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Biomedical subjects

D N Stephens

Publications and source records attributed to D N Stephens.

114 records · Page 7Linked to original sources
PubMed1975

Hypothalamic stimulation induces acid secretion, hypoglycemia, and hyperinsulinemia.

Electrical stimulation of the posterior hypothalamus brought about an increase in plasma insulin accompanied by a fall in blood glucose. If glucose fell below 55 mg/100 ml, gastric secretion of HCl ensued. The same relationship between acid secretion and glucose was observed when hypoglycemia was induced by intravenous injection of insulin. Stimulation outside the posterior hypothalamus did not give either a fall in glucose or an increase in gastric acid secretion. It is concluded that posterior hypothalamic stimulation causes gastric acid secretion by inducing insulin release and a consequent hypoglycemia.

Animals↗
PubMedDate not supplied

Catecholamines and self-stimulation: the action of amantadine and its interaction with amphetamine.

The antiparkinsonian drug amantadine HCl caused a dose-dependent depression of electrical self-stimulation, followed by a dose-dependent enhancement. Neither action was correlated with the differential effects of d- and l-amphetamine at different implantation sites. The initial depression was not prevented by pretreatment with anticholinergic or antiserotonergic agents nor by depression of catecholamine (CA) synthesis. The stimulant effects of amantadine and d-amphetamine summated but did not interact, response rates after d-amphetamine being augmented by pretreatment with amantadine except at intervals at which amantadine was by itself depressant. It is concluded that the initial effect of amantadien is caused by impulse-independent release of a pool of intraneuronal CA, causing dissociation between reinforcement signals and the rat's responses. This is followed by amphetamine-like facilitation of impulse-dependent release; the first action depresses performance, the second enhances it.

Amantadine↗
PubMedDate not supplied

Chronic treatment with diazepam or the inverse benzodiazepine receptor agonist FG 7142 causes differential changes in the effects of GABA receptor stimulation.

Daily treatment of mice with diazepam leads to the development of tolerance to the anxiolytic and anticonvulsant effect of the benzodiazepine, while daily treatment with the proconvulsant benzodiazepine receptor inverse agonist FG 7142 produces sensitization to its effects in that seizures develop (chemical kindling). In the present study, the effects of GABA receptor stimulation were studied 2 days after termination of 13 days treatment with diazepam, 20 mg/kg i.p./day, and FG 7142, 40 mg/kg i.p./day. For GABA receptor stimulation, the GABA agonist progabide was chosen because among several GABA receptor stimulants tested it was the only compound that induced increases in seizure threshold in non-toxic doses. Using the threshold for maximal (tonic extension) electroconvulsions as a measure for anticonvulsant efficacy, the anticonvulsant effect of progabide (100 mg/kg i.p.) was unchanged after chronic treatment with diazepam but was lost in FG 7142 kindled animals. Conversely, the hypothermic effect of progabide was reduced after treatment with diazepam but not with FG 7142. Baseline seizure threshold was unchanged 2 days after chronic administration of diazepam but increased in the FG 7142 pretreated mice. The data indicate that tolerance to benzodiazepines and kindling by FG 7142 are associated with different changes in GABA receptor function.

Animals↗