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Biomedical subjects

T Onaka

Publications and source records attributed to T Onaka.

At least 55 records · Page 3Linked to original sources
PubMed1997

Thermophilic carbon-sulfur-bond-targeted biodesulfurization.

Petroleum contains many heterocyclic organosulfur compounds refractory to conventional hydrodesulfurization carried out with chemical catalysts. Among these, dibenzothiophene (DBT) and DBTs bearing alkyl substitutions are representative compounds. Two bacterial strains, which have been identified as Paenibacillus strains and which are capable of efficiently cleaving carbon-sulfur (C--S) bonds in DBT at high temperatures, have been isolated for the first time. Upon attacking DBT and its various methylated derivatives at temperatures up to 60(deg)C, both growing and resting cells of these bacteria can release sulfur atoms as sulfate ions and leave the monohydroxylated hydrocarbon moieties intact. Moreover, when either of these paenibacilli was incubated at 50(deg)C with light gas oil previously processed through hydrodesulfurization, the total sulfur content in the oil phase clearly decreased.

Journal Article↗
PubMed1996

Norepinephrine depletion impairs neuroendocrine responses to fear but not novel environmental stimuli in the rat.

Emotional stimuli suppress vasopressin secretion and potentiate oxytocin and prolactin secretion by the pituitary in the rat. We studied effects of central norepinephrine depletion on these hormonal responses to novel environmental or fear stimuli. Male Wistar rats were injected intracerebroventricularly with 5-amino-2,4-dihydroxy-alpha- methylphenylethylamine, a selective neurotoxin to noradrenergic fibers. The neurotoxin treatment reduced the hypothalamic content of norepinephrine by 71% but did not significantly affect the dopamine content. Novel environmental stimuli suppressed vasopressin secretion and augmented secretion of oxytocin and prolactin in the vehicle-injected rats. The neurotoxin did not block the neuroendocrine responses. Intermittently applied electric footshocks also induced the similar neuroendocrine responses in the vehicle-injected rats. The neurotoxin significantly reduced the neuroendocrine responses. The drug, however, did not significantly alter vasopressin release after continuously applied footshocks. Environmental stimuli previously paired with footshocks (conditioned fear stimuli) suppressed vasopressin secretion and augmented secretion of oxytocin and prolactin in the vehicle-injected animals. Motor activity was suppressed during the conditioned fear stimuli. The neurotoxin impaired the neuroendocrine and behavioral responses whether the drug was injected before or after the conditioning. These data demonstrate the distinction between the neural mechanisms underlying the neuroendocrine responses to fear and to novel stimuli, suggesting that noradrenergic neurons are selectively involved in the hypothalamo-hypophysial responses to fear stimuli.

Animals↗
PubMed1996

A benzodiazepine, chlordiazepoxide, blocks vasopressin and oxytocin release after footshocks but not osmotic stimulus in the rat.

Noxious as well as hypertonic stimuli potentiate vasopressin and oxytocin secretion in rats. Neurohypophysial vasopressin- and oxytocin-secreting neurons receive inhibitory synaptic inputs mediated by gamma-aminobutyric acid (GABA). Benzodiazepines modulate GABA-A receptor activity in a facilitatory fashion. It is thus possible that benzodiazepines suppress vasopressin and oxytocin release after noxious stimuli. To test this hypothesis, we investigated whether chlordiazepoxide impairs the enhanced release of vasopressin and oxytocin after noxious or hypertonic stimuli in male rats. Chlordiazepoxide (5-20 mg/kg, i.p.) blocked dose-dependently the vasopressin and oxytocin responses to footshocks. Chlordiazepoxide, however, did not impair the hormonal responses to hypertonic stimulus. The results demonstrate that chlordiazepoxide selectively prevents vasopressin and oxytocin release after noxious stimuli and therefore suggest that the sites of chlordiazepoxide actions are not on the vasopressin or oxytocin neurons in rats.

Animals↗
PubMed1996

Chlordiazepoxide discriminates between the neural circuits mediating neuroendocrine responses to fear- and anxiety-producing stimuli in the rat.

Effects of a benzodiazepine, chlordiazepoxide (CDP), on neuroendocrine responses to emotional stimuli were studied in male rats. In the experiments with conditioned fear stimuli, rats received a pure tone paired with footshocks in the training session and were tested on the following day with the same environmental stimuli. CDP injected i.p. 30 min before training impaired the suppressive vasopressin and the augmentative oxytocin or adrenocorticotrophic hormone (ACTH) responses to the conditioned fear stimuli. However, the drug, administered 30 min after the training, did not significantly alter the hormonal responses to conditioned fear stimuli. CDP administered 30 min before testing also abolished the hormonal responses to conditioned fear stimuli. The stimuli which were identical to those used for training or unconditioned fear stimuli (intermittent footshocks) also produced the vasopressin, oxytocin and ACTH responses, and CDP prevented these hormonal responses. The drug, however, did not prevent the hormonal responses to novel environmental stimuli. Novel stimuli are known to produce a state of anxiety. Thus the present experiments demonstrate that CDP discriminates between the neural circuits mediating fear- and anxiety-producing stimuli in the rat.

Adrenocorticotropic Hormone↗
PubMed1996

A selective role of brainstem noradrenergic neurons in oxytocin release from the neurohypophysis following noxious stimuli in the rat.

Noxious stimuli facilitate oxytocin release from the neurohypophysis. Oxytocin-secreting hypothalamic magnocellular neurosecretory neurons receive excitatory synaptic inputs from noradrenergic neurons in the medulla oblongata. The medulla oblongata includes the A2 noradrenergic and the A1 noradrenergic cells. Here we investigated whether medullary noradrenergic neurons mediate oxytocin release after noxious stimuli in male rats. 5-Amino-2,4-dihydroxy-alpha-methylphenylethylamine, a neurotoxin selective for noradrenergic fibers, was injected into the lateral cerebral ventricle or the medulla. Seven days after the injection, the hypothalamic content of noradrenaline was decreased. In the rats injected with the neurotoxin, the release of oxytocin but not vasopressin after footshocks was impaired. Surgical ablation by suction of the caudal dorsomedial medulla including the A2 cell region did not significantly affect oxytocin release after footshocks, though the surgery abolished oxytocin release after i.v. injection of cholecystokinin octapeptide. In the rats whose A2 cell region had been ablated, an i.c.v. injected alpha 1 adrenoreceptor antagonist, benoxathian, blocked oxytocin release after footshocks. These results demonstrate that brainstem noradrenergic neurons mediate oxytocin release following noxious stimuli in the rat and suggest that responsible noradrenergic neurons are the A1 cells in the caudal ventrolateral medulla.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1995

Presynaptic actions of morphine: blockade of cholecystokinin-induced noradrenaline release in the rat supraoptic nucleus.

1. This study aimed to establish the site at which morphine acts to inhibit oxytocin release in response to peripheral administration of cholecystokinin (CCK). 2. Conscious rats were given morphine or vehicle followed by CCK or vehicle (I.V.). Fos immunoreactivity was apparent 90 min after CCK injection in the supraoptic nucleus of vehicle- but not morphine-pretreated animals. 3. In the dorsomedial (C2/A2) and the ventrolateral (C1/A1) regions of the brainstem, about half of the cells immunoreactive for tyrosine hydroxylase (TH) expressed Fos-like protein after CCK injection. In the C2/A2 region, 20% of the Fos-positive cells also showed TH immunoreactivity, whereas in the C1/A1 region 68% did so. Morphine treatment did not significantly change the number of cells expressing Fos immunoreactivity, or the percentage of TH-positive cells expressing Fos-like protein. 4. Amine release was measured in the supraoptic nucleus of urethane-anaesthetized rats using a microdialysis probe. An I.V. injection of CCK increased the concentrations in the dialysate of noradrenaline and serotonin, but not of either adrenaline or dopamine. Pretreatment with morphine (I.V.) blocked the effects of CCK in a naloxone-reversible manner. 5. Inclusion of morphine in the dialysate also blocked the increase in noradrenaline and serotonin in response to CCK in a naloxone-reversible manner. 6. These observations indicate that morphine acts near or within the supraoptic nucleus to block CCK-evoked noradrenaline release presynaptically. This presynaptic action of morphine may be a cause of the blockade of oxytocin release after CCK.

Animals↗
PubMed1995

Involvement of the noradrenergic afferents from the nucleus tractus solitarii to the supraoptic nucleus in oxytocin release after peripheral cholecystokinin octapeptide in the rat.

Activation of abdominal vagal afferents by peripheral injection of cholecystokinin octapeptide induces oxytocin release into the circulation. To test the hypothesis that cholecystokinin increases oxytocin release via activation of noradrenergic afferents from the brainstem, we injected rats with 5-amino-2,4-dihydroxy-alpha-methylphenylethylamine, a selective neurotoxin to noradrenergic fibres, into a lateral cerebral ventricle. The neurotoxin treatment reduced the noradrenaline content in the hypothalamus by 75% and reduced the oxytocin secretion in response to cholecystokinin by over 90%. In separate experiments, the neurotoxin was injected unilaterally in the vicinity of the supraoptic nucleus to test whether direct noradrenergic afferents to the supraoptic nucleus are involved in the response to cholecystokinin. The injection reduced the immunoreactivity for dopamine beta-hydroxylase in the supraoptic nucleus and significantly decreased the number of the supraoptic neurons expressing Fos-like protein after cholecystokinin but not after hypertonic saline. In further experiments, rhodamine-conjugated latex microspheres were injected into the supraoptic nucleus to retrogradely label afferent neurons, and the brains were processed with double-immunohistochemistry for tyrosine hydroxylase and Fos-like protein. In the C2/A2 but not the C1/A1 region of the brainstem, cholecystokinin increased the expression of Fos-like protein in the population of retrogradely-labelled catecholaminergic cells. In the C2/A2 region, the majority of retrogradely labelled cells expressing Fos-like protein after cholecystokinin were catecholaminergic. We conclude that noradrenergic afferents from the A2 but not from the A1 region of the brainstem to the hypothalamus mediate, at least in part, oxytocin release following cholecystokinin.

Afferent Pathways↗
PubMed1995

Opioid-noradrenergic interactions in the control of oxytocin cells.

The nucleus tractus solitarii (NTS) projects directly to the oxytocin neurones of the supraoptic nucleus (SON), and relays afferent stimuli arising from the birth canal during parturition. About 80% of these projecting neurones are noradrenergic, and these same neurones are activated following systemic administration of cholecystokinin (CCK), which also results in an increased electrical and secretory activity in oxytocin neurones. Oxytocin release in response to CCK is abolished following selective neurotoxic destruction of these noradrenergic neurones. Oxytocin release following CCK (and that during parturition) is potently inhibited by morphine, which blocks the local noradrenaline release in the supraoptic nucleus. This acute opiate action involves presynaptic inhibition of the noradrenergic terminals, and occurs without marked suppression of the activity of noradrenergic cells in the NTS. During chronic exposure to morphine the oxytocin system becomes tolerant to, and dependent upon morphine. In the course of tolerance, oxytocin cell activation in response to CCK recovers from initial inhibition. However, the pathway that mediates this response does not appear to become dependent: the oxytocin cell response to CCK is unchanged by opiate withdrawal induced by naloxone, despite a large increase in the background electrical activity of oxytocin cells provoked by withdrawal. Nevertheless, expression of withdrawal excitation by oxytocin neurones is curiously contingent upon the activity of the noradrenergic input in that prior lesioning of this input has no effect upon the subsequent withdrawal excitation of oxytocin cells. Yet under urethane anaesthesia, acute pharmacological blockade of the noradrenergic input suppresses withdrawal. We discuss how these paradoxical observations might be reconciled, and note that the difference may be related to differing levels of tonic activity in the noradrenergic input. It is possible that dependence relies upon the input when it is there, but not when it is not.

Afferent Pathways↗
PubMed1993

Effects of novelty stress on vasopressin and oxytocin secretion by the pituitary in the rat.

Effects of novel environmental stimuli on vasopressin and oxytocin secretion by the pituitary were studied in dehydrated male rats. As the novel environmental stimuli, rats were transferred to an experimental room, placed in a box painted black and given a pure tone auditory stimulus of 2 kHz. Exposure of rats to the novel environmental stimuli for a period of 2 min decreased plasma concentrations of vasopressin and increased plasma levels of adrenocorticotrophic hormone (ACTH) and prolactin, but did not significantly change the plasma level of oxytocin. The stimuli, however, became ineffective for producing the suppressive vasopressin response as the period of exposure was prolonged to more than 5 and up to 30 min, although the prolonged stimuli were still effective for inducing facilitatory ACTH and prolactin responses. After repeated exposures of rats to the environmental stimuli once a day for 5 or 10 days, the stimuli became disabled from producing the suppressive vasopressin response. However, the rats were still capable of responding to the novel stimuli of another kind. All these data suggest that novelty stress suppresses vasopressin secretion but does not change oxytocin secretion. In order to test the possibility that glucocorticoids expectedly secreted by the adrenals in response to the stress might have suppressed vasopressin secretion, a large amount of dexamethasone was administered to the rat before testing. Dexamethasone pretreatment depressed plasma levels of ACTH and vasopressin as reported previously and blocked the facilitatory ACTH response to the novelty stress. However, dexamethasone treatment did not affect the suppressive vasopressin response to the novelty stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1992

A dopamine D1 receptor antagonist, SCH 23390, selectively blocks vasopressin release after noxious stimuli in the rat.

Effects of a dopamine D1 receptor antagonist, SCH 23390, were investigated on plasma level of vasopressin after stressful stimuli in rats. The antagonist markedly attenuated the increase in plasma level of vasopressin after electric footshocks but not after s.c. injected hypertonic saline. The antagonist, however, did not significantly change the suppressive vasopressin response to fear-related emotional stress, though the drug suppressed motor behavior of the rat during testing period. These data suggest that dopamine D1 receptors play an important role selectively in the facilitatory vasopressin response to noxious stimuli in rats.

Animals↗
PubMed1992

A histaminergic H2-receptor antagonist, ranitidine, blocks the suppressive vasopressin response to fear-related emotional stress in the rat.

The effects of intracerebroventricularly (i.c.v.) administered histaminergic receptor antagonists on plasma levels of vasopressin, oxytocin, prolactin and adrenocorticotrophic hormone (ACTH) after fear-related emotional stress were investigated in the male rat. Pyrilamine, a histaminergic H1-receptor antagonist did not significantly alter the suppressive vasopressin or the facilitative prolactin response to nonassociatively applied emotional stress. On the other hand, i.c.v. administered ranitidine, a histaminergic H2-receptor antagonist, blocked these responses to stress. Pyrilamine again did not significantly change the suppressive vasopressin response to the associatively applied emotional stress. However, the drug attenuated the prolactin response slightly but significantly. Ranitidine blocked the suppressive vasopressin and the facilitative prolactin responses to the associatively applied emotional stress, but the drug did not change the facilitative oxytocin or ACTH response to the stress. Suppression of motor activity during the associatively applied emotional stress was not significantly changed by either of these antagonists. These results suggest that histaminergic H2 receptors are selectively involved in the neural pathways which mediate the suppressive vasopressin and the facilitative prolactin responses to fear-related emotional stress.

Animals↗
PubMed1992

Neurohypophysial responses to emotional stress after deafferentation of sino-aortic baroreceptors in rats.

In an attempt to test the possibility that sino-aortic baroreceptors may mediate the previously reported stress response in hypothalamic magnocellular neurosecretory cell activity in rats, effects of deafferentation of sino-aortic baroreceptors on plasma levels of vasopressin and oxytocin after fear-related emotional stress were studied in male rats 28-33 days after the surgery. An alpha 1-adrenergic receptor agonist, phenylephrine (1 mg/kg) injected i.p. under anesthesia increased arterial blood pressure in the rats that had received surgical operation of sino-aortic denervation (SAD) and in the rats of sham-operation control (SHAM). Reflex bradycardia after phenylephrine occurred in the SHAM but not in the SAD group. These results indicate that afferent signals originating from sino-aortic baroreceptors were effectively blocked by the SAD surgery. In the similarly prepared SAD group, plasma level of vasopressin was decreased and plasma level of oxytocin was increased significantly to the same extent as in the SHAM group after low-frequency shocks (0.05 Hz, 5 min) or environmental cue signals previously paired with shocks. It is therefore suggested that afferent neural signals originating from sino-aortic baroreceptors are not primarily involved in the suppressive vasopressin or the facilitatory oxytocin response to fear-related emotional stress in rats.

Afferent Pathways↗
PubMed1991

Sino-aortic baroreceptors are not involved in the potentiation of vasopressin or oxytocin secretion observed after noxious stimuli in the rat.

The possibility that arterial baroreceptors may be involved in the potentiation of vasopressin or oxytocin secretion observed after noxious stimuli was tested in male rats after sino-aortic denervation (SAD). There was no significant difference in plasma level of vasopressin or oxytocin between the SAD and the corresponding sham-operation control (SHAM) groups with or without electric shocks. An i.p. injected alpha 1-adrenergic receptor antagonist, prazosin, decreased arterial blood pressure both in the SAD and in the SHAM groups. However, the increased levels of these hormones after prazosin were significantly lower in the SAD than in the SHAM groups. Reflexly evoked tachycardia after prazosin occurred in the SHAM but not in the SAD groups. These results suggest that afferent neural signals originating from arterial baroreceptors are not involved in potentiation of vasopressin and oxytocin secretion after noxious stimuli in the rat.

Animals↗
PubMed1990

Interactions between emotional stress due to fear and hypovolemic stimuli in the control of vasopressin secretion in rats.

Interactions between emotional stress due to fear and hypovolemic stimuli on vasopressin secretion were studied in rats. Intraperitoneally injected dextran did not significantly change plasma osmolality and arterial blood pressure but increased blood hemoglobin and plasma vasopressin level. An i.v. infused physiological solution reversed these changes. Emotional stress due to fear acquired by learning suppressed plasma vasopressin level in dextran-injected rats. Emotional stress due to fear produced by low-frequency footshocks also suppressed the increased plasma vasopressin level. These results suggest that emotional stress due to fear interacts with afferent neural signals originating from cardio-vascular volume receptors in the control of vasopressin secretion.

Animals↗
PubMed1990

Differential effects of naloxone on neuroendocrine responses to fear-related emotional stress.

The effects of an opioid receptor antagonist, naloxone (NAL), were studied on the changes in pituitary hormone secretion induced by emotional stress. Male Wistar rats were trained with tone stimuli paired with electric footshocks and tested with the tone and environmental cue signals for emotional stress of fear acquired by learning as described previously (Onaka et al. 1988). Rats received s.c. injected NAL 30 min before testing at doses of 0, 0.2, 1.0, 5.0 and 25.0 mg/kg b.w. Half the rats were injected with 0.5 M NaCl (20 ml/kg b.w.) together with NAL. In these hypertonic rats plasma vasopressin level was slightly increased after NAL. The increment was statistically significant in control groups but not in experimental groups. However the suppression of vasopressin secretion by emotional stimuli was not changed by NAL. Plasma oxytocin levels were extremely high and not significantly different among experimental, unshocked control and untested control groups. NAL further increased the oxytocin level dose-dependently. NAL did not significantly change plasma adrenocorticotrophic hormone (ACTH) levels and hence did not modify the augmentative response in ACTH secretion to emotional stimuli. Plasma prolactin level was significantly elevated after emotional stimuli and NAL depressed the prolactin level in each of experimental and control groups. After NAL, the magnitude of the facilitatory response in prolactin secretion to emotional stimuli was decreased. Motor activity and its suppressive response to emotional stimuli were not influenced by NAL. In another half of rats under a normal osmotic condition the vasopressin response to emotional stimuli was not affected by NAL. NAL further augmented potentiation of oxytocin secretion after emotional stimuli dose-dependently.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1989

Pre-weaning handling reduces adrenocorticotropin response to novel but not to noxious stimuli in adult rats.

Effects of handling stimuli given to the rat during pre-weaning period were investigated on plasma immunoreactive (ir) adrenocorticotropin (ACTH) level after electric footshocks or novel audiovisual stimuli in adult life. Plasma ir-ACTH levels after footshocks did not significantly differ between non-handled control and previously handled rats, while the hormone level after novel audiovisual stimuli was significantly lower in handled than in the control rats. These results demonstrate that pre-weaning handling reduces ACTH response to novel audiovisual stimuli but not to footshocks in adult life, and thus suggest the possibility that stress during pre-weaning period affects differentially the developmental plasticity of the hypothalamo-pituitary axis.

Adrenocorticotropic Hormone↗
PubMed1988

Vasopressin secretion: suppression after light and tone stimuli previously paired with footshocks in rats.

In an attempt to find whether vasopressin (VP) secretion is suppressed by learned emotional stress, we have given rats under a hypertonic condition simultaneously applied light and tone that had been paired previously with footshocks and have quantified immunoreactive VP (ir-VP) in the plasma. In a training session light (60 watt) and tone (2 kz) of 3-s duration which were paired with electric footshocks (50 Hz, 1-s duration) were given to rats 11 times at an interval of 30 s. Various lengths of time after the training, the rats were tested with light and tone, which were unpaired with footshocks and repeatedly applied every 15 s for 3 min in the box used for training. Hypertonic NaCl (0.5 M, 2 ml/100 g b.w.) was injected s.c. 30 min before testing to increase the basal level of plasma VP. After testing, plasma ir-VP was significantly less in the experimental group than in the 0-mA control group of rats that were trained without FS. The values for the experimental group were also significantly less than those of untested control rats that had been trained with FS but were not tested. Plasma osmolality and blood haemoglobin concentration were not significantly different between control and experimental groups. Plasma immunoreactive adrenocorticotrophic hormone (ir-ACTH) level was higher and motor activity as expressed by cumulative time period of body movement during testing was lower in the experimental group than in either of the control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗