Inhibition of gastric acid secretion and mucosal blood flow induced by intraventricularly applied neurotensin in rats.
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Biomedical subjects
Publications and source records attributed to Y Osumi.
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The nociceptive reflex activity and analgesic effect of morphine were studied in rats using the hind paw stimulation test. The stimulation threshold was significantly increased in animals with bilateral destruction of the locus coeruleus (LC), and was reduced after lesion of the dorsal raphe nucleus (DR). LC lesions produced a selective lowering of noradrenaline (NA) content in the forebrain, while DR lesions resulted in a reduction in serotonin levels. Lesioning both LC and DR significantly reduced both NA and serotonin contents even when the stimulation threshold was not altered. Morphine produced a significant and dose-dependent elevation of the stimulation threshold in sham-operated animals, while morphine analgesia was almost completely inhibited by destruction of LC, DR and both the nuclei. These results imply that a depression of LC-mediated noradrenergic tone results in a decreased sensitivity to painful stimuli, whereas a reduction of raphe-derived serotonergic tone produces the opposite effect against LC. It is suggested, however, that both of these monoamines from the LC and DR are necessary for the analgesic effect of morphine.
The possibility that hypothalamic noradrenaline (NA) plays a role in the formation of gastric ulcers under stress via ventral bundles (VB) was examined in rats after bilateral destruction of VB. After a 3-h restraint stress ulcerative changes were observed in the stomach of sham-operated rats. NA contents in the hypothalamus and cerebral cortex decreased as compared to the respective contents before stress. The VB-lesioning inhibited the stress-induced decrease of NA in the hypothalamus. Ulcer indices in the animals 1 or 7 days after the VB-lesioning, however, did not differ from those of controls. Pretreatment of sham-operated controls with tetrabenazine enhanced the stress-induced decrease of NA in the brain, and exacerbated the gastric ulceration. VB-lesioning completely blocked these effects of tetrabenazine. It appears that the tetrabenazine-induced mobilization of hypothalamic NA via VB causes an aggravation of gastric ulceration.
Twenty-four right-handed, right hemiparetic patients with Broca's aphasia were examined for their singing capacity. Twenty-one (87.5%) produced good melogy. Twelve of these (57%) produced good text words while singing. It is speculated that the right hemisphere is dominant over the left for singing capacity. The relationship between melodic and text singing was also discussed.
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The chonotropic response to noradrenaline, tyramine, acetylcholine and transmural electrical stimulation was compared in atria isolated from rabbits at different stages of developmental after birth (day 2 to day 210). Pacemaker rates understeady state conditions were related inversely to days after birth; the rate in atria from rabbits at day 2 was significantly greater than that at days 10-210. The rate of neonatal rabbit atria was not significantly reduced by propranolol and the positive chontropic response to noradrenaline was not significantly reduced by propranolol and the positive chronotropic response to noradrenaline was not significantly different in atria from ages of rabbits as far as threshold concentrations for inducing tachycardia and ED50's were concerned. The maximum rate induced by noradrenaline was higher in neonatal rabbit atria than in adult rabbit atria. The effect of tyramine was approx. the same regardless of age. Increase in the pacemaker rate induced by transmural neural stimulation varied directly with age. The negative chronotropic effect of acetylcholine was greater in neonatal than in adult rabbit atria; the ED50 in the former was significantly less than in the latter. Bradycardia induced by transmural stimulation of intracardiac cholinergic nerves was related directly to age. Tachycardia in the neonatal rabbit atria may be due to electrogenic characteristics of pacemaker cells which differ from those in adult rabbit atria. Our evidence strongly suggests that the adrenergic and cholinergic nerves innervating the S-A node develop at an early postnatal stage in the rabbit.
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Bilateral lesions in the locus coeruleus (LC) of rats induced a urinary disorder and hyperdipsia. Dilatation of the urinary bladder, urinary retention and hematuria with bleeding originating from the urinary bladder, occurred immediately after the lesioning and continued for 2-5 days. Water intake increased 4 days after the lesioning. This hyperdipsia persisted for at least 4 days and then gradually returned to the control level. Food intake decreased for the first 5 days, and then returned to the control level. Lesions in the ascending dorsal bundle (DB) originating from the LC also produced hyperdipsia, but not urinary disorder. Destruction of the ascending ventral vundle (VB) originating from the noradrenaline (NA) neurons in the medulla oblongata did not affect eating, drinking or urination. The LC- or DB-lesioning caused a significant reduction of NA in the whole forebrain except the hypothalamus, whereas VB-lesioning caused reduced NA in the hypothalamus. In LC-lesioned animals, no significant changes were observed in serum osmolarity, Na+, K+, albumin and glucose in serum, or in the excretion of urine in the water-loading test.
Effects of 2-chloro-1-(2, 4-dichlorophenyl) vinyl diethyl phosphate, chlorfenvinphos, on spontaneous EEG, EMG and ChE activity in the brain and red blood cells were investigated in male Wistar rats. Chlorfenvinphos up to 1 mg/kg p.o. did not affect the ChE activity and the awake-sleep cycle. In doses over over 2 mg/kg, the ChE activity in the brain and red blood cells significantly decreased. The spontaneous EEG showed a prominent arousal pattern and appearance of slow wave sleep and parasleep was markedly depressed. Maximum inhibition of brain ChE activity was obtained 3 hr after the treatment and lasted for more than 72 hr. The duration of arousal pattern was proportional to the doses, however, the awake-sleep cycle returned to control on the 2nd day and a rebound increase in parasleep occurred on the 3rd day. Atropine depressed the EEG arousal pattern induced by chlorfenvinphos, without affecting ChE activity in the brain. The brain noradrenaline level was not altered with chlorfenvinphos. These results indicate that the appearance of EEG arousal pattern after chlorfenvinphos may be derived from central cholinergic activation.
The mechanism of action of colicin E3 (E3) was investigated in an in vitro system. Purified ribosomes are less susceptible to E3 than crude or washed ribosomes. A factor was found in the supernatant fraction of normal Escherichia coli cells that stimulates inactivation of ribosomes by E3, and on addition of this factor, about one tenth as much E3 was required for inactivation of ribosomes. On heating a mixture of E3 and this factor above 60 degrees , the ribosome inactivating activity of E3 increased greatly, and an amount corresponding to 0.01 mug of E3 was sufficient to inactivate 1.0 A(260) unit of ribosomes completely. By this treatment bacteriocidal activity of E3 decreased considerably, as the ratio of the two activities of E3 (ribosome inactivating activity and bacteriocidal activity) increased to 6 x 10(4)-fold. It is evident that the two activities do not run in parallel. This heat-treated product cleaved 16S rRNA in the same way as E3. These results suggest that inactivation of ribosomes is not due to colicin molecules prepared by the standard procedure, but to a modified form of them.
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