein kinase C, and was enhanced by genistein, an inhibitor of tyrosine kinase. The water extracts incubated with phorbol 12-myristate 13-acetate markedly increased phosphorylation of serine residue of 28.5 kDa protein with time and the phosphorylation depended on the concentration of the water extracts, whereas the water extracts incubated with arachidonic acid decreased the phosphorylation of serine residue of 38 and 42 kDa proteins. The phosphorylation of 28.5 kDa protein induced by the water extracts was inhibited by staurosporine, an inhibitor of protein kinase C, but was not inhibited by genistein, an inhibitor of tyrosine kinase.

The effects of electrical stimulation of the hypothalamus paraventricular nucleus on the spontaneous firing of mitral and granule cells in the main olfactory bulb were examined in ovariectomized female rats under urethane anaesthesia. High-frequency stimulation (0.5-1.0 mA, 10-20 pulses at 100 Hz) of the paraventricular nucleus produced inhibitory responses in 80% of mitral cells tested and excitatory responses in 74% of granule cells tested, with latencies ranging from 2 to 150 s. Both responses were blocked by infusions into the olfactory bulb of [d(CH2)5, Tyr(Me)2]ornithine-vasotocin (10 pmol), an oxytocin antagonist, and mimicked by intracerebroventricular infusions (0.2 or 0.4 nmol) or microiontophoretic applications of oxytocin but not by intracerebroventricular infusions of vasopressin (1 or 2 nmol). Infusions of 0.5% lignocaine, a local anaesthetic, into either the medial olfactory tract or the medial forebrain bundle failed to block the responses of mitral and granule cells to the stimulation. Unilateral transections at various levels between the bulb and the paraventricular nucleus also failed to block the responses. There were cases in which significant responses of mitral and granule cells to the stimulation required 60 or more pulses after the lignocaine infusions or transections, however. These results suggest that oxytocin originating in the hypothalamic paraventricular nucleus reaches the olfactory bulb following its release partly into the cerebrospinal fluid and acts to decrease olfactory processing.

The presence of endogenous digitalis-like factors in the central nervous system suggests their functional significance in the central nervous system. Three-day infusions of three-stepped doses of the digitalis agent ouabain (1–100 ng.kg body wt-1.h-1) into the lateral cerebral ventricle of freely moving rats caused a dose-dependent increase in the number of central-apneic episodes during rapid-eye-movement sleep without affecting the time spent in rapid-eye-movement sleep or basic respiratory rate. These results suggest that endogenous digitalis-like factors may be involved in the genesis of central sleep apneas.

We studied the mechanisms of occurrences of apneas and bradyarrhythmias during sleep in five Wistar-Kyoto rats. We recorded electroencephalograms, electrocardiograms, chest wall movement, and diaphragmatic electromyograms (EMGdi) for three continuous days in each freely moving rat and demonstrated that: 1) 99% of the apneas and 99% of the bradyarrhythmias occurred during paradoxical sleep (PS), 2) 98% of the apneas were due to spontaneous cessations of respiratory drive, 3) the percentages among apneas accompanied with bradyarrhythmias were only about 30% and independent of the apneic durations, 4) every autoregressive power spectrum contained two significant components in the ranges of 50-80 and 110-140 Hz, which would be analogous to high-frequency oscillations postulated to originate in the synaptic input to the phrenic motoneurons from respiratory centers, and 5) spectral patterns of EMGdi signals varied with sleep states. These results suggest that "PS-related" neural activity modulating central respiratory output is important in inducing apneas and promoting bradyarrhythmias.

Some forms of olfactory learning require intact noradrenergic terminals in the olfactory bulb that originate from the locus coeruleus. To clarify the action of noradrenergic inputs on the dendrodendritic interaction between mitral and granule cells in the rat olfactory bulb, we analyzed field potentials in the granule cell layer of the olfactory bulb evoked by paired-pulse stimulation of the lateral olfactory tract before and after the activation of the locus coeruleus. Locus coeruleus activation by glutamate injection in the vicinity of the nucleus changed only the test response without any effect on conditioning response. Paired-pulse inhibition measured from the ratio of test response amplitude to conditioning response amplitude was significantly depressed immediately after locus coeruleus activation. Conversely, 2 min later, paired-pulse inhibition was significantly potentiated. The significant potentiation of inhibition lasted for several minutes. The depression-potentiation sequence of paired-pulse inhibition was blocked by infusion of timolol, a beta-antagonist, into the olfactory bulb, in a dose-dependent manner, but not by infusion of phentolamine, an alpha-antagonist. Infusion of isoproterenol, a beta-agonist, into the bulb mimicked the depression of paired-pulse inhibition by locus coeruleus activation. These results suggest that glutamate activation of the locus coeruleus produces a depression-potentiation sequence in granule cell-mediated feedback inhibition onto mitral cells in the olfactory bulb through beta-adrenergic receptors.

Observations that noradrenaline induces enduring enhancement of the efficacy of a second transmitter in central synapses are intriguing and have attracted considerable attention, as the process may serve as a neuronal substrate for learning and memory. This may be true for synapses in the olfactory bulb (OB), as the significance of noradrenergic centrifugal inputs to the OB in olfactory learning has been noted in a number of models [1]. Noradrenergic terminals in the OB originate in the locus coeruleus (LC) [2]. However, the role of LC noradrenergic neurons in OB function has not been fully clarified. We therefore examined the effect of stimulation of the LC on mitral-granule cell interactions in the rat OB.

1. The effects of continuous infusions of ouabain on bradyarrhythmias (cardiac pauses for 0.5 s or longer) during sleep were examined in freely moving Wistar-Kyoto rats. 2. In a control group (n = 7), saline was infused into both the lateral ventricle and the femoral vein. In an intracerebroventricular (i.c.v.) ouabain group (n = 7), ouabain was infused centrally, such that each rat received three stepped doses of 1, 10, and 100 ng kg-1 h-1 for 3 days at each dose, while saline was infused systemically. In an intravenous (i.v.) ouabain group (n = 7), ouabain was infused systemically at the same doses as the i.c.v. ouabain received, while the simultaneous i.c.v. infusion of saline was carried out. 3. Three-day i.c.v. infusions of the three stepped doses of ouabain caused a dose-dependent increase in the frequency of bradyarrhythmias during rapid-eye movement (REM) sleep without affecting the time spent in REM sleep, arterial pressure, average heart rate, or the frequency of bradyarrhythmias during non-REM sleep. Intravenous ouabain or i.c.v. saline had no effects on the frequency of bradyarrhythmias. 4. Intrinsic CNS activity during REM sleep may be involved in the centrally mediated arrhythmogenic properties of ouabain during sleep.

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 14 C transfer from 14 C-1-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 14 C transfer from 14 C-1-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

Twenty neurons in the subfornical organ (SFO) were antidromically activated by electrical stimulation of the hypothalamic supraoptic nucleus (SON) in the rat. Electrical stimulation of the lateral hypothalamic area (LHA) excited the activity of 12 identified units, but did not affect that of the remaining units. The excitatory responses to LHA stimulation were blocked by microiontophoretically applied saralasin (Sar), an angiotensin II (AII) antagonist. These results suggest that the LHA has an excitatory influence on the activity of SFO neurons projecting to the SON and that the influence may be mediated by AII receptors.

Extracellular recordings were obtained from 58 phasically active neurosecretory neurons in the hypothalamic paraventricular nucleus (PVN) of urethane-anesthetized male rats. Of these PVN neurons, 39 exhibited an increase and 11 displayed a reduction in ongoing activity following electrical stimulation of the subfornical organ (SFO), while the remaining neurons were unresponsive. Microinjection of the local anesthetic lidocaine into the medial septum reversibly abolished the SFO stimulus-eveoked reduction in 7 out of 9 PVN neurons tested, whereas similar injection was without effect on the stimulus-evoked increase in 18 out of 20 PVN neurons tested. These results suggest that the SFO efferents through the medial septum to the PVN exert a predominantly inhibitory influence on the excitability of putative vasopressin (VP)-secreting neurons in the PVN.

Electrical stimulation of the rat A1 noradrenergic region produced orthodromic inhibition (34%), excitation (23%) or excitation-inhibition sequence (25%) of the spontaneous activity of phasically firing units in the paraventricular nucleus of the hypothalamus (PVH). Excitatory responses could be distinguised into two types on the basis of their latency and duration. Both the primary and post-excitatory inhibitory responses were significantly attenuated by intravenous injection of propranolol, a β-adrenoceptor antagonist, whereas neither type of excitatory response was affected.

Firstly, a collective oscillation mode of the neural activity is derived from the neural network system by using the multicompartment equation and the projection operator technique. This technique takes into account higher order interactions among neurons. The solution of the equation gives a chain structure with an infinite number of circuit loops in which each of them is only composed of four neurons. The obtained eigenvalues are quite similar to the spectrum of frequencies of the EEG. Secondly, the time-dependent behavior of the observed EEG is simulated by starting from the elementary process of action potential trains of neurons, which includes the effect of the collective oscillation mode mentioned above. This gives a comprehensive derivation of the EEG from the neural activity of action potentials. The simulation assumes that information of the action potential trains can be transmitted to the EEG through the intermediate states of the postsynaptic potential trains and the slow waves. The paper reports that a slightly modulated activity of a relatively small amount of neurons can cause a strong influence on the shape of the global EEG and that the calculated results reproduce the characteristic features of the EEG in a rat such as the theta rhythm, the spindle wave and the arousal wave.

There was increase production of adrenocortical hormones (cortisol and corticosterone) in the adrenal during three different types of stress: immobilization, exposure to heat, and exposure to cold. Such a state of hypersecretion of adrenocortical hormones was inhibited by electroacupuncture at the Tsu-San-Li (St-36) locus.

Seventy neurons in the ventrolateral medulla oblongata were antidromically activated by electrical stimulation of the preoptic and anterior hypothalamic area (POA/AHA) in female rats under urethane anesthesia. These identified cells were located within and adjacent to the nucleus reticularis lateralis and could be readily distinguished into at least two types of neurons, designated as ‘fast’ and ‘slow’ cells, on the basis of their waveform and conduction velocity.

A study was made of the effect of acupuncture on citrate and glucose metabolism in the liver in terms of incorporation of 14C-1, 5-citric acid and 14C-u-glucose in some metabolites. The effect of acupuncture on citrate metabolism in the liver under control conditions was such as to increase production of G and reduce that of KB, FC and FFA. No effect of acupuncture on glucose metabolism in the liver under such conditions was observed. Both citrate and glucose metabolism were affected to a marked extent by immobilization stress or exposure to heat or cold. The deleterious effect of these types of stress was less prominent in animals receiving acupuncture at the Tsu-San-Li locus than in those treated otherwise or receiving no treatment.

Fifteen neurons in the region of the subfornical organ (SFO) were antidromically activated by electrical stimulation of the paraventricular nucleus (PVN) in the rat. Electrical stimulation of the lateral hypothalamic area (LHA) excited the activity of 9 of the identified units, but did not affect the remaining units. The excitatory response of the identified units was blocked by microiontophoretically (MIPh) applied saralasin (Sar), an angiotensin II (ANGII) antagonist, but not by atropine (Atr), a muscarinic antagonist. These results suggest that the LHA has an excitatory influence on the activity of neurons in the region of the SFO with efferent projections to the PVN and that the influence may be mediated by ANGII receptors.

The influence of arrhythmias on cerebral function was investigated in 8 patients with sick sinus syndrome (bradycardia tachycardia syndrome) and 8 patients with advanced or complete atrioventricular block using 24-hour continuous recordings of the electrocardiogram and conventional electroencephalogram recordings. Syncope was observed more frequently in the atrio-ventricular block group, and was observed frequently when the longest heart beat pause during a 24-hour day was longer than 2.2 sec. Cerebral infarction as a complication of these arrhythmias was observed only with the sick sinus syndrome group. The maximum heart rate during a 24-hour day and the difference between maximum and minimum heart rate were significantly lower in the atrioventricular block group than in the sick sinus syndrome group. The electroencephalogram results showed a slight slowing of the background activity and the appearance of slow wave bursts in both groups. These abnormal findings were improved during intracardiac pacing in the atrio-ventricular block group. A quantitative analysis of the frequency of the electroencephalogram at various heart rates demonstrated the optimum pacing rate for the cerebral function. These results suggest that both the cerebral function and the cardiac function must be considered in the treatment of patients with bradycardia arrhythmias.

Estradiol benzoate administered to ovariectomized female rats significantly elevated the mean spontaneous firing rate and frequency of successful antidromic propagation into the somatodendritic spike and significantly reduced the strength of post-stimulus inhibition in presumed A1 noradrenergic neurons projecting directly to the preoptic and anterior hypothalamic area. The occurrence of both antidromic spikes and post-stimulus inhibition of the majority of these neurons was completely abolished by the injection of 6-hydroxydopamine but not by 5, 7-dihydroxytryptamine directly into the medial forebrain bundle.

Electrical stimulation of the rat A1 noradrenergic region produced excitation (77%) of the activity of putative vasopressin (VP)-secreting neurons in the paraventricular nucleus (PVN) and produced excitation (4%), inhibition (26%) and excitation-inhibition (11%) of the activity of PVN neurons that were not antidromically identified by neurohypophysial stimulation. The excitatory response of putative VP-secreting neurons was blocked by microiontophoretically applied phentolamine, an α-adrenoceptor antagonist, but not by timolol, a β-adrenoceptor antagonist. The inhibitory response of unidentified PVN neurons, on the other hand, was blocked by timolol, but not by phentolamine.

The relationship between arrhythmias and sleep states was investigated in patients with night-type arrhythmias, which were detected by 24-hour electrocardiogram recordings using the Holter Avionics system. These patients were examined using all-night polygraphic recordings and sleep states were divided in to 5 groups according to the standard sleep stage scoring manual as stage I, II, III, IV, and REM sleep. Patients were divided into 5 groups: (1) grade 2 ventricular premature contractions (VPCs), (2) grade 4a VPCs, (3) grade 4b VPCs, (4) supraventricular premature contractions, and (5) paroxysmal tachyarrhythmias such as paroxysmal atrial fibrillation or paroxysmal supraventricular tachycardia. The paroxysmal tachyarrhythmia group showed a significant increase in arrhythmia incidence during REM sleep (p less than 0.05). However, the subjects with other arrhythmias showed no significant increase during REM sleep, but grade 2 VPCs showed a tendency to increase in sleep stage IV (0.05 less than p less than 0.1). These results suggest that there are 2 types of arrhythmias influenced by sleep. The first type is affected by a phasic increase in sympathetic nervous tone during REM sleep and the second type is related to an increase in vagal tone during the night.

Extracellular single-unit activity was recorded from phasically firing neurohypophyseal neurons (n = 41) in the hypothalamic paraventricular nucleus (PVN) of urethane-anesthetized male rats. Electrical stimulation of the subfornical organ (SFO) produced orthodromic long-duration (n = 18) or short-duration (n = 10) excitation or inhibition (n = 8) of the activity of PVN neurons. The long-duration excitatory response of about half (n = 7) the neurons (n = 15) tested was reversibly abolished by microinjection of the local anesthetic lidocaine into the median preoptic nucleus (MnPO), whereas neither the short-duration excitatory (n = 7) nor inhibitory (n = 6) responses were affected. These results suggest that the SFO efferents through the MnPO to the PVN may transmit the neuromodulatory signals which evoke long-duration increases in the excitability of putative vasopressin (VP)-secreting neurons in the PVN.

Sixteen neurons in the lateral hypothalamic area (LH) and 12 neurons in the zona incerta (ZI) were antidromically activated by electrical stimulation of the subfornical organ (SFO) area in urethane-anesthetized male rats. The activity of these LH and ZI units was examined for response to intracarotid injections of isotonic (0.15 M NaCl solution, 0.05 ml) or hypertonic (0.18 M or 0.3 M NaCl solution, 0.05 ml) saline. All the units did not change their activity to the injections of isotonic saline. Of these units, 9 LH and 5 ZI units displayed an increase and 2 LH and 3 ZI units exhibited a reduction in neuronal activity following the injections of hypertonic saline, while the remaining 5 LH and 3 ZI units were unresponsive. The present results suggest that the LH and ZI neurons with ascending projections to the SFO may carry the information from osmoreceptive elements for modulating the actions of the SFO.

Fifteen neurons in the subfornical organ (SFO) were antidromically activated by electrical stimulation of the supraoptic nucleus (SON) of the hypothalamus in urethane-anesthetized rats. Microiontophoretically (MIPh) applied angiotensin II (AII) excited the activity of all identified SFO neurons and the effect of AII was blocked by MIPh-applied saralasin (Sar), an AII antagonist. Intravenously administered AII excited the activity of most (n=13) of these identified SFO neurons and this exciting effect by intravenous AII was also blocked by MIPh-applied Sar.

The present study was designed to elucidate the differences in taste sensitivity in various strains of mice, and to study the relationship between taste sensitivity and color of the fur. Taste thresholds for four kinds of taste substance, i.e., sodium chloride, saccharine, acetic acid, and phenylthiocarbamide (PTC), were measured with three black and three white strains of mice. Taste sensitivity in mice with hypofunction of the suprarenal body, thyroid gland, and liver was also studied to clarify the bearing of the functions of those organs on the sense of taste. The taste sensitivity of mice differed according to strain. A white strain (aa) showed the lowest taste thresholds for all substances tested, whereas a black strain (0–61) showed the highest. Other strains showed intermediate thresholds, the white strains showing lower ones except in the case of saccharine. Hypofunction of the suprarenal body, thyroid gland, and liver caused a rise in the taste thresholds: a) after cauterization of the suprarenal body, the threshold for acetic acid was raised, whereas those for other taste substances were unchanged; b) reduction of thyroid and hepatic functions resulted in a rise of the taste thresholds for saccharine, acetic acid, and PTC.

Extracts of normal lung contain a surface-active substance which probably helps to stabilize the air spaces. Detailed lipid analysis of these extracts was made. The effect of prolonged administration of 100 per cent oxygen sufficient to produce pulmonary edema was studied in guinea pigs. In spite of the presence of severe edema, the surface tension and the lipid composition did not change significantly from those of control animals. The data indicate that it is unlikely that the pulmonary edema observed following oxygen administration is the result of alteration of the surface-active material.

The effect of electrical stimulation of the medial preoptic area (MPO) on integrated multiple unit activity (MUA) in the arcuate nucleus (ARC) during the estrous cycle of the Wistar rat was examined with reference to the release of “the ovulating hormone” from the anterior pituitary gland. The electrical stimulation (0.5ms, 200Hz, SW, 100-500μA) was applied for 30min between 14:00 and 16:00 under pentobarbital anesthesia. 1) When the stimulus induced ovulation on the following day, MUA changes in the ARC were observed during the electrical stimulation on the day of proestrus, in contrast to their appearance after the electrical stimulation on the day of diestrus II. 2) The electrical stimulation facilitated the release of “the ovulating hormone” on the day of proestrus, while on the day of diestrus II it increased pituitary potency to induce ovulation as well, tested by an injection of a crude extract from the anterior pituitary of the experimental animals into recipients of diestrus II. 3) The circulatory level of the luteinizing hormone (LH) elevated immediately after the electrical stimulation, reached the maximum level 30 min later and returned to the control level after 60min on the day of proestrus. However, on the remaining days of the cycle it elevated immediately, reached the maximum level at 60min, but did not return to the control level even 120min after the electrical stimulation.Therefore, that the electrical stimulation of the MPO induces neural excitation of the ARC and increase of LH content in the circulation with a discrepancy in the timing throughout the cycle, indicates that the stimulation induces both synthesis and release of LH in the pituitary gland.

By using the New Zealand White rabbits with chronically implanted bipolar electrodes in the several parts of the brain, studies of the influences of electrical stimulation of the limbic system and the hypothalamus upon progesterone and estrogen formation in the ovary and ovarian progesterone output were carried out. Effects were studied through observations upon inducement of ovulation and upon incorporation of radioactivity into progesterone and estrogen (estradiold-estrone) by the ovarian homogenates in vitro with (1-14C) acetate.The implanted rabbits were primed with estradiol benzoate in oil (0.1mg s. c.) for 2 days prior to stimulation to ensure an estrous state. Electrical stimulation, consisting of monophasic square wave pulses, was delivered unilaterally for 30 min., 60 sec. on and 60 sec. off, 260-280μA, at 0.1 msec. duration, 60 cps. The results were as follows:1. Ovulation was induced by 260-280μA electrical stimulation of the hippocampus in the estrogen primed rabbits in the 20 out of 30 cases. Almost no, differences were observed between the effect of electrical stimulation of the dorsal and the ventral parts of the hippocampus. Similar results were observed. in the effects of stimulation upon the intermediate nucleus of the amygdala and the periventricular arcuate nucleus. The ovulation induced thereby was. blocked by bilateral lesions of the dorsal or the ventral fornix, by a massive lesion of the septum, or by a localized lesion of the periventricular arcuate nucleus including the adjacent regions. On the contrary, when the stria terminalis was damaged bilaterally, hippocampal stimulation still produced hemorrhagic follicles in the ovaries.2. Electrical stimulation of the hippocampus enhanced progesterone formation in the ovary more than that of the amygdala and the periventricular arcuate nucleus. But, it showed an unappreciable difference in estrogen formation. among these three regions. The ratio of (14C)-incorporated estrogen to (14C)-incorporated progesterone (E/P) showed a lower value in the hippocampus than in the other areas.In respect to progesterone labelling from (1-14C) acetate by the ovarian homogenates, the ovarian progesterone output and the E/P ratio, little difference was observed between the effect of electrical stimulation of the amygdala. and the periventricular arcuate nucleus of the hypothalamus including the posterior tuberal region. When the dorsal or the ventral fornix was damaged bilaterally, the synthesis of ovarian progesterone and estrogen and the ovarian progesterone output were lower than those of the control without regard to hippocampal stimulation. But in the animals with lesion in bilateral stria terminalis hippocampal stimulation retained the facilitatory effect upon the formation of progesterone and estrogen and the progesterone output. These findings may suggest that the effect of hippocampal stimulation upon the ovary was exerted through the fornix and the basal hypothalamus including the arcuate nucleus, and not through the stria terminalis.

The anterior pituitary glands of sterilized rats secured by subcutaneous injection of 50μg estradiol benzoate contained a higher content of FSH and a little lower content of LH than those of normal proestrous glands. Serum contents of these hormones were not so different from those in normal proestrus and estrus. Electrical stimulations (0.1ms, 100Hz, 100μA) through chronically implanted electrodes into the medial preoptic area and medial part of amygdala induced the increases of serum LH and FSH. Stimulation into the dorsal hippocampus increased serum and pituitary concentrations of FSH and serum concentration of LH. Serum and pituitary concentrations of prolactin in the estrogenized rat were almost equivalent to those in normal proestrus and estrus, and stimulation of the hippocampus induced an increase of serum one. These results show that the brain of estrogenized rat differs in the function of hippocampus from that of normal cycling rat and in the function of amygdala from that of androgenized rat. However, the dramatic increase of serum and pituitary concentrations of both LH and FSH in response to bilateral ovariectomy indicates the right existence of steroid sensitive component in the brain.

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 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.

A study was made of adrenocortical hormone production under electroacupuncture stimulation of the Tsu-San-Li locus in rabbits with a lesion in the fornix, stria terminalis, ventromedial nucleus or arcuate nucleus. In rabbit with a lesion in the stria terminalis or ventromedial nucleus, electroacupuncture stimulation of Tsu-San-Li resulted in no increase in phase 1 but an increase in phase 2 of adrenocortical hormone production. In rabbits with a lesion in the fornix or arcuate nucleus electroacupuncture stimulation of Tsu-San-Li was followed by increased adrenocortial hormone production in the both phases. These results show that the stria terminalis and the ventromedial nucleus play a major role in the augmentation of adrenocortical hormone production by electroacupuncture of Tsu-San-Li.

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.