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Biomedical subjects

H Onoe

Publications and source records attributed to H Onoe.

49 records · Page 3Linked to original sources
PubMed1991

REM sleep-associated hemoglobin oxygenation in the monkey forebrain studied using near-infrared spectrophotometry.

The oxygenation state of hemoglobin (Hb) in the monkey forebrain was monitored continuously throughout nocturnal sleep using a near-infrared spectrophotometric technique. During rapid eye movement (REM) sleep, an increase in oxygenated Hb occurred concomitantly with a decrease in deoxygenated Hb, while no significant changes in Hb oxygenation were observed during slow wave sleep (SWS). A gradual increase in total Hb content was also observed to occur during each REM sleep episode but not during SWS.

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PubMed1991

Astrocytes possess prostaglandin F2 alpha receptors coupled to phospholipase C.

We examined the effect of prostaglandin (PG) F2 alpha on phosphoinositide (PI) hydrolysis in rat cultured astrocytes. PGF2 alpha stimulated the formation of [3H]inositol phosphates in [3H]inositol-labeled astrocytes with the ED50 value of 23 nM, whereas PGD2 and PGE2 were much less effective than PGF2 alpha. Transformation of astrocytes was accompanied by an increase in the stimulatory response of PGF2 alpha. Pretreatment of the astrocytes with pertussis toxin and cholera toxin did not affect the PGF2 alpha-evoked PI hydrolysis. In the digitonin-permeabilized astrocytes, PGF2 alpha significantly enhanced the GTP gamma S-evoked PI hydrolysis in the presence of Ca2+. These results indicate that rat cultured astrocytes possess PGF2 alpha receptors coupled to phospholipase C.

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PubMed1990

High density of prostaglandin E2 binding sites in the anterior wall of the 3rd ventricle: a possible site of its hyperthermic action.

Prostaglandin E2 (PGE2) exerts a potent hyperthermic action when injected into the preoptic-hypothalamic area (POHA) and is considered to be a central mediator of fever. To determine the exact functional sites of PGE2, we used in vitro quantitative autoradiography of [3H]PGE2 binding sites in the rat POHA. The highest density of [3H]PGE2 binding was found in the regions of the anterior wall of the 3rd ventricle (A3V). Within the A3V, binding density was especially high in regions closest to the third ventricle or surrounding the organum vasculosum laminae terminalis (OVLT) but was relatively low within the OVLT itself. It seems likely that the A3V PGE2 binding sites identified in this study are responsible for PGE2 mediation of fever.

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PubMed1989

Secretion of tumor necrosis factor during fetal and neonatal development of the mouse: ontogenic inflammation.

Inflammation plays an important role in homeostasis of the body. We therefore can assume that an inflammatory state occurs during ontogenesis of animals. To address this problem, we examined the ability of tumor necrosis factor (TNF), one of the inflammatory mediators, to be secreted by mouse cells during development. We cultured cells prepared from various parts of fetuses (10-19 days of gestation) and postnatal brains by collagenase digestion and assayed the secreted TNF activity by the L-929 cytotoxicity test. We found TNF activity by fetal cells without any stimulation. The spontaneous secretion of TNF was relatively high at around 13-15 days of gestation. The secretion was enhanced by lipopolysaccharide (LPS), showing that fetal cells are in an activated state for TNF secretion. These TNF activities were neutralized completely by rabbit anti-murine TNF antibody. Spontaneous and LPS-enhanced secretion by postnatal brain cells reached a peak around 7 days after birth, and thereafter declined rapidly. This time course was well correlated to the increase in the weight of brain. The producing cells were negative in macrophage marker surface antigen, and heterogeneous in relation to adherence and phagocytic activity, showing that TNF is secreted by various types of cells in the fetal body. These results suggest the presence of an inflammation-like state during ontogenesis. We consider that this "ontogenic inflammation" may be the prototype of inflammation, which can regulate homeostasis of the adult body.

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PubMed1988

Prostaglandin D2, a cerebral sleep-inducing substance in monkeys.

The sleep-inducing effect of prostaglandin D2 (PGD2) was studied in five conscious male rhesus monkeys (Macaca mulatta) maintained in a 12-hr light/dark cycle. PGD2 was infused into the lateral or the third ventricle of the cerebrum slowly and continuously for 6 hr in the light period. Infusion of PGD2 into the lateral ventricle at 15-2250 pmol/min induced natural sleep as identified by electroencephalogram, electromyogram, electrooculogram, body temperature, heart rate, and animal behavior. Although sensitivity to PGD2 was slightly different among individual animals, the amount of total sleep time increased maximally up to 3- to 4-fold over the control level. PGD2 infused into the third ventricle induced effects similar to those observed for the lateral ventricular route, but infusion into the third ventricle was about 1000 times more effective than infusion into the lateral ventricle. In three monkeys, PGD2 increased the amount of sleep in a dose-dependent manner. Bell-shaped dose-response curves were observed for the other two monkeys. Infusion of prostaglandin E2 or F2 alpha into the lateral ventricle caused sedation but slightly reduced the amount of slow-wave sleep and produced increases in heart rate and body temperature. These findings suggest that endogenous PGD2 may be involved in the regulation of sleep by acting on the brain structures surrounding the third ventricle in the rhesus monkey.

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PubMed1986

Assay of phospholipase A2 activity of synaptic membranes using a phospholipid transfer protein: stimulation by depolarization.

A phospholipid transfer protein from bovine liver was used to transfer exogenous ([14C]linoleoylphosphatidylethanolamine [14C]linoleoyl PE) into synaptic membranes and synaptosomes without modifying the lipid compositions in order to study the intrinsic activity of phospholipase A2 of the preparations. Results were compared with the conventional method in which the substrate was simply dispersed with the enzyme preparations. Liberation of [14C]linoleic acid from [14C]linoleoyl PE-preloaded synaptic membranes by the transfer protein continued almost linearly over 60 min of incubation in the presence of Ca2+. The dose-response curve of Ca2+ for the activity of phospholipase A2 obtained in the present method was slightly shifted to the left in comparison with the conventional method: Ca2+ even at the concentration of 100 microM significantly enhanced the enzyme activity. Requirement of Ca2+ for the reaction is more specific in the present method than in the conventional one. When synaptosomes were prelabeled with [14C]linoleoyl PE by the transfer protein, the liberation of [14C]linoleic acid during the incubation at 37 degrees C increased linearly over 2 min. The liberation of [14C]linoleic acid was significantly enhanced in the presence of 56 mM KCl, 50 microM veratridine and 50 microM calcium ionophore A23187. These agents did not stimulate the reaction in the absence of Ca2+.

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