PubMed Health⌕ Search

Biomedical subjects

J B Lucot

Publications and source records attributed to J B Lucot.

36 records · Page 2Linked to original sources
PubMed1987

Buspirone blocks motion sickness and xylazine-induced emesis in the cat.

Cats were tested for motion sickness following s.c. pretreatment with four doses of buspirone. Buspirone blocked motion sickness with an ED50 of 0.46 mg . kg-1 base. Buspirone pretreatment (4.0 mg . kg-1 base) also significantly blocked vomiting in cats later injected with 0.66 mg . kg-1 (base) s.c. of the emetic drug xylazine. The results are interpreted as showing that buspirone is acting at the vomiting center, the point of convergence for the separate mechanisms subserving chemically-induced emesis and motion sickness.

Animals↗
PubMed1986

Effects of serotonergic agonists and antagonists on the locomotor activity of neonatal rats.

The locomotor activity of neonatal rats was measured after treatment with serotonin agonists or antagonists. Treatment with the serotonin agonists 5-hydroxytryptophan or quipazine resulted in the elimination of the peak in activity which normally results from increases in activity from days 10 to 15 of life followed by decreases from days 15 to 20 of life. The drug-induced decreases in activity occurred at doses that did not alter locomotor activity after day 17, when most of the peak in activity had passed. The dose of 5 mg/kg of the serotonergic antagonist methysergide eliminated the peak in activity without changing locomotor activity after the peak had passed. The antagonists methiothepin and cinanserin only produced decreases in locomotor activity which did not appear to be related to the peak in activity. The serotonergic agonist data are compatible with the hypothesis that the development of the serotonin system contributed to the inhibition of locomotor activity. The methiothepin and cinanserin data neither confirm nor dispute the hypothesis, as their effects may have been either nonserotonergic or on serotonin receptors that were different than those acted on by the agonists.

5-Hydroxytryptophan↗
PubMed1986

Xylazine emesis, yohimbine and motion sickness susceptibility in the cat.

The possible role of the alpha-2 adrenoceptors in xylazine-induced vomiting and in motion sickness was investigated. Cats were divided into two groups according to motion sickness susceptibility and were observed after s.c. injections of xylazine. The incidence of vomiting increased with the dose, and at each dose, the high susceptibility group had a greater emetic incidence than the low susceptibility group. In another experiment with cats divided into two groups according to motion sickness susceptibility, s.c. administration of yohimbine effectively antagonized the xylazine-induced emesis in both susceptibility groups. The cats in the latter experiment were then challenged with a motion sickness stimulus, after s.c. pretreatment with yohimbine. Yohimbine failed to prevent motion sickness but did occasion an unexplained variability in the incidence of vomiting. These findings suggest that the emetic effect of xylazine results from stimulation of alpha-2 adrenoceptors but that these receptors are not fundamental to feline motion sickness. The fact that susceptibilities to xylazine-induced emesis and to motion sickness are correlated suggests a point of interaction other than the area postrema, which is known to be essential for xylazine-induced vomiting but not for motion sickness in the cat.

Animals↗
PubMed1985

A stimulator for laboratory studies of motion sickness in cats.

A motion sickness device is described which produces motion sickness in about 40% of an unselected population of unrestrained female cats during a 30-min exposure at 0.28 Hz. The apparatus provides a gentle wave stimulus, similar to that provided by an amusement park Ferris Wheel. Two cats may be tested at the same time. This device is useful for studies of putative antimotion sickness drugs or the biochemical basis of the emetic response to motion.

Animals↗
PubMed1983

Alpha-methyltyrosine attenuates and reserpine increases methamphetamine-induced neuronal changes.

The repeated administration of methamphetamine to rats has been shown to cause a long-lasting depletion of dopamine in various brain regions. In the first study, the effects of pretreatment with alphamethyltyrosine (AMT) or reserpine on the long-lasting methamphetamine-induced dopamine depletion were examined. In the second study, the effects of AMT and reserpine on central dopamine levels were measured in rats previously treated with methamphetamine. Pretreatment with AMT attenuated the long-lasting dopamine depletion induced by methamphetamine, whereas, pretreatment with reserpine increased the depletion. The acute effects of AMT and reserpine on brain dopamine were not altered when administered two weeks after the last methamphetamine injection.

Animals↗
PubMed1983

Catecholaminergic influences on motion sickness.

The evidence for possible roles of catecholamines in motion sickness is reviewed. l-Dopa is implicated in that it is the precursor to catecholaminergic neurotransmitters. Dopamine may have a role in stimulating motion sickness, though much basic information is lacking. Epinephrine may have a stimulatory role, since anatomical, pharmacological and physiological evidence is consistent with such a role. Norepinephrine probably inhibits motion sickness, as indicated by anatomical, physiological and pharmacological evidence. Information is missing that is critical to the understanding of the roles of each neurotransmitter in motion sickness.

Animals↗
PubMed1982

The effects of intracerebroventricular administration of 5,6-dihydroxytryptamine to neonatal rats.

5,6-Dihydroxytryptamine was administered intracerebroventricularly to neonatal rats on days 3 and 6 (25, 50, 75 or 100 micrograms) or on day 12 (50, 75 or 100 micrograms) after birth. Administration on days 3 and 6 increased serotonin (5-HT) in the diencephalon, decreased it in the telencephalon and produced variable results in the brainstem. The dose of 100 micrograms eliminated the peak in locomotor activity that normally occurs at day 15. Administration on day 12 produced increased 5-HT levels in the diencephalon and the brainstem. The dose of 100 micrograms delayed the decrease in activity after the peak. Administration on days 3 and 6 or on day 12 produced non-specific damage throughout the brain, although dopamine levels were normal. The behavioral effects did not correspond with the neurochemical effects and probably were due to the pronounced non-specific effects of the treatment.

5,6-Dihydroxytryptamine↗
PubMed1982

Effects of neonatal administration of 5,7-dihydroxytryptamine on locomotor activity.

Neonatal rats treated on day 3 of life with 50 or 100 micrograms 5,7-dihydroxytryptamine exhibited long-lasting selective depletions of serotonin (5-HT). The 5-HT depletions produced a shift in the peak in locomotor activity from its normal occurrence at 15 days of age to later days of age. The observation that the decreases in activity after the peak were delayed, rather than eliminated, suggests that the inhibition of locomotor activity produced by 5-HT may be of transient importance in the developing rat. The transience of the inhibition may be the result of the continuing development of nonserotonergic systems during this time period that are involved in the regulation of activity.

5,7-Dihydroxytryptamine↗
PubMed1980

The effects of dopaminergic agents on the locomotor activity of rats after high doses of methylamphetamine.

Treatment of rats with 100 mg/kg/day of methylamphetamine for four days produced long lasting (16 week) depletions of central nervous system levels of dopamine but not of norepinephrine. This methylamphetamine treatment also attenuated the ability of methylamphetamine and apomorphine to produce increases in locomotor activity without shifting the dose-response curve to the right or left. These rats underwent significant decreases in activity after lower doses of haloperidol while the response to L-Dopa was virtually unchanged.

Animals↗
PubMed1977

Toxic interactions of stimulants, narcotics and narcotic antagonists.

This study examines the lethality of combinations of central nervous system stimulants, narcotics and narcotic antagonists in rodents housed individually. The lethality of mice and rats from d-amphetamine was potentiated by methadone, cyclazocine and morphine, in that order of potency. Naloxone did not enhance lethality from d-amphetamine in mice, whereas it did antagonize lethality from morphine-d-amphetamine interactions. Naloxone did slightly enhance lethality from d-amphetamine in rats, but at a higher dose than those found to antagonize the lethality from morphine-d-amphetamine combinations. Methadone also enhanced the lethality from cocaine. These results have important implications for drug abusers and for patients being treated for narcotic addiction with either a methadone maintenance program or a cyclazocine administration program.

Animals↗
PubMed1976

Characteristics of ethanol drinking patterns under schedule-induced polydipsia.

Rats were induced to consume concentrations of ethanol between 5% and 10% (w/v) using the schedule-induced polydipsia technique. Although the substitution of ethanol solutions for water disrupted the usual post-pellet pattern of drinking, large amounts of ethanol were consumed and sound-induced convulsions were observed during ethanol withdrawal. In subsequent experiments, other rats chose 5% and sometimes 10% ethanol solutions over water where both water and ethanol were freely available during the first session of exposure to ethanol. Convulsions and wild running behavior could be observed in some of these rats after only 8 days of drinking, even though ethanol was freely available at all times. Use of the schedule-induced polydipsia technique served to bring the rats into early contact with the ethanol, but rats that received the same number of food pellets in a dish rather than by the schedule drank almost as much ethanol as did the rats receiving ethanol by the schedule. Rats with free access to food pellets drank very little ethanol.

Alcohol Drinking↗
PubMedDate not supplied

alpha-Fluoromethylhistidine but not diphenhydramine prevents motion-induced emesis in the cat.

PURPOSE: This study seeks to evaluate the comparative role of alpha-fluoromethylhistidine and diphenhydramine in the prevention of motion sickness. METHOD: The role of histaminergic mechanisms in motion sickness were evaluated in a feline model. Twenty-six female cats were studied. A variety of doses of fluoromethylhistidine and diphenhydramine were administered before motion testing. RESULTS: Fluoromethylhistidine was effective in preventing motion sickness. The efficacy was dose dependent. In contrast, diphenhydramine failed to prevent motion sickness in any of the tested doses. CONCLUSIONS: The failure of diphenhydramine to prevent motion sickness was unexpected. This may reflect the route of administration or the animal model studied. Depletion of histamine with fluoromethylhistidine prevented motion sickness in cats. Our results suggest that this drug may provide a very long duration of protection in cats.

Animals↗