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Biomedical subjects

J C Stoof

Publications and source records attributed to J C Stoof.

120 records · Page 7Linked to original sources
PubMed1978

Changes in the behavioral response to a novel environment following lesioning of the central dopaminergic system in rat pups.

During the third week of life, a hyperactive period for laboratory rat, the occurrence of 8 behavioral categories was recorded in individual littermates transferred to a novel environment. Neonatal destruction of the catecholaminergic system by intraventricular injection of 6-OH-DA resulted in increased motor activity during the third week of life. Selective lesioning of the dopaminergic system by the combined treatment of 6-OH-DA + desmethylimipramine also induced a significant increase in some active behavioral categories. It appeared that in contrasts to the gross behavioral sequence, as seen in controls, which compromised locomotion and rearing leads to grooming leads to sitting and lying down, the lesioned animals showed a prolonged phse of restless locomotion. These data are interpreted as a disability to habituate adequately to a novel environment after neonatal lesioning of the dopaminergic system.

Aging↗
PubMed1977

Increased dopamine release from rat striatal slices by inhibitors of GABA-aminotransferase.

The effects were examined of two inhibitors of GABA-aminotransferase, amino-oxyacetic acid (AOAA) and RMI-71645-16, on depolarization-induced (30 mM K+) dopamine (DA) release from rat striatal slices. When added to the medium, these drugs increased the release of radiolabeled DA, either accumulated by high-affinity uptake or synthesized from 14C-tyrosine. AOAA did not modify the release of 14C-acetylcholine from striatal slices or 3H-noradrenaline from cortical slices. Moreover, 3H-DA release from substantia nigra was not affected. The data suggest the possibility that the effects of GABA-T inhibitors on striatal DA release are mediated by intrinsic GABA-ergic neurons.

4-Aminobutyrate Transaminase↗
PubMed1977

Evaluation of the red blood cell cytopherometric test for the diagnosis of multiple sclerosis.

The effect of linoleic acid on the electrophoretic mobility of red blood cells from both MS patients and normal subjects was studied. An extensive statistical evaluation of the data clearly demonstrated that there was no difference in behaviour of red blood cells from patients and normal subjects in the presence of linoleic acid. Even a tendency for the mobility of erythrocytes to be decreased in patients and increased in normal subjects after addition of linoleic acid was not observable.

Electrophoresis↗
PubMed1976

Release and receptor stimulating properties of p-tyramine in rat brain.

Radiolabeled p-tyramine could be released from rat striatal slices, which were previously allowed to accumulate this amine, upon depolarization with media containing 40 mM potassium. This depolarization-induced release did not occur in the absence of calcium ions in the medium and over 75% of the labeled material released was identified chromatographically as tyramine. The possible existence of a direct receptor-stimulating activity of p-tyramine was examined by injecting this amine intraventricularly into rats, after pretreatment with various drugs, which inhibit catecholaminergic function, and measuring their motor activity. If injected into rats, which were pretreated with reserpine or alpha-methyl-p-tyrosine, p-tyramine induced a marked increase in the motor activity, which was not accompanied by a significant decrease in brain catecholamines, ruling out the possibility of indirect receptor stimulation. Since the presence of endogenous p-tyramine in the brain has been reported, these data may indicate a specific synaptic role for this amine, perhaps as a neurotransmitter.

Animals↗
PubMed1975

Reserpine and calcium: interaction at the injection site.

The subcutaneous administration of calcium prior to reserpine prevented the development of the well-known reserpine effects. Pretreatment with other bivalent cations induced a similar effect. The inhibitory effect of reserpine on the in vitro uptake of labelled catecholamines in brain homogenates was also prevented in rats pretreated with bivalent cations. On the other hand when calcium was injected at a site other than that of reserpine, there was no antagonistic effect. The latter results suggest an interaction between bivalent cations and reserpine at the injection site that prevents the systemic absorption of reserpine.

Animals↗
PubMedDate not supplied

Localization and pharmacology of some dopamine receptor complexes in the striatum and the pituitary gland: synaptic and son-synaptic communication.

The striatum receives massive dopaminergic projections from neurons in the ventral tegmental area, the substantia nigra and the retro-rubral cell group. Dopaminergic neurons in the arcuate nucleus and periventricular hypothalamic nuclei project to the median eminence and the neuro-intermediate lobe of the pituitary gland. The anterior lobe of the pituitary gland is not innervated by dopaminergic neurons, but receives dopamine via a vascular route from the median eminence. Two categories of dopamine receptors (D-1 and D-2) can be identified on the basis of the ability of various drugs to discriminate between these two entities. Dopamine stimulates both D-1 and D-2 receptors. The affinity of dopamine for the D-2 receptor is approximately 1000 times higher than for the D-1 receptor. Dopamine is involved in synaptic as well as non-synaptic communication. Examples of non-synaptic communication via D-2 receptors are the dopamine induced inhibition of prolactin release from the anterior pituitary gland and most likely the D-2 receptor mediated inhibition of the release of acetylcholine in the striatum. Examples of synaptic communication have been found in the striatum where (with ultrastructural techniques) synaptic contacts between dopaminergic nerve terminals and elements from cells containing GABA, substance P or enkephalin have been demonstrated. It is tempting to speculate that synaptic and non-synaptic communication occurs via D-1 and D-2 receptors respectively.

Acetylcholine↗