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M T Lin

Publications and source records attributed to M T Lin.

At least 253 records · Page 14Linked to original sources
PubMed1987

Bombesin-induced hypothermia: possible involvement of cholinergic and dopaminergic receptors in the rat hypothalamus.

The thermal responses of rats which were pretreated with 5,7-dihydroxytryptamine to deplete hypothalamic 5-hydroxytryptamine, 6-hydroxydopamine to deplete hypothalamic catecholamines, phentolamine and propranolol to inhibit adrenergic receptors, haloperidol to inhibit dopamine receptors, or atropine to inhibit cholinergic receptors, to intrahypothalamic administration of bombesin were compared with those of control rats. The bombesin-induced hypothermia was attenuated by pretreatment of the rats with either hypothalamic dopamine depletion or receptor blockade, or hypothalamic cholinergic receptor blockade. The reduction in the bombesin-induced hypothermia in the treated rats was due to the reduction of metabolic and vasomotor response. The data indicate that bombesin may act on hypothalamic dopamine and/or cholinergic receptor mechanisms to induce hypothermia by promoting a reduction in metabolic heat production and an enhancement in heat loss in rats.

Animals↗
PubMed1987

Diazepam facilitates reflex bradycardia in conscious rats.

The effects of diazepam on cardiovascular function were assessed in conscious rats. Intravenous administration of diazepam (1-30 mg kg-1) produced a dose-dependent decrease in both the mean arterial pressure and the heart rate. Also, reflex bradycardia was produced in rats by intravenous infusion of adrenaline (1.25-2.5 micrograms kg-1). Intravenous pretreatment of the rats with diazepam, although causing no change in the adrenaline-induced pressor effect, did enhance the adrenaline-induced reflex bradycardia. However, the diazepam enhancement of adrenaline-induced reflex bradycardia was antagonized by pretreatment of rats with an intravenous dose of picrotoxin (an agent blocks chloride channels by binding to sites associated with the benzodiazepine-GABA-chloride channel macromolecular complex). The data indicate that diazepam acts through the benzodiazepine-GABA-chloride channel macromolecular complex within the central nervous system to facilitate reflex bradycardia mediated through baroreceptor reflexes in response to an acute increase in arterial pressure.

Animals↗
PubMed1987

Pain sensitivity, thermal capability, and brain monoamine turnover in hypertensive rats.

This study compared the pain sensitivity, thermal capability, and brain monoamine turnover in normotensive and hypertensive rats. Either the spontaneously hypertensive rats, the experimentally (renal or deoxycorticosterone acetate) hypertensive rats, or their normotensive controls were tested for pain sensitivity by the hot-plate procedure, with the plate maintained at 55 degrees C. The spontaneously hypertensive rats, but not the experimentally hypertensive rats, showed an elevated level of spontaneous pain threshold compared with their appropriate controls. However, both the spontaneously and the experimentally hypertensive rats displayed a reduced sensitivity of analgesic responses to morphine administration. In addition the thermal responses to external stresses in these groups of animals were assessed. It was found that, over an ambient temperature range of 8-30 degrees C, either spontaneously or experimentally hypertensive rats maintained their rectal temperature within a normal limit displayed by their appropriate controls. However, the metabolic rate levels of both spontaneously and experimentally hypertensive rats were elevated at ambient temperatures less than 22 degrees C. Furthermore, compared with their appropriate controls, these hypertensive rats also showed a greater degree of hypothermic responses to chlorpromazine injection. Biochemical examination revealed that either the spontaneously or the experimentally hypertensive rats had a lower serotonin, but a higher catecholamine, turnover in both the hypothalamus and the brain stem compared with their appropriate normotensive controls. The data indicate that, in a hypertensive state, changes in the monoamine turnover of different brain regions may be correlated with the above-mentioned alterations in pain sensitivity and in thermal capability.

5-Hydroxytryptophan↗
PubMed1987

Hypothalamic involvement in the hyperglycemia and satiety actions of somatostatin in rats.

To determine whether the anorexic and the hyperglycemia actions of somatostatin were mediated through the hypothalamic nuclei, rats were infused with somatostatin and normal saline through previously implanted hypothalamic cannulae. Administration of somatostatin (0.5-1.5 microgram in 1.0 microliter) into the lateral hypothalamus, but not the ventromedial or the anterior hypothalamus, caused a reduction in food consumption without affecting relative water intake (or water-to-food ratio) in conscious rats in a freely moving state. On the other hand, administration of somatostatin into the lateral hypothalamus, but not the anterior or the ventromedial hypothalamus, caused an increase in blood glucose level in rats. This hyperglycemia was antagonized by vagotomy, but not by spinal transection or adrenalectomy. The data indicate that the lateral hypothalamus is the most sensitive site of the somatostatin-induced anorexia and the action of somatostatin on the lateral hypothalamus-vagus efferent activity is also a possible mechanism mediating hyperglycemia in rats.

Animals↗
PubMed1987

Participation of a bulbospinal serotonergic pathway in the rat brain in clonidine-induced hypotension and bradycardia.

The effects of microinjection of clonidine (1-10 micrograms in 1 microliter) into a region adjacent to the ventrolateral surface of the medulla oblongata on cardiovascular function were assessed in urethane-anesthetized rats. Intramedullary administration of clonidine, but not saline vehicle, caused a dose-dependent decrease in both the mean arterial pressure and the heart rate. The clonidine-induced hypotension was antagonized by prior spinal transection, but not bilateral vagotomy. On the other hand, the clonidine-induced bradycardia was antagonized by prior bilateral vagotomy, but not spinal transection. Furthermore, selective destruction of the spinal 5-HT nerves, produced by bilateral spinal injection of 5,7-dihydroxytryptamine, reduced the magnitude of the vasodepressor or the bradycardiac responses to clonidine microinjected into the area near the ventrolateral surface of the medulla oblongata in rats. The data indicate that a bulbospinal serotonergic pathway is involved in development of clonidine-induced hypotension and bradycardia. The induced hypotension is brought about by a decrease in sympathetic efferent activity, whereas the induced bradycardia was due to an increase in vagal efferent activity.

5,7-Dihydroxytryptamine↗
PubMed1987

Interferon produces hyperthermic responses in rats.

The effects of administration of alpha human leukocyte interferon into the anterior hypothalamic preoptic area on metabolic, respiratory and vasomotor activities, as well as body temperatures, were assessed in unanesthetized rats at various ambient temperatures (Ta). Intrahypothalamic administration of interferon produced dose-dependent fever in rats at Ta = 8-30 degrees C. The interferon-induced fever was due to increased metabolism and/or cutaneous vasoconstriction (or decreased heat loss). Furthermore, the fever induced by interferon was antagonized by pretreatment of animals with indomethacin, an inhibitor of prostaglandin synthesis. The data indicate that the fever induced by intrahypothalamic interferon is due to the endogenous release of prostaglandins in the anterior hypothalamic preoptic area of rat's hypothalamus.

Animals↗
PubMed1986

Hypertension and tachycardia produced by inhibition of reuptake of 5-hydroxytryptamine by fluoxetine in the rat.

In rats anaesthetized with urethane, increasing the activity of 5-hydroxytryptamine receptors or the level of cuntional serotonin in the brain with the inhibitors of the reuptake of serotonin, fluoxetine, produced both hypertension and tachycardia. The hypertension induced by fluoxetine was significantly inhibited by pretreatment of the animals with ketanserin (a serotonin receptor antagonist), by bilateral vagotomy, spinal transection or bilateral adrenalectomy. On the other hand, the tachycardia induced by fluoxetine was significantly inhibited by pretreatment with ketanserin or bilateral vagotomy, but not by spinal transection or adrenalectomy. The data indicate that fluoxetine acts through serotonin receptors in the central nervous system by influencing autonomic outflow to induce both hypertension and tachycardia.

Adrenalectomy↗
PubMed1986

Effects of bombesin on thermoregulatory responses and hypothalamic neuronal activities in the rat.

Direct administration of bombesin (1, 10, and 100 ng/microliter) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures (Ta) of 8 and 22 degrees C. The hypothermia in response to bombesin was brought about by a decrease in metabolism at Ta 8 degrees C, whereas at Ta 22 degrees C the hypothermia was brought about by both a decrease in metabolism and an increase in cutaneous temperature. However, at Ta 30 degrees C, intrahypothalamic administration of bombesin caused an insignificant change in thermoregulatory responses. On the other hand, 51 single neurons in the preoptic anterior hypothalamic area were examined in 20 rats under urethan anesthesia. Each animal was subjected to scrotal warming or cooling and to the administration of bombesin. Microiontophoretic application of bombesin resulted in inhibition of the majority (62.5%) of cold-responsive neurons as well as excitation of the majority (50%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (74%) of thermally unresponsive neurons were not affected by bombesin application. The data indicate that bombesin, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.

Animals↗
PubMed1986

Effect of chlordecone exposure on thermoregulation in the rat.

Intraperitoneal administration of chlordecone (20-80 mg/kg) caused a dose-related fall in the rectal temperatures of rats at ambient temperatures of 8 and 22 degrees C. The chlordecone-induced hypothermia was brought about by a decrease in metabolism. The chlordecone hypothermia was antagonized by pretreatment of animals with haloperidol (a dopaminergic receptor antagonist), but not by phentolamine (an alpha-adrenergic receptor antagonist), propranolol (a beta-adrenergic antagonist), atropine (a cholinergic receptor antagonist), or p-chlorophenylalanine (a serotonin depletor). In addition, the dopamine levels in the hypothalamus were elevated significantly when evaluated 1 h after an intraperitoneal dose of chlordecone. The data suggest that systemic administration of chlordecone may act through the dopaminergic mechanisms in the hypothalamus to induce hypothermia (or decreased metabolic heat production) in rats.

Animals↗
PubMed1986

Alterations in physiologic functions and in brain monoamine content in streptozocin-diabetic rats.

In the present study, we used streptozocin (STZ) to induce diabetes in rats and observed alterations in several physiologic functions and in monoamine content of different brain regions. Rats with STZ diabetes displayed a thermoregulatory deficit in the cold. Both the body temperature and metabolic rate of the diabetic animals were reduced at ambient temperatures below 22 degrees C. These diabetic animals had a higher level of the spontaneous pain threshold, but displayed a reduced sensitivity of analgesic responses to morphine injection. In addition, these diabetic animals had a lower level of spontaneous motor activity, but displayed an increased sensitivity of locomotor stimulant responses to amphetamine administration. Biochemical examination revealed that the diabetic animals had a lower serotonin level in both the hypothalamus and the brainstem without changes in the serotonin levels of the corpus striatum. These diabetic animals also had a lower catecholamine level in the hypothalamus, but a higher catecholamine level in the corpus striatum. The alterations in brain monoamine content and in the above-mentioned physiologic parameters were reversed after insulin replacement therapy. The data suggest that alterations in various autonomic, somatosensory, and motor neural functions of untreated STZ-diabetic rats correlated with a reproducible pattern of monoamine content in various brain regions (a pattern that differed from that observed in healthy control rats), and that both the altered neural function and the altered brain monoamine pattern were reversed after insulin therapy.

Amphetamine↗
PubMed1986

Alterations in physiological functions and in brain monoamine content in the sympathectomized rats.

In the present study, we conducted pre-ganglionic decentralization (or sympathetic trunk resection) of the superior cervical ganglia and observed alterations in several physiological functions and in the monoamine content of different brain regions. Over an ambient temperature range of 8-30 degrees C, these sympathectomized rats maintained their rectal temperatures within a normal limit displayed by the intact controls. These sympathectomized animals, although showing no change in the level of spontaneous pain threshold or motor activity, did display an increased sensitivity of analgesic responses to morphine administration or locomotor stimulant responses to amphetamine administration. Biochemical examination revealed that these sympathectomized animals had a higher level of norepinephrine, dopamine or 5-hydroxytryptamine in the hypothalamus, as well as a higher level of dopamine in the corpus striatum. However, in the brainstem, these sympathectomized animals had a unaltered monoamine level. The data indicate that, in a sympathectomized condition, changes in the monoamine content of different brain regions may be correlated with the above-mentioned alterations in somatosensory and motor neural functions.

Animals↗
PubMed1985

Effects of cholecystokinin octapeptide on thermoregulatory responses and hypothalamic neuronal activity in the rat.

Rats were chronically implanted with a hypothalamic cannula to allow chemical stimulation of the hypothalamus on the conscious animals in repeated experiments. Direct administration of cholecystokinin octapeptide (CCK-8) (20-60 ng) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures of 8 degrees C and 22 degrees C. The hypothermia induced by CCK-8 was produced by a decrease in metabolism at an ambient temperature of 8 degrees C, whereas at 22 degrees C, it was caused by both a decrease in metabolism and an increase in cutaneous temperature. However, at an ambient temperature of 30 degrees C, intrahypothalamic administration of CCK-8 caused an insignificant change in thermoregulatory responses. Furthermore, neither intrahypothalamic injection of 0.9% saline nor intraperitoneal injection of CCK-8 (60 ng) had any effect on thermoregulatory responses at the ambient temperatures of 8 degrees-30 degrees C studied. Under urethane anaesthesia, 59 single neurons in the preoptic anterior hypothalamic area were examined in 29 rats. Each animal was subjected to scrotal warming or cooling and to the administration of CCK-8. Microiontophoretic application of CCK-8 resulted in inhibition of the majority (75%) of cold-responsive neurons as well as excitation of the majority (77.8%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (69%) of thermally unresponsive cells were not affected by CCK-8 application. The data indicate that CCK-8, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.

Animals↗
PubMed1985

Hypothalamic monoaminergic mechanisms of aspirin-induced analgesia in monkeys.

Microinjection of sodium acetylsalicylate (aspirin, 0.2-0.6 mg) into the preoptic anterior hypothalamic area, but not the dorsal raphe region or the periaqueductal central gray matter, produced a dose-related analgesia in conscious monkeys. The analgesia induced by intrahypothalamic administration of aspirin was antagonized by pretreatment of monkeys with either a serotoninergic receptor blocker (cyproheptadine) or two catecholaminergic receptor blockers (haloperidol and yohimbine). These suggest the existence of a monoaminergic pain-inhibitory mechanism in the preoptic anterior hypothalamic area activated by aspirin.

Analgesics↗
PubMed1985

The site and the mode of analgesic actions exerted by clonidine in monkeys.

We used intracerebral administration of clonidine in monkeys to map effective sites for analgesia. The jaw opening reflex elicited by tooth pulp stimulation was used for analgesia testing. We found that the most consistently effective sites for analgesia in monkeys are in at least three brain regions: the diencephalic periventricular gray, the dorsal raphe nuclei, and the periaqueductal gray. In addition, the analgesia induced by intracerebral administration of clonidine was effectively antagonized by pretreatment of animals with either naloxone (a narcotic antagonist) or yohimbine (an alpha-adrenergic antagonist). These results suggest the existence of an opiate and an adrenergic antinociceptive mechanism in the diencephalic periventricular gray, the dorsal raphe nuclei, and the periaqueductal gray activated by clonidine in primates.

Analgesics↗
PubMed1985

Effects of brain epinephrine depletion on thermoregulation, reflex bradycardia, and motor activity in rats.

Two hours after i.p. administration of 2-cyclooctyl-2-hydroxyethylamine (CONH), 1-aminomethylcycloundecanol (CUNH), 2,3-dichloro-alpha-methylbenzylamine (DCMB), or 7,8-dichloro-1,2,3,4-tetrahydroisoquinoline (SKF64139), the hypothalamic and brain stem epinephrine (EPI) contents of rat brain were decreased. Depletions of brain EPI with these phenylethanolamine N-methyltransferase (PNMT) inhibitors reduced the rectal temperatures of rats at ambient temperatures of 8 and 22 degrees C. The hypothermia in response to these PNMT inhibitors was due to decreased metabolism and cutaneous vasodilatation. The locomotor stimulant responses induced by thyrotropin-releasing hormone were also reduced by administration of any one of these PNMT inhibitors. On the other hand, acute administration of any of these PNMT inhibitors enhanced the reflex bradycardia induced by i.v. infusion of EPI. The data suggest that brain (particularly the hypothalamus and brain stem) EPI-containing neurons are involved in the regulation of body temperature, reflex bradycardia, and motor performance in the rat.

Adrenal Glands↗
PubMed1985

Effects of subdiaphragmatic vagotomy on thermoregulatory responses of rats to different ambient temperatures.

Rats 4 weeks after bilateral transections of the subdiaphragmatic vagus nerve displayed a thermoregulatory deficit. Rectal and skin temperatures and metabolic rate were reduced at ambient temperatures of 22 and 8 degrees C. However, these vagotomized animals maintained their body temperatures within the normal limits displayed by normal animals at an ambient temperature of 30 degrees C.

Animals↗
PubMed1985

Depletion of noradrenaline in the hypothalamus reduces the febrile responses induced by prostaglandin E2, thyrotropin-releasing hormone and beta-endorphin in rats.

The effects of pretreatment of rats with an intrahypothalamic injection of 6-hydroxydopamine on the thermal responses induced by intrahypothalamic injection of noradrenaline, prostaglandin E2, thyrotropin-releasing hormone or beta-endorphin were assessed. Administration of either noradrenaline (2-10 micrograms), prostaglandin E2 (10-40 ng), thyrotropin-releasing hormone (0.5-2.0 micrograms) or beta-endorphin (1-3 micrograms) into the preoptic anterior hypothalamus caused a dose-dependent rise in rectal temperature in conscious rats at an ambient temperature of 22 degrees C. In addition, it was found that three intrahypothalamic doses of 10 micrograms of 6-hydroxydopamine at intervals of 2 days caused a significant depletion of noradrenaline in the hypothalamus to 26.4% of control while the concentration of dopamine in the hypothalamus was not significantly reduced at 95.3% of control. Furthermore, the hyperthermic responses induced by prostaglandin E2, thyrotropin-releasing hormone, or beta-endorphin were greatly attenuated after selective depletion of noradrenaline in the hypothalamus in rats. However, selective depletion of noradrenaline did not affect the noradrenaline-induced hyperthermic responses. The data indicate that either prostaglandin E2, thyrotropin-releasing hormone or beta-endorphin may act through the endogenous release of noradrenaline from the hypothalamus to induce hyperthermic responses in rats.

Animals↗