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Biomedical subjects

J Vetulani

Publications and source records attributed to J Vetulani.

At least 127 records · Page 7Linked to original sources
PubMed1978

Effect of clonidine, amphetamine, and their combinations on the locomotor activity of CD-1 and C57BL/6 mice.

Clonidine inhibited the exploratory motor activity of C57BL/6 mice non-habituated to the testing conditions. In CD-1 mice clonidine did not depress exploratory activity but did elevate the basal locomotor activity of animals both non-habituated and habituated to testing conditions. Amphetamine increased the locomotor activity of many C57BL/6 mice and conversely inhibited the locomotion of many CD-1 mice. In both strains, amphetamine in doses up to 2 mg/kg was unable to alter effects produced by clonidine. Results suggest that the locomotor activity of C57BL/6 mice is more sensitive than that of CD-1 mice to drugs affecting the central noradrenergic system.

Amphetamine↗
PubMed1978

The influence of pharmacological agents on the accumulation of egzogenic noradrenalin in nervous tissue cultivated in vitro. I. Effect of desipramine.

The authors investigated absorption of noradrenalin by neurons and glia cells cultivated in vitro. Material was taken from locus coreuleus of 3, 6, 12, 18, 24, and 36 days old rats. On the basis of observations, the authors found out that absorption of egzogenic noradrenalin changes with the growth of animals. In animals less than 24 days old, noradrenalin is absorbed not only by neurons but also by glia cells. Desipramin affects the egzogenic noradrenalin absorption clearly over the 12th day of life.

Absorption↗
PubMed1977

Effect of clonidine on the noradrenergic cyclic AMP generating system in the limbic forebrain and on medial forebrain bundle self-stimulation behavior.

The present results show that clonidine does not mimic the agonist action of norepinephrine (NE) on the noradrenergic cyclic AMP generating system of the limbic forebrain, but antagonizes the stimulatory effect of NE while not influencing the action of isoprenaline. In self-stimulation behavior, clonidine decreases responding and blocks the facilitation caused by d-amphetamine.

Adenosine Monophosphate↗
PubMed1977

Improvement of shuttle-box performance of mice by combinations of benzodiazepines and morphine given during training.

Chlorodiazepoxide, diazepam and morphine, given alone or in combination, were tested in naive mice subjected to five 100-trial avoidance sessions in the shuttle-box. When given alone before each training session all three drugs improved avoidance behaviour. However, facilitation of avoidance responding was much more evident when either benzodiazepine derivative was given in combination with morphine.

Animals↗
PubMed1976

A possible common mechanism of action of antidepressant treatments: reduction in the sensitivity of the noradrenergic cyclic AMP gererating system in the rat limbic forebrain.

The response of the noNEpinephrine (NE) sensitive cyclic AMP generating system in slices of the rat limbic forebrain after both the acute and chronic administration of the tricyclic antidepressants desipramine (DMI) and iprindole as well as electro-convulsive treatment (ECT) was investigated. Neither the basal level of cyclic AMP nor the hormonal response to NE were altered after administration of a single dose of short term treatment with DMI and iprindole. However, the administration of the antidepressants on a clinically more relevant time basis markedly reduced the sensitivity of the cyclic AMP generating system to NE. This change in sensitivity was not related to the levels of the drugs in brain. The response of cyclic AMP to NE was also reduced by ECT, but the onset of this action was shorter than that observed with the antidepressants. ECT also antagonized the enhanced response of cyclic AMP to NE following destruction of central adrenergic nerve terminals with 6-hydroxydopamine. It thus appears that the therapeutic action of tricyclic antidepressants could be related to postsynaptic adaptive changes in the sensitivity of the noradrenergic adenylate cyclase receptor system rather than to acute presynaptic events.

Animals↗
PubMed1976

The noradrenergic cyclic AMP generating system in the limbic forebrain: pharmacological characterization in vitro and possible role of limbic noradrenergic mechanisms in the mode of action of antipsychotics.

The cyclic AMP generating system in slices of the rat limbic forebrain was investigated. In consists of: (u) A noradrenergic system which responds to norepinephrine (NE) and isoproterenol. Though the rise of the nucleotide elicited by isoproterenol is more rapid than that caused by NE, the maximal effect is less than half of that induced by NE; (2) an adenosine-dependent system. The noradrenergic cyclic AMP generating system in the limbic forebrain displays a number of properties of a central NE receptor: it develops supersensitivity to NE and isoproterenol following prolonged deprivation of NE at postsynaptic sites (chronic treatment with reserpine or chemosympathectomy with 6-hydroxydopamine). When noradrenergic terminals are protected from 6-hydroxydopamine by desmethylimipramine, the responses to NE are not enhanced. Responses to NE are blocked by both propranolol and phentolamine, while responses to isoproterenol are blocked by propranolol but not by phentolamine. The adenosine-dependent system does not develop supersensitivity after central chemosympathectomy and is not blocked by either alpha- or beta-antagonists. While not altering the basal level of the nucleotide, clinically effective antipsychotic drugs caused a dose-dependent inhibition of the limbic noradrenergic cyclic AMP response with clozapine and pimozide being particularly potent (IC50 0.06 and 0.08 muM, respectively). Antipsychotic drugs do, however, not affect cyclic AMP responses elicited by adenosine. The results are compatible with the view that the central NE receptor is closely related to or may be an integral part of an adenylate cyclase system and that its blockade in the limbic forebrain by antipsychotic drugs may contribute to their therapeutic action.

Adenosine↗
PubMedDate not supplied

Recognition cue in the rat's social memory paradigm.

The cue used by an adult resident rat for recognition of a just met juvenile in the social memory paradigm was assessed by manipulating the amount of olfactory information and enhancing the recognition with arginine8-vasopressin (AVP). Social recognition was impaired in anosmic resident rats, suggesting that the recognition cue is olfactory in nature. Washed juveniles were recognized by AVP but not placebo treated residents, independently of whether after washing they were marked with previously collected urine of the residents or not. Preputialectomized juveniles were recognized neither by placebo nor by AVP treated residents. The results suggest that the scents originating from the preputial gland of the juvenile serve as the recognition cue in the social memory paradigm of rats.

Animals↗