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Biomedical subjects

H Lai

Publications and source records attributed to H Lai.

At least 127 records · Page 7Linked to original sources
PubMed1984

Apomorphine-induced hypothermia affected by acute treatment with apomorphine, haloperidol, or ethanol.

Apomorphine-induced hypothermia was studied in rats pretreated with a dose of apomorphine (mg/kg, IP), haloperidol (0.25 mg/kg, IP), ethanol (3 g/kg, PO), or apomorphine + ethanol. Pretreatment with apomorphine attenuated the hypothermic response, pretreatment with either haloperidol or ethanol potentiated it, and pretreatment with apomorphine together with ethanol did not alter it. These data show that an acute treatment with a dopaminergic drug can alter the responsiveness of the dopaminergic thermoregulatory system, and also that ethanol has an inhibitory effect on the dopamine mechanism.

Animals↗
PubMed1984

Effects of treatments with apomorphine, haloperidol and ethanol on apomorphine-induced changes in body temperature in the rat.

In previous research, we discovered two DA-related thermoregulatory mechanisms in the rat: a haloperidol-sensitive, hypothermia-inducing mechanism and a haloperidol-nonsensitive, hyperthermia-inducing mechanism. The latter mechanism must also involve serotonin, since its activity can be blocked by serotonin antagonists. We have now found that the responsiveness of these mechanisms to apomorphine could be selectively affected by acute pretreatments with apomorphine, haloperidol and ethanol. The hypothermia-inducing mechanism was supersensitized by pretreatment with either haloperidol (0.25 mg/kg, administered 5 days earlier) or ethanol (3 g/kg, 15 h), but was not affected by pretreatment with apomorphine (1 mg/kg, 15h). In contrast, the hyperthermia-inducing mechanism was supersensitized and desensitized by similar pretreatments with apomorphine and ethanol, respectively, but was not affected by pretreatment with haloperidol.

Animals↗
PubMed1983

Psychoactive-drug response is affected by acute low-level microwave irradiation.

The effects of various psychoactive drugs were studied in rats exposed for 45 min in a circularly polarized, pulsed microwave field (2450 MHz; SAR 0.6 W/kg; 2-microseconds pulses, 500 pps). Apomorphine-induced hypothermia and stereotypy were enhanced by irradiation. Amphetamine-induced hyperthermia was attenuated while stereotypy was unaffected. Morphine-induced catalepsy and lethality were enhanced by irradiation at certain dosages of the drug. Since these drugs have different modes of action on central neural mechanisms and the effects of microwaves depend on the particular drug studied, these results show the complex nature of the effect of microwave irradiation on brain functions.

Amphetamines↗
PubMed1983

Dopaminergic and serotonergic mechanisms of thermoregulation: mediation of thermal effects of apomorphine and dopamine.

The effects of dopaminergic and serotonergic antagonists on apomorphine- and dopamine-induced changes in body temperature were studied in the rat. Intraperitoneal administration of apomorphine produced dose-dependent hypothermia. At a dose of 0.1 mg/kg, apomorphine caused either no significant effect or a slight decrease in body temperature. However, it caused hyperthermia in rats pretreated with the DA antagonist, haloperidol, and hypothermia in rats pretreated with the serotonin depletor, p-chlorophenylalanine or serotonin antagonists, cyproheptadine, metergoline or cinanserin. Intracerebroventricular injection of 100 micrograms/2 microliter of DA transiently decreased body temperature. Pretreatment with cyproheptadine potentiated and prolonged the responses. However, the same injection of DA produced hyperthermia in haloperidol-pretreated animals. These data suggest that both dopaminergic and serotonergic mechanisms in the brain mediate the effects of apomorphine on body temperature. We propose that apomorphine can simultaneously activate two opposing DA-related thermoregulatory mechanisms with different sensitivities to haloperidol: a haloperidol-sensitive hypothermia and a haloperidol-nonsensitive hyperthermia mechanisms. Furthermore, the action of the latter mechanism is mediated by a secondary activation of serotonergic mechanisms.

Animals↗
PubMed1982

Chronic haloperidol treatment potentiates apomorphine- and ethanol-induced hypothermia in the rat.

Supersensitivity developed in the central dopaminergic system of the rat after 21 days of chronic haloperidol injection. This was indicated by a higher level of apomorphine-elicited stereotypic behavior and by higher concentrations of striatal 3H-spiroperidol binding sites in haloperidol-treated rats compared to saline-treated controls. The chronic haloperidol treatment did not affect the baseline body temperature but potentiated both apomorphine- and ethanol-induced falls in core temperature. Such potentiation may also be related to dopamine supersensitivity. However, no significant correlation was found between apomorphine- or ethanol-induced hypothermia and apomorphine-elicited stereotypic behavior or the concentration of striatal 3H-spiroperidol binding sites. Hence, the nigrostriatal dopamine system does not appear to be involved in the development of hypothermic responses to these agents.

Animals↗
PubMed1981

Chronic treatments with zotepine, thioridazine, and haloperidol affect apomorphine-elicited stereotypic behavior and striatal 3H-spiroperidol binding sites in the rat.

Apomorphine (AP)-elicited sterotypic behavior and striatal 3H-spiroperidol binding sites were studied in rats given 3 weeks of chronic treatment with one of the following neuroleptic drugs: zotepine (10 or 20 mg/kg/day IP); thioridazine (10 or 20 mg/kg/day IP); haloperidol (2 or 5 mg/kg/day IP). On days 10-12 after the chronic neuroleptic treatment, enhancement of AP-elicited stereotypy was seen in the high- and low-dose haloperidol-treated, as well as in the high-dose thioridazine and zotepine-treated rats when compared to that of saline-injected controls. No significant change in the response to AP was found in the low-dose thioridazine and zotepine-treated animals. Significant increases in the concentration of striatal 3H-spiroperidol binding sites were seen after treatment with all three neuroleptics, both high and low doses. A positive correlation was found between AP-elicited stereotypy and the concentration of striatal 3H-spiroperidol binding sites in the haloperidol-treated and control rats. However, no such correlation was seen after chronic thioridazine and zotepine treatments.

Animals↗
PubMed1980

Effects of thioridazine on apomorphine-elicited stereotypic behavior and motor activity.

Bilaterally injected thioridazine (10 micrograms) into the striata of rats augmented the stereotypic behavior elicited by apomorphine. The enhancing effect was attenuated by pretreatment with alpha-methyl-p-tyrosine. At 48 hr postinjection of thioridazine (1.0 mg/kg, IP), motor suppression from a low dose of apomorphine (0.2 mg/kg, IP) was enhanced; however, motor response to a high dose of apomorphine (1 mg/kg, SC) was not affected. Possible mechanisms of action of thioridazine are discussed.

Animals↗
PubMed1979

Effects of ethanol on turnover and function of striatal dopamine.

Acute oral administration of ethanol increased the rate of depletion of dopamine in the striata of rats injected with alpha-methyl-p-tyrosine. This effect was eliminated by pretreatment with atropine or by lesioning of the striato-nigral tract. Ethanol also attenuated the inhibitory effect of apomorphine on turnover of striatal dopamine. Unilateral injection of ethanol into the neostriatum of rats followed by intraperitoneal injection of either apomorphine or amphetamine elicited marked ipsilateral head-to-tail body turning. This turning was blocked by pretreatment with haloperidol. Chronic intubation of ethanol to rats enhanced contralateral body turning elicited by unilateral intrastriatal injection of dopamine. Injection of 6-hydroxydopamine into the substantia nigra led to denervation supersensitivity of dopaminergic functions in the neostriatum. This effect was not seen in rats that were given ethanol postinjection of 6-hydroxydopamine. These results suggested that ethanol has an inhibitory effect on the nigrostriatal dopaminergic system.

Animals↗
PubMed1978

Methylazoxymethanol acetate: effect of postnatal injection on brain amines and behavior.

The antimitotic drug, methylazoxymethanol acetate (MAMA), was injected into newborn rats during the first four days of life. At 48 days of age, these rats weighed one-third less than controls, as did the cerebella of their brains, but the rest of their brains weighed only 7% less than those of controls. The cerebella structures of the drug-injected rats was highly disorganized. Purkinje cells were scattered haphazardly in the granular layer instead of forming a monolayer. More foldings and short folia were found in the cerebella of drugged animals. In spite of these large morphological differences, the total amounts of norepinephrine and serotonin in the cerebella of the drugged rats were not different from those of the control rats. Behavioral effects of postnatal injection of MAMA include retarded development of the righting reflex,i.e., the drugged pups took longer time to right themselves when placed on their backs during the first nine days after birth; and scondly, MAMA reduced locomotor activity measured 45 days after birth.

Animals↗
PubMedDate not supplied

TRH analog MK-771 reverses neurochemical and learning deficits in medial septal-lesioned rats.

Microinjection of ibotenic acid into medial septum of rats decreased choline acetyltransferase (CAT) and high-affinity choline uptake (HACU) activities in hippocampus and retarded the learning of a spatial memory task in the radial-arm maze. Administration of MK-771, a stable TRH analog, to such animals restored HACU activity in hippocampus to normal levels. Daily treatment of rats with MK-771 prior to maze running also restored the animals' learning ability. MK-771 did not enhance hippocampal HACU activity or maze performance in sham-lesioned rats. These results suggest that MK-771 reversed the ibotenic acid-induced memory deficit by restoring septohippocampal cholinergic function. MK-771 and other TRH analogs may represent novel agents for improving memory deficits produced by cholinergic insufficiency in Alzheimer's disease.

Animals↗
PubMedDate not supplied

Age-related decreases in dopamine receptors in the caudate nucleus and putamen of the rhesus monkey (Macaca mulatta).

Specific binding of the dopamine receptor ligand 3H-spiroperidol to cell membranes prepared from the caudate nuclei and putamens of 29 rhesus monkeys (M. mulatta), ranging in age from 2 to 22 years, was investigated. Receptor concentration (Bmax) decreased in the caudate nucleus and putamen with age at mean rates of 2.1 and 1.7% per year, respectively, whereas binding affinity (Kd) did not change significantly with age. The rate of decline in Bmax appeared to be more rapid before adulthood and in old age than during young adulthood and middle age. These data are compared with the results from similar studies of other animal species including human, rabbit, rat, and mouse. The rate of decline in striatal dopamine receptors is closely related to the rate of aging and maximal life span of the species. It may reflect both maturational and senescent processes modifying the behavior of animals as they age.

Aging↗