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Biomedical subjects

G B Glavin

Publications and source records attributed to G B Glavin.

At least 91 records · Page 5Linked to original sources
PubMed1985

Selective noradrenaline depletion markedly alters stress responses in rats.

Rats were given FLA-63, followed by R04-1284 0.5 h later to relatively selectively deplete brain NA. After 8 h, some animals were examined for regional brain NA and MHPG-SO4, while some were subjected to 3 h of cold-restraint stress and then examined. All brain regions examined showed significant NA and MHPG reduction. Specific NA depletion markedly exacerbated restraint ulcer formation and plasma corticosterone levels. NA depletion without restraint stress did not induce ulcers or elevate corticosterone. Intact brain NA activity appears to be essential for coping with stress.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1985

Neuronal mechanisms involved in drug-induced jumping behavior in mice.

Previously we have found that lithium chloride (250 mg/kg i.p.) plus haloperidol (4 mg/kg i.p.), or apomorphine (0.25 mg/kg i.p.) plus thyrotropin releasing hormone (TRH, 20 mg/kg i.p.), elicited a jumping behavior which involves dopaminergic and cholinergic inhibition, and noradrenergic activation. Pretreatment with antiserotonergic agents such as methysergide (5 and 10 mg/kg i.p.) and cyproheptadine (5 mg/kg i.p.) enhanced the jumping behavior induced by these drugs. 5-Methoxy-N,N-dimethyltryptamine (5-MDMT, 5 mg/kg i.p.), a serotonergic receptor agonist, inhibited the jumping behavior. Muscimol, a GABA receptor agonist, at 2 mg/kg, potentiated jumping. GABA receptor antagonists such as bicuculline (4 mg/kg i.p.) and picrotoxin (0.2 and 1 mg/kg i.p.) depressed jumping. An antihistamine agent, diphenhydramine (5 mg/kg i.p.), also potentiated the jumping behavior. Furthermore methysergide (10 mg/kg i.p.), but not muscimol (2 mg/kg i.p.) elicited jumping behavior when combined with clonidine (0.5 mg/kg i.p.), TRH (20 mg/kg i.p.), haloperidol (4 mg/kg i.p.) or atropine (5 mg/kg i.p.). These results suggest that in addition to dopaminergic, cholinergic and noradrenergic mechanisms, serotonergic inhibition may be directly contributing to the initiation of jumping behavior, whereas GABAergic activation appears to be a modulating factor in this behavior.

Animals↗
PubMed1985

Early weaning predisposes rats to exacerbated activity-stress ulcer formation.

Rats were weaned early (Day 15), normally (Day 21) or late (Day 27). When they reached 200 g (+/- 10) they were placed into the activity-stress paradigm. Half the rats in each weaning group were housed in activity-wheel cages and fed only 1 hr each day. The remaining rats served as food-yoked home cage controls and were fed only that amount of food eaten by their wheel-housed partners. Early weaned rats ran more than normally or late weaned animals. Early weaned rats also died at a faster rate and exhibited a significantly greater cumulative ulcer length than did normally or late weaned rats, although ulcer incidence did not differ between the groups. No ulcers occurred in home cage control rats. Early maternal deprivation may generally predispose rats to stress-induced gastrointestinal disease, whether or not such disease has an acid etiology.

Age Factors↗
PubMed1985

Methylphenidate effects on activity-stress gastric lesions and regional brain noradrenaline metabolism in rats.

Methylphenidate (5, 10, or 20 mg/kg/day) or saline were administered to rats in the activity-stress ulcer paradigm. Running-wheel activity and food consumption did not differ among groups. Methylphenidate produced dose-related increases in gastric ulcer severity, decreases in hypothalamic noradrenaline (NA) and increases in 3-methoxy-4-hydroxy-phenylethyleneglycol sulfate (MHPG-SO4) in the hypothalamus, amygdala, hippocampus and thalamus. These results differ markedly from the effects seen with a related substance, d-amphetamine, and suggest different mechanisms of action for these drugs.

Animals↗
PubMed1985

Stress and brain noradrenaline: a review.

Noradrenergic neural systems have been expressly implicated in pathophysiological conditions induced by stress. The majority of experimental evidence supports a central role for brain noradrenaline in mediating the effects of stress and predisposing an organism to stress pathology as well as in producing a well-documented consequence of stress exposure-behavioral depression. This review briefly discusses the noradrenergic (NA) pathways involved, the functioning of NA synapses and their associated receptors and focuses directly upon the effects of stress on NA activity in the brain. These broad categories are discussed in terms of: 1. behavioral versus neurochemical explanations for the effects of stress; 2. the methods used to produce stress; 3. measurement of NA and its major metabolite ("turnover"); 4. regional brain effects of stress; 5. effects of pre-stress alterations in brain NA activity upon subsequent stress-induced brain NA changes; 6. correlation of stress-induced brain NA changes with peripheral manifestations of stress; and 7. predisposing factors in stress-induced neurochemical alterations.

Animals↗
PubMed1985

Zinc sulphate reduces activity-stress gastric lesions in rats.

Daily i.p. injections of zinc sulphate significantly reduced the frequency and severity of activity-stress gastric lesions in rats in a dose-related fashion. These lesions are believed to be of a non-acid etiology and respond primarily to centrally-acting agents. The present results suggest that some local factors contribute to activity-stress gastric damage.

Animals↗
PubMed1985

Effects of morphine and naloxone on restraint-stress ulcers in rats.

Rats were starved for 24 h. Morphine sulphate (1.0, 2.0 or 4.0 mg/kg i.p.) or naloxone-HCl (12.5, 25 or 50 mg/kg i.p.) was administered prior to 3 h of cold-restraint stress. Morphine at 4.0 mg/kg significantly reduced the ulcer severity relative to saline-injected controls and to naloxone-treated rats. Naloxone increased the ulcer incidence and ulcer severity when compared to controls and morphine-treated rats. These results suggest that endogenous opioids released during stress may attenuate the pathological effects of stress.

Animals↗
PubMed1984

Aggression, body temperature, and stress ulcer.

Female rats which were exposed to supine restraint plus cold for 3 hr and were able to bite a passing nylon brush, developed fewer gastric lesions as compared to control rats which were similarly restrained but did not have access to the aggressive biting response. A second study, wherein rats were exposed to two restraint sessions, replicated the results obtained from the first experiment. Core body temperature measures revealed that rats with access to the biting response were more successful in maintaining body temperature. The protective effect of aggression may thus be due to the reduction in restraint hypothermia and not necessarily the affective qualities of the aggressive response per se.

Aggression↗
PubMed1983

Fat-supplemented diet protects against activity-stress ulcers in rats.

Rats were exposed to a fat-supplemented (32.5% beef tallow) diet from weaning until they were 200 g in weight. Half the animals were exposed to the activity stress paradigm consisting of housing in standard activity-wheel cages while restricting their food intake to 1 h each day. Control rats were treated in the same fashion but on a fat-free (0.08%) diet. Fat-supplemented activity-stressed rats exhibited high levels of running wheel activity but less mortality and less gastric pathology than fat-free controls which were exposed to the activity-stress procedure. Ulcers were not observed in home cage housed rats in either diet condition.

Animals↗
PubMed1983

Regional rat brain noradrenaline turnover in response to restraint stress.

Male Wistar rats were starved for 12 hr and then subjected to either 2 hr of wire mesh "envelope" restraint at room temperature; 2 hr of supine restraint in a specially constructed harness at room temperature or were not restrained. Eight brain regions were examined for NA level and the level of its major metabolite, MHPG-SO4. Plasma corticosterone and gastric ulcer incidence were also measured. All restrained rats displayed marked elevations in MHPG-SO4 levels in most brain regions. In addition, several brain regions in restrained animals showed a reduction in NA level. All restrained rats showed elevated plasma corticosterone levels and evidence of gastric lesions. In general, supine restraint produced greater alterations in regional brain NA turnover, greater evidence of ulcer disease, and higher plasma corticosterone levels than did wire mesh restraint. These data suggest that acute but intense stress in the form of restraint causes markedly altered brain NA activity--a possible neurochemical mechanism underlying the phenomenon of stress-induced disease.

Animals↗
PubMed1982

Nicotine and ascorbic acid effects on cold-restraint ulcers in rats.

Rats were orally administered 1-ascorbic acid, nicotine 1-ascorbic acid and nicotine, or distilled water for 10 days. Following this treatment they were fasted for 24 h and then restrained in a cold environment for 2 h. Nicotine alone produced significantly more gastric ulcers than any other treatment. 1-Ascorbic acid increased ulceration relative to controls. The combined effects of 1-ascorbic acid and nicotine resulted in reduced ulcer incidence and severity. It appears that l-ascorbic acid and nicotine do not act synergistically to augment stress-induced gastric ulcer.

Animals↗
PubMed1980

Effects of aluminium hydroxide on restraint-induced and restraint delay-induced gastric ulceration in rats.

Rats given aluminium hydroxide after cold-restraint stress but before the 'post-stress delay' period, ulcerated significantly less severely and less frequently than rats given the drug before cold-restraint stress or those given water at either time period. Both aluminium hydroxide treated groups exhibited less ulceration than non-drug groups. These data suggest profound parasympathetic and hence, gastric acid, involvement in restraint delay-induced ulceration in rats.

Aluminum Hydroxide↗
PubMed1980

Restraint ulcer: history, current research and future implications.

A relatively new ulcerogenic procedure, supine restraint-cold, is described. This procedure is simple, effective andproduced a reliably high incidence of gastric glandular lesions in a variety of animal species. In some cases, these lesions penetrate the muscularis mucosa and as such may be called ulcers. They are responsive to known therapeutic agents (cimetidine, aluminum hydroxide). Drugs which modify autonomic activity (scopolamine, carbachol) affect the extent of supine restraint-cold induced gastric lesions. Animals which differ in open-field behaviors indicative of emotionality, show marked differences in gastric lesions induced by this procedure. It is suggested that the supine restraint-cold procedure meets the established criteria for a useful experimental ulcer model [25] and thus represents a viable research tool.

Aluminum Hydroxide↗
PubMed1978

Effects of cimetidine on stress ulcer and gastric acid secretion in the rat.

Cimetidine at 25, 50, and 100 mg/kg significantly inhibited gastric acid secretion in rats with chronic gastric cannulas. Rats receiving either 50 or 100 mg/kg of cimetidine secreted significantly less gastric acid 3 hr after injection. Cimetidine failed to reduce the number or size of gastric lesions in rats exposed to the activity-stress procedure, but cimetidine at 100 mg/kg significantly reduced the number and size of gastric lesions in rats subjected to a supine restraint procedure.

Animals↗