Search PubMed⌕ Search

Biomedical subjects

S Ueki

Publications and source records attributed to S Ueki.

At least 127 records · Page 7Linked to original sources
PubMed1986

Inhibitory action of insulin on suprachiasmatic nucleus neurons in rat hypothalamic slice preparations.

In order to elucidate a role of insulin on neurons in the suprachiasmatic nucleus (SCN) involved in the generation of circadian feeding behavior, we examined the effect of insulin on SCN neuronal activity at in vitro condition. Bath application of insulin (1-100 microU) mainly inhibited the SCN neuronal activity, and this inhibitory effect was still observed in a Ca2+-free Krebs solution. The present result strongly suggests that insulin directly inhibits SCN neurons and may explain an increase in food intake by insulin infusion into the SCN during the light period.

Animals↗
PubMed1986

Changes in brain catecholamine levels following olfactory bulbectomy and the effect of acute and chronic administration of desipramine in rats.

Bilateral olfactory bulbectomy of the rat caused marked changes of noradrenaline level in several brain regions accompanied with the development of mouse-killing behavior (muricide). Noradrenaline level increased in the medial amygdala, ventromedial and lateral hypothalamus in muricidal olfactory bulbectomized rats (OB rats) but not in non-muricidal OB rats, while dopamine level decreased in the lateral hypothalamus in muricidal OB rats. Acute administrations of desipramine not only suppressed muricide of OB rats but normalized noradrenaline change in ventromedial hypothalamus and dopamine change in lateral hypothalamus. Chronic administration of desipramine also suppressed muricide and normalized noradrenaline changes in ventromedial and lateral hypothalamus and medial amygdala. These findings suggest that the increase in noradrenaline levels in the medial amygdala, ventromedial and lateral hypothalamus may be important for the induction of muricide in OB rats, and muricide was suppressed by desipramine in accordance with the normalization of increased noradrenaline levels, and that the change in dopaminergic function in the lateral hypothalamus may also be important for this muricide.

Aggression↗
PubMed1986

Optic nerve stimulation-induced increase of release of 3H-glutamate and 3H-aspartate but not 3H-GABA from the suprachiasmatic nucleus in slices of rat hypothalamus.

This study investigates the possibility of glutamate and/or aspartate as an excitatory transmitter in the retinohypothalamic fibers' terminal within the anterior hypothalamus, including the suprachiasmatic nucleus (SCN). We studied the release of 3H-Glu and 3H-Asp from the SCN of rat hypothalamic slices produced by optic nerve stimulation. Stimulation of the optic nerve released 3H-Glu, 3H-Asp but not 3H-GABA, while stimulation of the SCN released all three. These releases were suppressed in both Ca2+ free Krebs and tetrodotoxin (TTX) 1 microM containing Krebs. The present result with previous electrophysiological observations strongly suggest that glutamate and/or aspartate are included in this retinohypothalamic termination, while GABA is included in intrinsic and/or extrinsic neurons of the SCN, excluding the terminal of the retinohypothalamic fibers.

Animals↗
PubMed1986

Endogenous prostaglandins in gastric alkaline response in the rat stomach after damage.

A role of endogenous prostaglandins in gastric alkaline response (an increase of luminal pH) and functional recovery was investigated in the rat stomach after damage with acidified taurocholate (TC, 20 mM) or aspirin (ASA, 40 mM). Exposure of the stomach to TC or ASA similarly produced a transmucosal potential difference (PD) reduction and enhancement of H+ backdiffusion. The PD was restored gradually with time, and this process was much faster in the case of TC compared with ASA. After exposure to TC, acid secretion ceased and bicarbonate (0.5-1 mu eq/10 min) appeared in the lumen, whereas acid secretion persisted in the stomach exposed to ASA. However, in the presence of cimetidine (8 mg . kg-1 . h-1), these two agents produced a similar degree of luminal alkalinization (approximately 1 mu eq/10 min of HCO3-). Pretreatment with indomethacin (5 mg/kg, sc) significantly inhibited luminal alkalinization and PD recovery seen after exposure to TC. Concurrent administration of 16,16-dimethyl prostaglandin E2 (3 micrograms/kg, sc) antagonized the effects of indomethacin in stomachs exposed to TC and also unmasked luminal alkalinization and expedited the PD recovery in stomachs exposed to ASA. The levels of PGE2 and 6-keto-PGF1 alpha in the corpus mucosa were significantly increased in stomachs exposed to TC, but decreased in those exposed to ASA. These results indicate that luminal alkalinization of the stomach after damage with TC results from both an inhibition of acid secretion caused by endogenous prostaglandins and an increased appearance of HCO-3, and may play a role in functional recovery of the damaged mucosa. Gastric alkalinization seems to be a common phenomenon after exposure to mucosal damaging agents unless they have an inhibitory effect on prostaglandin biosynthesis.

16,16-Dimethylprostaglandin E2↗
PubMed1986

Mechanisms of antisecretory action of intragastric FPL-52694: a mast cell stabilizer in anesthetized rats.

Mechanisms of antisecretory action of intragastric FPL-52694, a mast cell stabilizer, were investigated in anesthetized rats. In Schild's rat preparation, intravenous FPL-52694 (10 mg/kg) significantly suppressed acid secretion in response to only tetragastrin (20 micrograms/kg, i.v.) (42.1 +/- 19.4%), while intragastric application of FPL-52694 (100 mg/kg) for 30 min produced a marked, unequivocal inhibition (over 70%) in acid secretory responses to histamine (1 mg/kg, i.v.) and carbachol (2.5 micrograms/kg, i.v.) as well as tetragastrin. The inhibitory effect of intragastric FPL-52694 was confirmed in the lumen-perfused rats, where acid secretion (24-25 mumol/10 min) induced by intravenous infusion of histamine (8 mg/kg/h) was abolished for 1 h after exposure of the stomach for 30 min to this agent. Inhibition of histamine-stimulated acid secretion by intragastric FPL-52694 was much greater and lasted longer (2 h) as compared with xylocaine (4% solution), but significantly mitigated by pretreatment of the rats with subcutaneous administration of indomethacin (3 mg/kg). Furthermore, application of FPL-52694 but not of xylocaine to the stomach caused a reduction of transmucosal potential difference, an increase of luminal appearance of HCO-3 (1-2 mumol/10 min), and an enhancement of H+ back-diffusion, although no damage was appreciated in the mucosa. These results suggest that antisecretory action of intragastric FPL-52694 may involve local mechanisms such as neutralization of acid with HCO-3, a loss of acid due to H+ back-diffusion, and inhibition of acid production mediated by endogenous prostaglandins, but is not related to the local anesthetic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1986

[Effects of misoprostol, (+/-)-methyl (11 alpha, 13E)-11, 16-dihydroxy-16-methyl-9-oxoprost-13-en-l-oate, on various gastric and duodenal lesions in rats].

Male Sprague-Dawley rats (230-280 g), either fasted for 15-24 hr or non-fasted prior to experiments, were used. Misoprostol (3-100 micrograms/kg, p.o.) dose-dependently inhibited the development of 150 mM HCl X aspirin (100 mg/kg)-, 150 mM HCl X 60% ethanol-, and aspirin (150 mg/kg)-induced gastric lesions. Misoprostol (30, 100 micrograms/kg, p.o.), given twice daily for 4 days, significantly inhibited prednisolone (50 mg/kg given once daily for 4 days)-induced gastric lesions. Misoprostol (30 or 2 X 300 micrograms/kg, p.o.) also significantly inhibited water-immersion stress (21 degrees C, 10 hr)-induced gastric lesions or mepirizole (200 mg/kg)-induced duodenal lesions, respectively. In contrast, misoprostol (30-300 micrograms/kg, p.o.) had no effects on indomethacin (25 mg/kg)- and mepirizole (200 mg/kg)-induced gastric lesions. Misoprostol (30 micrograms/kg, p.o.) had no effect on gastric secretion in pylorus-ligated preparations (4 hr), but it (100 or 300 micrograms/kg, p.o.) significantly increased the volume and pepsin output. Gastric motility, either normal or enhanced with indomethacin (25 mg/kg), was inhibited by misoprostol (30 or 300 micrograms/kg, p.o.). Misoprostol (30 micrograms/kg, i.d.) significantly stimulated duodenal HCO3- secretion. Mechanisms by which misoprostol inhibits various gastric lesions remain unknown. However, the stimulatory activity on duodenal HCO3- secretion appears to be involved in the preventive effect of misoprostol on the development of duodenal lesions. The effects of cimetidine and 16,16-dimethyl PGE2 were also studied and compared with those of misoprostol.

Alprostadil↗
PubMed1986

[Electroencephalographic effects of 450191-S and its metabolites in rabbits with chronic electrode implants].

Electroencephalographic (EEG) effects of 450191-S and its metabolites were investigated in unanesthetized rabbits with chronic electrode implants, and they were compared with those of nitrazepam and estazolam. 450191-S at doses of 0.1-0.5 mg/kg, i.v., induced a drowsy pattern of spontaneous EEG: high voltage slow waves and spindle bursts increased in the cortex and amygdala, while the hippocampal theta rhythm was desynchronized. In addition, low voltage fast waves appeared particularly in the cortical EEG. The EEG arousal response to auditory stimulation and to electric stimulation of the mesencephalic reticular formation, posterior hypothalamus and centromedian thalamus was markedly suppressed by 450191-S. The photic driving response elicited by a flash light in the visual cortex was significantly suppressed by 450191-S. 450191-S showed no significant effect on the recruiting response. The EEG effects of nitrazepam were qualitatively similar but less potent and shorter in duration of action than those of 450191-S. The effects of estazolam were approximately as potent as those of 450191-S, but its duration of action was much shorter than that of 450191-S. 450191-S was more potent than nitrazepam and approximately equipotent to estazolam in suppressing hippocampal and amygdaloid after-discharges. The EEG effects of M-1 and M-2 were similar to those of 450191-S in both qualitative and quantitative aspects. The effects of M-A were quantitatively similar but less potent and shorter in duration of action than those of 450191-S.

Animals↗
PubMed1986

Pathogenic mechanisms involved in mepirizole-induced duodenal damage in the rat.

Mepirizole (60 and 200 mg/kg) administered s.c. induced damage in the surface epithelial cells of the rat proximal duodenum as early as 2 hr after the treatment. 16,16-Dimethyl prostaglandin E2 (dmPGE2, 30 micrograms/kg) administered s.c. significantly protected the duodenal mucosa against mepirizole-induced damage for up to 6 hr. Gastric acid secretion in acute fistula preparations was significantly reduced 1 hr after administration of mepirizole (60 and 200 mg/kg). The secretion reverted to the control level 2 hr later. In the 60 mg/kg-treated group, however, there was a significant increase in the acid output for up to 6 hr. Duodenal HCO3- secretion, stimulated with 10 mM HCl was significantly inhibited with mepirizole (60 and 200 mg/kg). Mepirizole (60 and 200 mg/kg) significantly increased the amount of acid in the duodenum for 2 to 6 hr after the treatment. dmPGE2 (30 micrograms/kg) significantly inhibited gastric acid secretion, stimulated duodenal HCO3- secretion, and reduced the increased amount of acid in the duodenum in response to mepirizole. Endogenous prostaglandin E2 and 6-keto prostaglandin F1 alpha in the duodenal mucosa were significantly reduced by mepirizole (200 mg/kg) 1 to 2 hr later. Mepirizole-induced duodenal damage appears to be caused by the increased amount of acid in the duodenum.

16,16-Dimethylprostaglandin E2↗
PubMed1986

Effects of indomethacin on the duodenal mucosa of rats: comparative study with cysteamine.

Effects of indomethacin and cysteamine on the duodenal mucosa of rats were studied microscopically (using scanning electron microscopy) and also functionally. Indomethacin (5 mg/kg, s.c.) induced no microscopic damage to the duodenal epithelium for up to 6 hr after administration. Indomethacin had no effects on gastric H+ output and the amount of H+ in the duodenum, but did reduce the duodenal HCO3- secretion (both basal and 10 mM-HCl stimulated). PGE2 contents in the duodenal mucosa were markedly reduced by indomethacin for 6 hr. These results suggest that reductions of duodenal HCO3- secretion and endogenous prostaglandins per se do not impair the H+ disposal system of the duodenum and so do not damage the epithelial cells. In contrast, cysteamine (100 mg/kg, s.c.) produced microscopic damage to the duodenal epithelium as early as 2 hr later. Cysteamine significantly increased gastric H+ output and reduced duodenal HCO3- secretion, resulting in an increased amount of H+ in the duodenum 3 hr later. Cysteamine had no effect on PGE2 contents in the duodenum. The time lag between damage formation and functional changes suggests that the earliest damage caused by cysteamine occurs by mechanisms other than erosive action of H+ emptied by the stomach. The increased amount of H+ may contribute to an enhancement of the initial damage.

Animals↗
PubMed1985

delta 9-Tetrahydrocannabinol elicited ipsilateral circling behavior in rats with unilateral nigral lesion.

The present study was designed to examine the influence of delta 9-tetrahydrocannabinol (THC) on the central dopaminergic system using circling behavior. THC 5 mg/kg i.p. produced ipsilateral circling in rats with unilateral nigral lesion by 6-hydroxy-dopamine. THC-induced ipsilateral circling was completely antagonized by 0.2 mg/kg of haloperidol. These findings suggest that THC may cause a presynaptic stimulation of nigrostriatal dopaminergic neurons.

Animals↗
PubMed1985

Effects of small amygdaloid lesions on pancreatic exocrine secretion.

To investigate the role of the amygdala in central regulation of pancreatic exocrine secretion, the effects of electrolytic lesions on pancreatic secretion were studied in rats. Small bilateral electrolytic lesions in amygdaloid body restricted to basolateral, medial and central nuclei were produced. Eight days after the lesions, bile-pancreatic juice was collected following anesthetization with urethane and chloralose. Basal secretion and secretion stimulated by exogenous pancreozymin and secretin were evaluated in terms of amylase output. In the group with basolateral nucleus lesions, both basal and stimulated secretion were significantly increased. After medial nucleus lesions, mean body weight was reduced to 59% of initial, and basal and stimulated secretion were significantly lower than in the control group and also significantly lower than in an unoperated group, whose mean body weight was reduced to the same level as that of the medially lesioned group by restricting daily food intake. After lesions of the central nucleus, basal secretion was significantly increased, while stimulated secretion was not affected. These results indicated that the amygdala is involved in regulating pancreatic exocrine secretion and that its various nuclei exert different effects.

Amygdala↗
PubMed1985

Influence of prednisolone on gastric alkaline response in rat stomach. A possible explanation for steroid-induced gastric lesion.

Exposure of the rat stomach for 10 min to 1 M NaCl produced an increase of luminal pH (alkaline response) with a concomitant reduction of the transmucosal potential difference (PD) and an increased generation of mucosal prostaglandins of E2 and 6-keto F1 alpha. Prednisolone (3-50 mg/kg), given subcutaneously 4 hr before exposure to 1 M NaCl, dose-dependently inhibited alkaline response without affecting the PD reduction, and at 50 mg/kg completely prevented the increased production of mucosal prostaglandins after exposure to 1 M NaCl. The inhibitory effect of prednisolone on alkaline response was significantly antagonized by pretreatment with 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2) (3 micrograms/kg) or cycloheximide (1.5 mg/kg). A repeated administration of prednisolone (3-50 mg/kg), once daily for 4 days, produced gastric lesions dose-dependently. At 50 mg/kg, gastric lesions appeared after administration of this drug for more than 2 days, and the inhibition of alkaline response caused by 1 M NaCl became more potent as the days of treatment increased. Either 16,16-dmPGE2 (10-100 micrograms/kg) or cycloheximide (1 or 3 mg/kg), given daily in two divided doses for 4 days, dose-dependently inhibited formation of gastric lesions in response to prednisolone (50 mg/kg). These results indicate that prednisolone inhibits gastric alkaline response caused by 1 M NaCl by reducing generation of endogenous prostaglandins. The weakened self-defense mechanisms caused by prednisolone may be involved in the pathogenesis of steroid-induced gastric lesions.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Qualitative and quantitative analysis of muscarinic acetylcholine receptors in the piebald lethal mouse model of Hirschsprung's disease.

Cholinergic innervation in the aganglionic bowel of the piebald lethal mouse model of Hirschsprung's disease was investigated by analysis of muscarinic acetylcholine receptors before and after administration of hexamethonium. After hexamethonium administration in the normal rectum, the maximum specific binding (Bmax) of [3H]quinuclidinyl benzilate increased from 196.6 to 346.2 fmol/mg protein without affecting the dissociation constant. This increase of muscarinic acetylcholine receptors was associated with a decrease in the 50% effective dose (ED50) of contractile response to oxotremorine from 3.8 X 10(-7) M to 6.5 X 10(-8) M. In the aganglionic rectum, hexamethonium administration did not change the Bmax (166.4 fmol/mg protein) or dissociation constant value. The ED50 of contractile response to acetylcholine and oxotremorine (4.3 X 10(-8) M, 6.5 X 10(-8) M) was lower than that in the normal rectum (1.9 X 10(-7) M, 2.0 X 10(-7) M), but it was not changed by hexamethonium. It is concluded that cholinergic innervation is congenitally absent in the aganglionic rectum in piebald lethal mice.

Acetylcholine↗
PubMed1985

Effect of L-glutamate, injected into the posterior hypothalamus, on blood pressure and heart rate in unanesthetized and unrestrained rats.

In unanesthetized and unrestrained rats, microinjection of L-glutamate into the posterior hypothalamus produced hypertension and tachycardia. These cardiovascular responses were mostly accompanied with behavioral excitation such as searching the cage, rearing and sniffing. The cardiovascular responses elicited by L-glutamate were attenuated by prior injection with propranolol and hexamethonium but not with glutamate diethylester, phentolamine and atropine. The behavioral responses to L-glutamate were suppressed by propranolol, hexamethonium and phentolamine. These results suggest that catecholaminergic and/or cholinergic systems in the posterior hypothalamus may be involved in the mediation of the cardiovascular and behavioral responses induced by L-glutamate.

Animals↗
PubMed1985

The role of central noradrenergic neurons in electroconvulsive shock-induced muricide inhibition in olfactory bulbectomized rats.

In order to elucidate the role of central monoaminergic neurons in electroconvulsive shock (ECS)-induced muricide inhibition in the olfactory bulbectomized rat (OB rat), we examined the effect of chemical or electrical lesions of each monoamine-containing neuron on ECS-induced muricide inhibition. ECS-induced muricide inhibition was antagonized by 6-hydroxydopamine (6-OHDA) treatment and locus coeruleus lesions, while it was unaffected by desipramine + 6-OHDA, substantia nigra lesion, and desipramine + 5,7-dihydroxytryptamine. The present results strongly suggest that ECS-induced muricide inhibition of the OB rat is due to increased activity of the noradrenaline but not of dopamine and serotonin neurons.

Adrenergic Fibers↗
PubMed1985

Effects of chronic LiCl and RbCl on muricide induced by midbrain raphe lesions in rats.

Midbrain raphe lesions in rats (raphe rats) induce aggressive behavior including muricide. A single administration of LiCl (Li) 100 mg/kg to raphe rats produced only 25% of muricide inhibition. However, the inhibitory effect of muricide in raphe rats significantly increased from the 5th day following repeated administration of Li. Chronic Li also inhibited muricide in olfactory bulbectomized (OB) rats. The inhibition of muricide lasted until the next day to some extent. In this point, the effect of Li on muricide is similar to that of antidepressants, but not of neuroleptics. On the contrary, RbCl (Rb) showed a tendency to induce muricide. The single re-administration of Li 100 mg/kg on the withdrawal on the 7th day after repeated administration for 14 days showed a significant inhibition of muricide in raphe rats, unlike that in OB rats. Li also showed a partial prophylactic effect on muricide when Li 100 mg/kg was administered for 1 week before raphe lesions. These results suggest that raphe rats may serve not only as an experimental model of depression, but also as that of manic illness.

Aggression↗
PubMed1985

Effects of psychotropic drugs on discrimination conditioning in olfactory bulbectomized rats.

In the acquisition process of discrimination avoidance conditioning, bilateral olfactory bulbectomized rats showed poor discrimination conditioning since both the avoidance responses to positive conditioned stimuli (CS) and the incorrect responses to negative CS increased. The effects of various psychotropic drugs upon this poor discrimination conditioning were examined. Chlordiazepoxide 5 mg/kg, IP, produced an increase in the avoidance responses with simultaneous decrease in the incorrect responses, thus making the discrimination possible. Chlorpromazine 2 mg/kg, IP, worsened the discrimination by decreasing both the avoidance and incorrect responses as compared with saline-treated rats. Amitriptyline 10 mg/kg, IP, decreased the incorrect responses without affecting the avoidance responses, thus making the discrimination possible. Methamphetamine 0.5 mg/kg, IP, increased both the avoidance and incorrect responses resulting in poor discrimination conditioning. From these results, it was found that the poor discrimination conditioning of O.B. rats was improved by psychotropic drugs like chlordiazepoxide and amitriptyline.

Amitriptyline↗