[Regulatory factors in food intake: glucoreceptor neuron and gluco-sensitive neuron].
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Adenosine Triphosphate↗
Biomedical subjects
S Aou
Publications and source records attributed to S Aou.
[Progress in research on the central mechanism of feeding behavior--neuronal network].
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Animals↗
[Role of miscellaneous substances (organic acids, lactone, etc) in regulation of food intake].
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4-Butyrolactone↗
Hypothalamus regulates calcium metabolism in rats.
Hypothalamic mechanisms of blood calcium homeostasis and their functional heterogeneity were investigated in rats. Electrical and chemical stimulation of the lateral hypothalamic area (LHA), the paraventricular nucleus (PVN) and the ventromedial nucleus of the hypothalamus (VMH) induced hypocalcemia. The hypocalcemic effect of PVN stimulation was suppressed by vagotomy of the thyroid/parathyroid branches, while that of LHA and VMH stimulation was eliminated by gastric vagotomy. Immobilization (IMB) stress elicited hypocalcemia through VMH-gastric vagal activation. Both IMB- and LHA stimulation-induced hypocalcemia was antagonized by muscarinic antagonist and histamine H2 blocker. The former was also blocked by alpha-blocker and gastrin release inhibitor, while the latter was antagonized by an beta-blocker. The results suggest that hypothalamic nuclei are involved in regulation of blood calcium homeostasis via the gastric or thyroid/parathyroid vagus. Muscarinic, histamine H2, adrenergic and gastrin receptors mediate the hypocalcemic effect of the hypothalamo-vagal activation depending on behavioral conditions and receptor subtypes.
Animals↗
Intracerebroventricular injection of prostaglandin E2 induces thermal hyperalgesia in rats: the possible involvement of EP3 receptors.
To determine what types of prostanoid receptors are involved in the central effect of prostaglandin E2 (PGE2) on nociception, we administered PGE2 and its agonists, i.e., 17-phenyl-omega-trinor PGE2 (an EP1 receptor agonist), butaprost (an EP2 receptor agonist), 11-deoxy PGE1 (an EP2/EP3 receptor agonist, EP2 >> EP3) and M&B28767 (an EP3 receptor agonist) into the lateral cerebroventricle (LCV) of rats and observed the changes of paw-withdrawal latency on a hot plate. The LCV injection of PGE2 (10 pg/kg-10 ng/kg), 11-deoxy PGE1 (100 pg/kg-10 ng/kg) and M&B28767 (1 pg/kg-100 pg/kg) produced a significant reduction in the paw-withdrawal latency. The maximal reduction was observed 15 min after the LCV injection of these drugs. Neither 17-phenyl-omega-trinor PGE2 (1 pg/kg-1 microgram/kg) nor butaprost (1 pg/kg-100 microgram/kg) induced any significant changes in the paw-withdrawal latency. The LCV injection of PGE2 (1 microgram/kg) and 17-phenyl-omega-trinor PGE2 (50 micrograms/kg) increased the latency only 5 min after LCV injection. These findings indicate that the LCV injection of PGE2 induces thermal hyperalgesia through EP3 receptors and analgesia through EP1 receptors by its central action in rats.
Alprostadil↗
Intracerebroventricular injection of interleukin-1 beta enhances nociceptive neuronal responses of the trigeminal nucleus caudalis in rats.
To assess the effect of interleukin-1 (IL-1) in the brain on nociception electrophysiologically, recombinant human IL-1 beta (rhIL-1 beta) (1 pg/kg to 1 microgram/kg, i.e., 0.29 pg-0.33 microgram/rat) was microinjected into the lateral cerebral ventricle of urethane-anesthetized rats and the changes of responses in the wide dynamic range (WDR) neurons in the trigeminal nucleus caudalis to noxious pinching of facial skin were observed. A significant enhancement in the responses of the WDR neurons to noxious stimuli was observed after the injection of rhIL-1 beta between 10 pg/kg and 1 ng/kg, which showed a maximal response at a dose of 100 pg/kg (29-33 pg/rat) which began to appear 5 min after injection, reached a peak within 25 min and then gradually subsided. However, this dose of rhIL-1 beta did not affect the responses of low threshold mechanoreceptive neurons to skin brushing. An increase in the dose of rhIL-1 beta by more than 10 ng/kg (up to 1 microgram/kg) had no effect on the nociceptive responses of the WDR neurons. The rhIL-1 beta-induced enhancement of nociceptive responses of WDR neurons was completely abolished by pretreatment with either IL-1 receptor antagonist, Na salicylate or alpha-melanocyte stimulating hormone. These results therefore provide electrophysiological evidence that IL-1 beta which is produced in the brain induces hyperalgesia in the rat.
Animals↗
The effect of B-HT 920, a dopamine D2 agonist, on bar-press feeding in the monkey.
Although the dopamine (DA) system has been shown to regulate food intake, the function of the DA receptor subtypes on behavior still remains to be elucidated. In the present study, we examined the effect of B-HT 920, a selective agonist of DA D2 receptors that preferentially affect presynaptic autoreceptors, on both food consumption and execution of a high fixed-ratio bar-press task for food reward in monkeys. Two kinds of bar-press task were used: 1) a cue-triggered bar-press task during the first 40 trials, and 2) a self-paced bar-press task in which the monkeys freely performed bar-press trials until they were satiated. A SC injection of B-HT 920 (25 micrograms/kg) increased food consumption in the home cage. The same facilitatory effect on food consumption was also observed in the operant task condition. During the cue-triggered bar-press task, however, both the latency of the bar-press responses to a cue light and the time required to complete the bar-press trials were prolonged after the injection of B-HT 920. The results suggest that the activation of D2 autoreceptors suppresses the operant food acquisition behavior and increases food consumption through an inhibition of the satiety mechanism rather than an activation of any hunger-related drive.
Animals↗
Hypothalamic stimulation induces vagally mediated hypocalcemia in the rat.
To elucidate hypothalamic involvement in blood calcium homeostasis, the effects of unilateral electrical stimulation (0.1 mA, 0.5 ms, 30 Hz, 60 min) of the lateral hypothalamic area (LHA), the paraventricular nucleus (PVN), and the ventromedial nucleus of the hypothalamus (VMH) on the blood concentration of ionized calcium were examined in the anesthetized rats. LHA stimulation induced a sustained decrease (0.05-0.07 mM fall) in the blood calcium level during the period of 60 to 150 min (end of the measurements) after stimulation. In contrast, PVN stimulation elicited a transient hypocalcemia (0.07 mM decrease) 60 min after stimulation. The hypocalcemic effects of LHA and PVN stimulation were eliminated by vagotomy of the gastric branches and the thyroid/parathyroid branches, respectively. VMH stimulation, using the same parameters, did not induce any significant change in blood calcium. The results suggest that the LHA and the PVN have a hypocalcemic function that is mediated, at least in part, by the vagus nerve innervating the stomach and the thyroid/parathyroid glands, respectively.
Anesthesia↗
Ventromedial hypothalamus mediates stress-induced hypocalcemia via the gastric vagus in rats.
A hypothalamo-vagal mechanism of immobilization (IMB) stress-induced hypocalcemia was investigated in rats. Bilateral lesions in the ventromedial nucleus of the hypothalamus (VMH), but not those of the lateral hypothalamic area (LHA) or the paraventricular nucleus (PVN), eliminated the calcium-lowering effect of IMB. None of these lesions, however, affected the basal levels of the blood calcium. An electrical stimulation of the VMH induced a significant decrease in the blood calcium level (0.07 mM fall) 60 min after stimulation. The hypocalcemic response was eliminated by a vagotomy of the gastric branches but not by that of the thyroid/parathyroid branches. These results suggest that the VMH mediates IMB-induced hypocalcemia through its influence on the gastric vagus.
Animals↗
Effects of 2-buten-4-olide, an endogenous satiety substance, on plasma glucose, corticosterone, and catecholamines.
Effects of 2-buten-4-olide (2-B4O), an endogenous satiety substance, on levels of plasma glucose, corticosterone, and catecholamines were examined in fed, conscious, and unrestrained rats. A vascular indwelling catheter was inserted into the right atrium of the animal from the jugular vein 1 wk before the experiment. Injection of 2-B4O and blood sampling were performed through the catheter in an unanesthetized condition. The levels of plasma glucose, corticosterone, epinephrine, and norepinephrine increased significantly for 2 h after the start of intravenous injection of 2-B4O in a dose-dependent manner. The increases in glucose and catecholamines induced by 2-B4O injection were abolished by bilateral splanchnicotomy (SPX) but not by pretreatment with anti-corticotropin-releasing factor (CRF) antibody. The increase in corticosterone was abolished not by the SPX but by pretreatment with anti-CRF antibody. These findings suggest that 2-B4O, endogenously produced during food deprivation, may facilitate sympathoadrenal and hypothalamopituitary-adrenal functions through the central nervous system.
4-Butyrolactone↗
Linkage of stress-induced hypocalcemia, gastric lesions, and emotional behavior in Wistar-Kyoto rats.
The effects of water-restraint stress on blood calcium levels and gastric pathology and their behavioral relevance were examined in Wistar-Kyoto (WKY) and Wistar rats. The stress induced more severe hypocalcemia (0.32 mM decrease) and gastric lesions (34.6 mm in mean length) in WKY rats than in Wistar rats (0.19 mM and 17.7 mm, respectively). The magnitude of hypocalcemia correlated positively with that of gastric lesions in both strains (WKY, r = 0.59; Wistar, r = 0.69). In the forced-swimming test, WKY rats exhibited a longer immobility time (6.53 min) and a shorter struggling time (0.54 min) than Wistar rats (3.33 and 1.90 min, respectively). The severity of hypocalcemia and gastric lesions correlated positively (r = 0.59 and 0.69, respectively) with the length of immobility time in the WKY rats, while it correlated negatively (r = -0.70 and -0.61, respectively) with the length of struggling time in the Wistar rats. These results suggest that stress-induced hypocalcemia and gastric lesions are closely related and are also influenced by behavioral responsiveness in a strain-dependent manner.
Animals↗
Hypothalamic linkage in stress-induced hypocalcemia, gastric damage, and emotional behavior in rats.
The effects of hypothalamic lesions on stress-induced hypocalcemia, gastric damage, and swim test-evoked behavior were examined in rats. Bilateral lesions of the ventromedial nucleus in the hypothalamus (VMH) eliminated water-restraint stress-induced hypocalcemia and attenuated any gastric damage compared with those in the sham-operated rats. In contrast, lesions in the paraventricular nucleus (PVN) exacerbated both the stress-induced hypocalcemia and gastric lesions in comparison with those in the control rats. In a forced-swimming test, the VMH-lesioned rats showed a significantly shorter time of immobility as well as a longer duration of struggling than the control rats, respectively, while the PVN-lesioned animals spent a longer time in immobility and a shorter period struggling than the control rats. These results suggest that the VMH has an accelerative action in stress-induced hypocalcemia, gastric lesions, and behavioral despair, while the PVN has an opposite effect.
Animals↗
Intracerebroventricular injection of interleukin-1 beta induces hyperalgesia in rats.
To determine whether interleukin-1 beta (IL-1 beta) in the brain may modulate nociception, recombinant human IL-1 beta (rhIL-1 beta) (1 pg/kg to 1 microgram/kg) was microinjected into the lateral cerebral ventricle of rats and the latency before initiating the licking of their hindpaws after being placed on a hot plate (50.0 +/- 0.1 degrees C) was measured. A significant reduction of the paw-lick latency was observed after injections of nonpyrogenic doses (10 pg/kg to 1 ng/kg) of rhIL-1 beta, showing a maximal response at a dose of 100 pg/kg which began to appear 5 min after injection, reached a peak within 30 min and then gradually subsided. An increase in the amount of rhIL-1 beta to > 1 ng/kg (up to 1 microgram/kg) had no effect on the nociceptive threshold. The rhIL-1 beta-induced hyperalgesia was completely abolished by pretreatment with an IL-1 receptor antagonist (IL-1ra) or Na salicylate. Similar pretreatment with alpha-melanocyte-stimulating hormone (alpha-MSH) also inhibited the rhIL-1 beta-induced hyperalgesia. However, pretreatment with alpha-helical corticotropin-releasing factor (CRF)9-41 failed to affect it. The results suggest that IL-1 beta in the brain produces hyperalgesia by its receptor-mediated and prostaglandin-dependent action which is sensitive to alpha-MSH. The hyperalgesic action of central IL-1 does not appear to depend on the CRF system.
Animals↗
Hypothalamic involvement in stress-induced hypocalcemia in rats.
Although hormonal regulation of blood calcium homeostasis has been intensively investigated in the peripheral organs, the involvement of the central nervous system in calcium regulation is still poorly understood. In the present study, we found that (1) bilateral lesions of the ventromedial nucleus of the hypothalamus (VMH), but not those of the paraventricular hypothalamic nucleus or the lateral hypothalamic area, eliminated immobilization (IMB)-induced hypocalcemia, and (2) electrical stimulation of the VMH decreased the blood calcium level. The results suggest that the VMH has a hypocalcemic function and plays a role in IMB-induced hypocalcemia.
Animals↗
Gastric vagus mediates immobilization-induced hypocalcemia in rats.
The involvement of the parasympathetic nervous system in the etiology of stress-induced hypocalcemia was investigated in the rat. Atropine methyl bromide (0.1 and 0.6 mg/kg ip) given 20 min before immobilization (IMB) was observed to suppress the induction of hypocalcemia in a dose-dependent manner. A vagotomy of the bilateral cervical trunks also abolished the IMB-induced hypocalcemia. A vagotomy on either the thyroid/parathyroid branches or the celiac branches had no effect on the IMB-induced hypocalcemia, but a vagotomy on the gastric branches completely abolished it. Pretreatment with either secretin (2 and 6 micrograms/kg ip), an inhibitor of gastrin release, or cimetidine (5 and 10 mg/kg ip), a histamine H2-receptor antagonist, diminished the IMB-induced hypocalcemia. The concentration of serum gastrin increased significantly during IMB. It is thus concluded that the decreased levels of plasma calcium caused by IMB are due to the activation of the vagus innervating the stomach. Gastrin and histamine are also involved as a consequence of the activation of the vagus.
Animals↗
The stomach is the etiologic organ for immobilization-induced hypocalcemia in rats.
Our previous study revealed that the gastric vagus nerve plays an etiologic role in immobilization (IMB) stress-induced hypocalcemia. The purpose of the present study is to identify exactly what parts of the stomach are involved in the development of IBM-induced hypocalcemia and to determine whether or not gastric acid secretion is involved. A total gastrectomy, but not a resection of the upper intestine, eliminated the hypocalcemic effect of IMB. In addition, either an antrectomy (removal of the source of gastrin) or a fundectomy (depriving the origin of gastric histamine and gastric acid) was sufficient for eliminating IMB-induced hypocalcemia, while a partial (50%) fundectomy failed to suppress it. An intraperitoneal injection of galanin (an inhibitor of gastrin release) or ranitidine (a blocker of histamine H2-receptor) also suppressed the calcium-lowering effect of IBM, whereas omeprazole (an inhibitor of the proton pump) had no effect. These findings suggest that the antrum and the fundus of the stomach play essential roles in IMB-induced hypocalcemia through the vagus-induced release of gastrin and histamine but not through the secretion of gastric acid per se.
Animals↗
Gustatory neural coding in the amygdala of the alert macaque monkey.
1. Neurons in the amygdala are implicated in mediating hedonic appreciation, emotional expression, and conditioning, particularly as these relate to feeding. The amygdala receives projections from the primary taste cortex in monkeys, offering a route by which it could gain access to the gustatory information required to guide feeding behavior. We recorded the activity of 35 neurons in the amygdala of alert rhesus macaques in response to a range of gustatory intensities and qualities to characterize taste-evoked activity in this area. 2. The stimulus array comprised 26 chemicals, including four concentrations of each of the four basic taste stimuli, a series of other sugars, salts, and acids, monosodium glutamate, and orange juice. 3. Neurons responsive to taste stimulation could be found in a 76-mm3 region of the amygdala, centered 9.1 mm lateral to the midline, 14.9 mm anterior to the interaural line, and 25.7 mm below the surface of the dura. They composed 7.2% (35/484) of the cells tested for gustatory sensitivity in the amygdala. 4. The mean spontaneous activity of taste cells was 8.2 +/- 2.3 (SE) spikes per second. This rather high level provided an opportunity for reductions from spontaneous rate that was used regularly in the amygdala. When these negative response rates were included, the mean breadth-of-tuning coefficient of this sample of taste cells was 0.82. There was no strong evidence for gustatory neuron types, nor were functionally similar cells located together in a chemotopic arrangement. 5. Responses across 1.5 log units of stimulus concentration were nearly flat, with increasing excitation in some neurons largely offset by increasing inhibition in others. Taking the absolute value of the evoked activity, concentration-response functions rose monotonically to all basic stimuli except HCl, but were not sufficiently steep to account for human psychophysical data. The neural response to HCl did not rise with stimulus concentration within the range used. 6. Neural patterns representing the taste qualities of the basic stimuli were less sharply separated in the amygdala than at lower-order gustatory relays. Glucose elicited activity patterns that were most distinct from those of the nonsweet chemicals; those associated with NaCl were next most distinct. There was no clear separation between the patterns generated by chemicals that humans describe as sour and bitter. Monosodium glutamate evoked responses that did not correlate well with those of any basic stimulus, implying that its quality cannot be subsumed under the four basic tastes.(ABSTRACT TRUNCATED AT 400 WORDS)
Amygdala↗
Feeding suppression elicited by electrical and chemical stimulations of monkey hypothalamus.
The effects of electrical (ES) and chemical stimulations of the hypothalamus were investigated in monkeys during bar-press feeding. ES elicited both prolonged and nonprolonged types of suppression of bar-press feeding in hungry animals. Prolonged type suppression persisted for greater than 1 min beyond one or more post-ES trials and was found after ES of the dorsomedial hypothalamus (DMH), the ventromedial hypothalamus (VMH), and the ventromedial part of the lateral hypothalamic area (LHA). Non-prolonged type suppression was observed only during ES at some sites of both in hypothalamic and extrahypothalamic areas. A microinjection of glutamate into the VMH and the DMH, but not into the LHA, was able to reproduce the ES-induced prolonged type suppression. In contrast, the ES of the LHA, but not the VMH and DMH, in a satiated state provoked feeding. The results, together with the previous findings, suggest that the neuronal inhibitory mechanism of feeding exists in the VMH and DMH, while both the neuronal facilitatory and axonal inhibitory mechanisms in the LHA are involved in the feeding regulation, and these mechanisms of the LHA are affected by the hunger/satiety state.
Animals↗