Biomedical subjects

M T Lin

Publications and source records attributed to M T Lin.

At least 271 records · Page 15Linked to original sources

PubMed1985

Striatal neuronal responses to scrotal temperature changes and dopaminergic drugs.

Seventy-nine units in the striatal region were examined in 48 urethan-anesthetized rats. When these units were classified by their thermal responsiveness, proportions of the cold-responsive, warm-responsive, and thermally unresponsive units were 25.4, 35.4, and 39.2%, respectively, of the total units tested. Either microiontophoretically or systemically administered apomorphine (a dopamine agonist) and haloperidol (a dopamine antagonist) affected (inhibited and/or excited) most (86.5-100%) cold-responsive units. In contrast, only a small percentage of the warm-responsive (28.6-43.8%) or thermally unresponsive (0-19.2%) units were affected by both apomorphine and and haloperidol. Furthermore it was found that most (73-100%) cold-responsive units were inhibited by apomorphine but excited by haloperidol; the inhibitory responses of the unit activity induced by apomorphine were antagonized by haloperidol. The reciprocal relationships between apomorphine and haloperidol were not observed in most warm-responsive (76.2-85.7%) or thermally unresponsive (80.8-100%) units. The data demonstrate that many striatal neurons are influenced by thermal afferent activation in the scrotum. The results also provide a neuronal basis for the hypothesis that the dopaminergic receptors located in the cold-responsive neurons of the striatum have effects on metabolic heat production in rats.

Animals↗

PubMed1985

Decreasing brain epinephrine levels with 2-cyclooctyl-2-hydroxyethylamine induces hyperglycemia in rats.

Intraperitoneal administration of 2-cyclooctyl-2-hydroxyethyl-amine (CONH; 25-75 mg/kg) produced dose-related reductions in the epinephrine (EPI) concentrations in both the hypothalamic and brainstem regions, but not in the adrenal glands. The reductions in the hypothalamic and brainstem EPI concentrations in rats anesthetized with pentobarbital sodium were accompanied by parallel increases in blood glucose. These data suggest that CONH induces its hyperglycemia action at least in part by altering central EPI biosynthesis. This hyperglycemic was antagonized by spinal transection or adrenalectomy, but not by vagotomy. This indicates that CONH increases the adrenal-sympathetic efferent activity and leads to hyperglycemia in rats.

Adrenal Medulla↗

PubMed1985

Thyrotropin-releasing hormone-induced hyperglycemia: possible involvement of cholinergic receptors in the lateral hypothalamus.

The influence of the site of action of thyrotropin-releasing hormone (TRH) on the production of hyperglycemia was studied in rats by comparing the effectiveness of TRH administered by different routes. Administration of TRH (5 micrograms) into the lateral hypothalamus (LH) produced a hyperglycemia with a peak elevation of blood glucose of 140 mg/dl. Injection of 5 micrograms TRH into the ventromedial hypothalamus (VMH) produced a blood glucose elevation of 44 mg/dl, while injection of the same dose of TRH into the anterior hypothalamus (AH) produced a blood glucose elevation of 23 mg/dl. These findings indicate an LH site of action of TRH. Indeed, intra-LH administration of TRH (1-10 micrograms) caused dose-related increases in blood glucose. Administration of acetylcholine into the same site was also shown to induce hyperglycemia. The hyperglycemic effects of TRH and acetylcholine were antagonized by previous treatment of the LH site with atropine, a cholinergic receptor antagonist. Furthermore, the TRH-induced hyperglycemia was not observed or was greatly reduced in spinal rats or in adrenalectomized rats. The results indicate that TRH may act through the cholinergic receptor mechanisms within the LH region to induce hyperglycemia by promoting an increase in the sympathetic-adrenal medullary efferent activity.

Acetylcholine↗

PubMed1985

Effects of insulin on thermoregulatory responses and hypothalamic neuronal activity.

In the first series of experiments, the effects of administration of insulin (0.04-0.12 IU/microliter) into the preoptic anterior hypothalamic area on thermoregulatory responses were assessed in unanesthetized rats at various ambient temperatures (Ta). Intrahypothalamic administration of insulin induced a dose-dependent rise in rectal temperature. At Ta = 8 degrees C, the hyperthermia in response to insulin was due to increased metabolism, whereas at Ta = 30 degrees C, the hyperthermia was due to cutaneous vasoconstriction. However, at Ta = 22 degrees C, the insulin-induced hyperthermia was due to both increased metabolism and cutaneous vasoconstriction. In the second series of experiments, the effects of intracerebroventricular administration of insulin on 35 hypothalamic units classified as cold-responsive, warm-responsive, or thermally unresponsive were assessed in 35 rats anesthetized with urethane. It was found that the majority (80%) of the warm-responsive units were depressed by insulin, whereas the majority (70%) of the cold-responsive units were excited by insulin. The data indicate that insulin acts on the hypothalamic thermally responsive neurons to induce hyperthermia by promoting an increase in heat production and/or vasoconstriction.

Action Potentials↗

PubMed1985

Hypothalamic involvement in the locomotor stimulant or satiety action of thyrotropin-releasing hormone and amphetamine.

To determine whether the locomotor stimulant and the anorexic actions of thyrotropin-releasing hormone (TRH) and amphetamine were mediated through the hypothalamic nuclei, rats were infused with either TRH or amphetamine through previously implanted hypothalamic cannulae. Administration of TRH or amphetamine into the ventromedial hypothalamus, but not the lateral hypothalamus and the anterior hypothalamus, caused locomotor stimulation in rats. On the other hand, administration of TRH or amphetamine into the lateral hypothalamus, but not the ventromedial hypothalamus or the anterior hypothalamus, caused a reduction in food consumption without affecting relative water intake (or water-to-food ratio) in the rat. The data indicate that the ventromedial hypothalamus is the most sensitive site of the TRH- or amphetamine-induced locomotor stimulation and the action of TRH or amphetamine on the lateral hypothalamus is also a possible mechanism mediating anorexia.

Amphetamine↗

PubMed1985

Cholecystokinin-induced hypothermia: possible involvement of serotoninergic mechanisms in the rat hypothalamus.

The thermal effects of rats which were pretreated with 5,7-dihydroxytryptamine to deplete hypothalamic 5-hydroxytryptamine (5-HT) or with a 5-HT receptor blocker to intrahypothalamic administration of cholecystokinin (CCK) were compared with those of control rats. The CCK-induced hypothermic response was attenuated by pretreatment of the rats with either hypothalamic 5-HT depletion or receptor blockade. The reduction in the CCK hypothermia in the treated rats was due to the reduction of metabolic and vasomotor response. The data indicate that CCK may act on a 5-HT pathway within the hypothalamus to induce its hypothermia by promoting a reduction in metabolic heat production and an enhancement in heat loss in rats.

5,7-Dihydroxytryptamine↗

PubMed1984

Effects of hypothalamic noradrenaline depletion with 6-hydroxydopamine on the body temperature regulation of the rat.

Rats which had been pretreated with 3 intrahypothalamic doses of 10 micrograms of 6-hydroxydopamine (6-OHDA) to cause a selective depletion of hypothalamic noradrenaline to 26.7% of control hypothalamic noradrenaline maintained rectal temperature within the normal limits displayed by the control group. However, noradrenaline-depleted rats displayed a decrease in both cutaneous temperature and metabolic heat production in the cold (8 degrees C). Intrahypothalamic injections of 6-OHDA in normal rats at room temperature (22 degrees C) caused an acute hyperthermia of up to 1.1 degree C which lasted for about 6 h. The acute hyperthermia in response to 6-OHDA was due to both cutaneous vasoconstriction and increased metabolism in the rat. Selective depletion of hypothalamic noradrenaline without affecting hypothalamic dopamine by prior treatment with 6-OHDA markedly reduced the hyperthermic responses to a subsequent dose of 6-OHDA. Therefore, the acute hyperthermic responses to 6-OHDA may be related to a release of noradrenaline in the hypothalamus. The data indicate that activation of noradrenergic pathways in the hypothalamus facilities heat production and inhibits heat loss mechanisms in the rat.

Animals↗

PubMed1984

Clonidine-induced hypothermia: possible involvement of cholinergic and serotonergic mechanisms.

The thermoregulatory effects (including metabolic, vasomotor and respiratory activities) produced by an injection of clonidine (1-3 micrograms in 0.5 microliter) into the preoptic anterior hypothalamus were assessed in conscious rats at ambient temperatures (Ta) of 8, 22 and 30 degrees C. Intrahypothalamic administration of clonidine caused a dose-dependent fall in rectal temperature at Ta 8 degrees C and 22 degrees C. The hypothermia in response to clonidine was due to decreased metabolic heat production and/or cutaneous vasodilation. There was no change in respiratory evaporative heat loss. The clonidine-induced hypothermic response was attenuated by pretreatment of the rats with either 5,7-dihydroxytryptamine (10 micrograms, administered intrahypothalamicly, 14 days before clonidine injection), yohimbine (0.2 microgram, administered intrahypothalamicly, 10 min before clonidine injection), cyproheptadine (1 microgram, administered intrahypothalamicly, 10 min before clonidine injection), or atropine (0.1 microgram, administered intrahypothalamicly, 10 min before clonidine injection). The data indicate that clonidine may act on alpha-adrenoceptors located on a serotonin-acetylcholine pathway within the preoptic anterior hypothalamus to induce hypothermia by promoting a reduction in metabolic heat production and/or an enhancement in dry heat loss in rats.

5,7-Dihydroxytryptamine↗

PubMed1984

Demonstration of specific glucocorticoid binding sites in bovine cornea.

Specific [3H]-dexamethasone binding sites were demonstrated in bovine corneal cytosol using titration analyses. Specific glucocorticoid binding to corneal cytosol exhibited a single class of sites with apparent dissociation constants of 4-6 nM and 68-72 fmol binding sites mg-1 cytosolic protein. Association of steroid with these binding sites was temperature- and time-dependent. Specific binding was maximal at 4 degrees C after 6 hr and was somewhat lower at 25 degrees C and lowest at 37 degrees C. Presence of increasing amounts of certain unlabeled steroids with glucocorticoid activity inhibited [3H]-dexamethasone binding in a dose-dependent manner. The order, beginning with the most potent inhibitor of binding, was triamcinolone acetonide greater than fluorometholone greater than dexamethasone greater than medroxy progesterone acetate greater than 11 beta-OH-progesterone greater than prednisolone acetate greater than prednisolone greater than cortisol greater than corticosterone . Other steroids exhibiting less inhibition of [3H]-dexamethasone binding were cortexolone greater than prednisone greater than dexamethasone phosphate greater than progesterone greater than prednisolone phosphate greater than cortisone greater than 17 alpha-OH progesterone greater than estradiol-17 beta greater than testosterone greater than 11 alpha,17 alpha,21-OH-progesterone. These data suggest that the influence of glucocorticoids and drugs with this type of normal activity on corneal cells is mediated by an intracellular receptor protein.

Animals↗

PubMed1984

Possible role of central serotoninergic neurons in the development of dental pain and aspirin-induced analgesia in the monkey.

The effects of aspirin or 5-hydroxytryptamine (5-HT)-related drugs on the dental pain induced by electrical stimulation of tooth pulp afferent fibers were assessed in conscious monkeys. The electrical current required for producing jaw opening is referred to as the pain threshold. Both systemic (25 to 75 mg/kg, i.p.) or central (0.5 to 1.5 mg, third cerebral ventricle) administration of aspirin produced analgesia in monkeys. In addition, activation of central 5-HT receptors with central injection of either 5-HT or its precursor, 5-hydroxytryptophan, also produced analgesia. On the other hand, inhibition of central 5-HT receptors with central administration of either cyproheptadine (a blocking agent of 5-HT receptors), p-chlorophenylalanine (PCPA, an inhibitor of 5-HT synthesis) or 5,7-dihydroxytryptamine (5,7-DHT, a depletor of central 5-HT nerve fibers) produced an enhancement in pain sensitivity (or a decrease in pain threshold). Furthermore, the analgesia induced by aspirin was antagonized by pretreatment of monkeys with either cyproheptadine, PCPA, or 5,7-DHT. The results indicate that increases in the activity of central 5-HT neurons are associated with reduced dental pain and enhanced aspirin-induced analgesia, whereas decreases in the activity of those neurons correlate with dental hyperalgesia and diminished aspirin-induced analgesia in monkeys.

5,7-Dihydroxytryptamine↗

PubMed1984

Effects of kainic acid injections in the striatum on physiologic and behavioral functions in conscious rats.

Alterations in both physiologic and behavioral functions were assessed in unanesthetized rats after a unilateral injection of kainic acid (KA) in the striatum. The immediate behavioral effects were dyskinesias, head swaying, circling, tail elevation, hyperpnea and marked salivation. The induced behavioral responses lasted for about 14 to 18 h. Rats with intrastriatal KA injection, although showing no thermoregulatory deficit at both moderate (22 degrees C) and hot (30 degrees C) environmental temperatures, displayed a lower metabolism and a lower rectal temperature than the preinjection controls in the cold (8 degrees C) environment. In addition, the hypothermia induced by intrastriatal administration of apomorphine (dopamine agonist) was greatly antagonized by pretreatment with intrastriatal injection of KA. Furthermore, intrastriatal infusions of KA (1 microgram in 0.5 microliter) also caused a decrease in pain threshold (or in the latency to the hind-paw lick on the hot plate test), hypophagia, polydipsia, and weight loss. The induced alterations in thermoregulation, pain reflex, and ingestive behavior lasted for about 7 days. These data indicate that striatal neurons are involved in the central control of motor activity, thermoregulation, the pain reflex, and ingestive behavior.

Animals↗

PubMed1984

Administration of prostaglandin E2 into the striatum induces hyperthermia in rats.

Changes in thermoregulatory function were assessed in unanesthetized rats after a unilateral injection of prostaglandin E2 (PGE2) into the striatum or the substantia nigra. Intrastriatal injection of PGE2, but not vehicle solution, induced a dose-dependent rise in rectal temperature. The hyperthermia in response to intrastriatal injection of PGE2 was due to increased metabolism and/or cutaneous vasoconstriction. Furthermore, the PGE2-induced hyperthermia was antagonized by prior intrastriatal injection of kainic acid (to destroy cell bodies in the striatum) but not by pretreatment with 6-hydroxydopamine (to destroy the dopaminergic nerve fibers in the striatum). On the other hand, administration of PGE2 into the substantia nigra induced no significant change in thermoregulatory functions. The data showed that PGE2, when injected into the striatum, may act on cell bodies in the striatum to induce hyperthermia by promoting an increase in heat production and/or vasoconstriction.

Animals↗

PubMed1984

Hypothalamic neuronal responses to iontophoretic application of morphine in rats.

Effects of thermal stimulation of the scrotum and of iontophoretic application of morphine on the activity of neurones in the preoptic anterior hypothalamic area were observed in 30 urethane-anaesthetised rats. The proportions of cold-responsive, warm-responsive and thermally unresponsive units were 20.7, 28.3 and 51%, respectively, of the total number of neurones tested. Iontophoretic application of morphine to neurones in the preoptic anterior hypothalamic area in rats resulted in excitation of the majority of cold-responsive cells and inhibition of the majority of warm-responsive cells tested. However, most of the thermally unresponsive cells were unaffected by application of morphine. These results provide a neuronal basis for the hypothesis that morphine, when administered directly into the hypothalamus, facilitates heat production and inhibits heat loss, which leads to hyperthermia.

Animals↗

PubMed1984

Tachycardia, hypertension and decreased reflex bradycardia produced by striatal lesions induced by kainic acid.

The effects of intra-striatal injection of kainic acid on cardiovascular function were assessed in urethane-anesthetized rats. Intra-striatal administration of 2 micrograms of kainic acid (in a volume of 0.5 microliter) produced both tachycardia and hypertension. The tachycardia induced by intra-striatal injection of kainic acid was antagonized by either prior bilateral vagotomy or spinal transection of the animals (at C7). On the other hand, the hypertension induced by intra-striatal administration of kainic acid was antagonized by prior bilateral vagotomy, but not spinal transection. In addition, reflex bradycardia was produced by intravenous infusion of adrenaline in rats. Over the dose range (1.25-5.0 micrograms/kg, i.v.) of adrenaline used, a dose-dependent bradycardia was obtained. It was found that pretreatment of animals with intra-striatal injection of kainic acid, although causing no change in the adrenaline-induced pressor effect, did reduce the adrenaline-induced bradycardia. Intravenous administration of same dose of kainic acid had no effect on these cardiovascular responses. Thus, the data indicate that striatal neurones are involved in the central control of cardiovascular function.

Animals↗

PubMed1984

Cholecystokinin acts through catecholaminergic mechanisms in the hypothalamus to influence ingestive behaviour in the rat.

Administration of cholecystokinin (CCK) (0.2 - 0.6 micrograms in a volume of 2 microliter) into the lateral cerebral ventricle caused a decrease in intake of food but a relative increase in intake of water (or water-to-food ratio) in rats. To determine whether the anorexic actions of CCK were mediated through the hypothalamic nuclei, rats were infused with CCK (0.02 - 0.12 microgram in a volume of 0.5 microliter) through previously implanted hypothalamic cannulae. Administration of CCK into the lateral hypothalamus, but not the anterior hypothalamus or ventromedial hypothalamus, caused decreased intake of food and a relative increased intake of water. In addition, the responses induced by injection of CCK into the hypothalamus were completely abolished by selective depletion of catecholamines in the hypothalamus (eg. noradrenaline and dopamine) with intra-hypothalamic injection of 6-hydroxydopamine. Intraperitoneal administration of 0.12 microgram of CCK had no effect on the intake of food and water in rats. The data indicate that CCK acts through catecholaminergic mechanisms in the hypothalamus to influence feeding behaviour.

Animals↗

PubMed1984

Both dopaminergic and adrenergic receptors in the brain are involved in the behavioural excitation induced by dibutyryl 3',5'-adenosine monophosphate and aminophylline in the rat.

Following administration of dibutyryl cyclic-AMP or aminophylline, but not vehicle solution, into the lateral cerebral ventricle of rats produced locomotor stimulation, head and body rearing, circling, (as indicated by an enhancement of gross movement), increased grooming, head swaying and scratching (as indicated by an enhancement of fine movement), tail elevation, piloerection and convulsion. The behavioural excitation produced by either dibutyryl cyclic-AMP or aminophylline was antagonized by pretreatment with intraventricular injection of either two alpha-adrenergic antagonists (phentolamine and yohimbine) or a dopaminergic antagonist (haloperidol), but not with either a beta-adrenergic antagonist (propranolol) or a narcotic antagonist (naloxone). In addition, direct administration of dibutyryl cyclic-AMP into either the anterior hypothalamus, the nucleus accumbens or the caudate-putamen complex of rats produced the same behavioural responses as those produced by the intraventricular injection. Again, the behavioural responses induced by intracerebral injection of dibutyryl cyclic-AMP was antagonized by pretreatment with either alpha-adrenergic antagonists or a dopaminergic antagonist. The present data indicate that both the dopaminergic and the adrenergic receptors in the brain are involved in the behavioural excitation induced by dibutyryl cyclic-AMP and aminophylline in the rat.

Aminophylline↗

PubMed1984

Experimental study on the pathogenesis of heat stroke.

A heat-balance study was carried out on conscious rabbits exposed to ambient temperatures (Ta) from 8 degrees to 40 degrees C. At Ta = 40 degrees C, heat gain exceeded heat loss and led to hyperthermia and heat stroke, and the latency for the onset of heat stroke was found to be around 87 minutes. At the onset of heat stroke, the comatose animals showed higher levels of rectal temperature, ear skin blood flow, respiratory evaporative heat loss, metabolic rate, intracranial pressure (ICP), and cerebral water content as compared to those of control animals (kept at an ambient temperature of 24 degrees C). Before the start of heat stress, the animals had an average mean arterial blood pressure (MABP) of 94 mm Hg and cerebral perfusion pressure (CPP) of 80 mm Hg. However, at the onset of heat stroke, the average MABP and CPP decreased to 67 and 19 mm Hg, respectively. The reduction in CPP at the onset of heat stroke was due to both a decrease in MABP and an increase in ICP. In addition, the comatose animals which received an intravenous infusion of 10% glycerol (3 ml/min) had a survival time (interval between onset of heat stroke and death) longer than that of the comatose animals which received the control-vehicle solution. The prolongation of survival time in the glycerol-treated animals may be due to lower rectal temperature, lower cerebral water content, or lower ICP during the development of heat stroke. The present data indicate that not only hyperthermia but also cerebral edema, intracranial hypertension, decreased MABP, and decreased CPP are the main causes of heat stroke. The therapeutic values of glycerol on heat stroke may be related to the depressant action on cerebral edema, intracranial hypertension, and body temperature.

Animals↗

PubMed1983

Serotonergic mechanisms in the hypothalamus mediate thermoregulatory responses in rats.

1. Either electrical stimulation of midbrain raphe nuclei or administration of 5-hydroxytryptamine (5-HT; serotonin) into the preoptic anterior hypothalamus caused hypothermia in conscious rats at ambient temperatures (Ta) of both 8 degrees C and 22 degrees C. The hypothermia was due to decreased metabolic heat production at Ta = 8 degrees C, while at Ta = 22 degrees C the hypothermia was due to both decreased metabolism and increased heat loss (cutaneous vasodilatation). However, at Ta = 30 degrees C, electrical stimulation of midbrain raphe or intrahypothalamic injection of 5-HT caused an insignificant change in the thermoregulatory responses. There was no changes in respiratory evaporative heat loss in response to these treatments at various Ta's. 2. Direct administration of the serotonergic receptor antagonists such as cyproheptadine and methysergide into the preoptic anterior hypothalamus caused hyperthermia in conscious rats at Ta's of 8 degrees C, 22 degrees C and 30 degrees C. The hyperthermia was due to increased metabolism and cutaneous vasoconstriction. 3. The hypothermia induced by intrahypothalamic administration of 5-HT was antagonized by pretreatment with an intrahypothalamic dose of either cyproheptadine or methysergide in rats at Ta = 22 degrees C. 4. Inhibition of 5-HT neuronal activity with administration of 5-HT into the midbrain raphe regions also caused hyperthermia, increased metabolism and cutaneous vasoconstriction in rats at Ta's of 8 degrees C, 22 degrees C and 30 degrees C. 5. These observations tend to suggest that the functional activity of serotonergic receptors in the preoptic anterior hypothalamus mediates thermoregulatory responses in the rat. Activation of serotonergic receptors in the hypothalamus decreases heat production and/or increases heat loss, while inhibition of serotonergic receptors in the hypothalamus increases heat production and/or decreases heat loss in the rat.

Animals↗