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A Horita

Publications and source records attributed to A Horita.

At least 19 recordsLinked to original sources
PubMed1992

Single vs. repeated microwave exposure: effects on benzodiazepine receptors in the brain of the rat.

We studied the effects of single (45 min) and repeated (ten daily 45-min sessions) microwave exposures (2450-MHz, 1 mW/cm2, average whole-body SAR of 0.6 W/kg, pulsed at 500 pps with pulse width of 2 microseconds) on the concentration and affinity of benzodiazepine receptors in the cerebral cortex, hippocampus, and cerebellum of the rat. We used a receptor-binding assay with 3H-flunitrazepam as ligand. Immediately after a single exposure, an increase in the concentration of receptor was observed in the cerebral cortex, but no significant effect was observed in the hippocampus or cerebellum. No significant change in binding affinity of the receptors was observed in any of the brain-regions studied. In rats subjected to repeated exposures, no significant change in receptor concentration was found in the cerebral cortex immediately after the last exposure, which may indicate an adaptation to repeated exposures. Our data also show that handling and exposure procedures in our experiments did not significantly affect benzodiazepine receptors in the brain. Because benzodiazepine receptors in the brain are responsive to anxiety and stress, our data support the hypothesis that low-intensity microwave irradiation can be a source of stress.

Animals↗
PubMed1992

Opioid receptor subtypes that mediate a microwave-induced decrease in central cholinergic activity in the rat.

We performed experiments to investigate subtypes of opioid receptors in the brain involved in the effect of acute (45 min) pulsed microwave exposure (2,450-MHz, 2-microseconds pulses, 500 pps, average power density 1 mW/cm2, peak-power density, 1 W/cm2, average whole body SAR 0.6 W/kg) on cholinergic activity in the rat brain. Rats were pretreated by microinjection of specific antagonists of mu, delta, and kappa opioid-receptors into the lateral cerebroventricle before exposure to microwaves. The data showed that all three subtypes of opioid receptors are involved in the microwave-induced decrease in cholinergic activity in the hippocampus. However, the microwave-induced decrease in cholinergic activity in the frontal cortex was not significantly affected by any of the drug treatments, confirming our previous conclusion that the effect of microwaves on the frontal cortex is not mediated by endogenous opioids.

Animals↗
PubMed1992

A possible 5-HT3 component of thyrotropin-releasing hormone-induced increases in gastric motility in developing rats.

Intracisternal injection of thyrotropin-releasing hormone (TRH) increases gastric motility primarily via a vagal cholinergic mechanism. However, a serotonergic (5-HT) component may also exist. Rats (7, 10, 14, and > or = 50 days of age) were anesthetized and gastric motility monitored via an extraluminal strain gauge. Following baseline, ICS 205-930 which blocks 5-HT3 and 5-HT4 receptors (0.01, 0.10, or 1.0 mg/kg) was administered intraperitoneally, then 30 min later intracisternal TRH (5 or 10 micrograms). ICS 205-930 0.1 and 1.0 mg/kg blocked TRH-induced motility in 7-day-old rats. Results support a 5-HT3 or 5-HT4 receptor contribution to TRH-induced gastric motility stimulation, and suggest that receptor expression is dynamic during development.

Animals↗
PubMed1991

D-1 agonist, SKF 38393, but not a D-2 agonist, produces a cholinergically mediated analeptic effect in rabbits.

SKF 38393 (2-15 mg/kg, IV), but not quinpirole, shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rabbits. This effect was blocked by atropine (2-5 mg/kg, IV), but not by atropine methylbromide, suggesting that a central cholinergic mechanism was involved. The analeptic effect was also blocked by SCH 23390 (0.1 mg/kg, IV) or raclopride (5 mg/kg, IV). These results indicate that SKF 38393 activates central cholinergic neurons, which in turn initiate the analeptic effect. However, the fact that raclopride also blocked the SKF 38393 analeptic effect, but quinpirole did not exert any analeptic effect, suggests that a D-1/D-2 modulation of cholinergic systems may be involved in the SKF 38393-induced analeptic effect. These results also support our earlier findings and view that cocaine-induced analeptic activity is mediated by a dopaminergic-cholinergic mechanism.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
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

Neuropharmacology and aging.

This review has attempted to convey the idea that the current concepts of psychotropic drug actions are based largely around the monoamine transmitter systems. Several of the hypotheses which implicate abnormalities of these systems as factors involved in the aging brain are discussed. It is suggested that the current lack of specific geriatric psychotropic agents is in part a reflection of our ignorance of the neurochemical basis of the aging process.

Acetylcholine↗
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↗
PubMed1977

Thyrotropin-releasing hormone: physiological concomitants of behavioral excitation.

Two doses (10 microng and 100 microng) of thyrotropin-releasing hormone (TRH) or saline were injected intraventricularly in rabbits pretreated with either saline, pentobarbital or phenobarbital. Behavior, EEG patterns, respiration rate and heart rate were monitored for 100 min posttreatment. TRH significantly altered all physiological indices except heart rate in both barbiturate- and saline-pretreated animals. The results support the contention that TRH modified central functioning by direct action. Results are discussed in terms of barbiturate antagonism and excitatory effects of TRH.

Animals↗