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Biomedical subjects

J C Gilbert

Publications and source records attributed to J C Gilbert.

At least 55 records · Page 3Linked to original sources
PubMed1982

The effects of dopamine agonists and antagonists on Na+,K+-ATPase and Mg2+-ATPase activities of synaptosomes.

The effects of dopamine agonists and antagonists on the Na+,K+-ATPase and Mg2+-ATPase activities of rat cerebral cortex synaptosomes have been determined. Dopamine, ADTN, apomorphine and S-584, but not piribedil, stimulated the activities of the enzymes. The stimulatory effect of dopamine was not antagonised by dopamine antagonists and apparently the catechol group is responsible for the enzyme stimulation.

Adenosine Triphosphatases↗
PubMed1980

The relationship between nerve terminal adenosine triphosphatases and neurotransmitter release: as determined by the use of antidepressant and other CNS-active drugs.

1 The role of adenosine triphosphatases (ATPases) in neurotransmitter release was studied using nerve terminals (synaptosomes) prepared from rat cerebral cortex as a model. 2 Amitriptyline, nortriptyline, protriptyline, desipramine and imipramine were found to inhibit ATPases at concentrations of 10(-5) M and above. The drugs inhibited both the basal and electrically evoked release of acetylcholine (ACh) and noradrenaline (NA) at concentrations of 10(-4) M and above. 3 At low concentrations of antidepressants (10(-8) and 10(-7) M) release of NA was enhanced but there was no effect on ACh release. 4 Other drugs which inhibit Na+, K+-ATPase increase basal NA release as did drugs which inhibited vesicular MG2+-ATPase. 5 A model is proposed suggesting that transmitter release/re-uptake depends on (1) active Na+, K+-ATPase at the presynaptic membrane and (2) an active synaptic vesicular MG2+-ATPase.

Acetylcholine↗
PubMed1980

[Beta blockers and disturbances of the microcirculation (author's transl)].

Study of 192 cases of hypertensive patients, 89 of whom were treated by diet, general advice and correction of risk factors for an average period of 8 months. The group of patients treated beta blockers consisted of 103 subjects, 28 of whom received Propranolol, 29 Oxyprenolol, 20 Atenolol and 26 Practolol. The prevalence of Raynaud's phenomenon was markedly greater in the patients treated with beta blockers, in comparison with the group not receiving any drugs. The highest incidence of vasomotor problems was seen in the group of subjects treated with Propranolol, with 57% of patients having a Raynaud-type paroxysmal acrosyndrome. In more than half of the cases attributed to Propranolol, the clinical picture of Raynaud's syndrome was severe. Discussion of the mode of action of beta blockers on the microcirculation.

Adrenergic beta-Antagonists↗
PubMed1980

Stimulation and inhibition of synaptosome ATPases by noradrenaline. The involvement of cytoplasmic factor.

The activity of Na+, K+-ATPase was determined in synaptosomes and in pellets, (containing membranes, mitochondria and vesicles) and cytoplasm prepared from synaptosomes from rat cerebral cortex. The activity of the pellets was more than two fold higher than that of the synaptosomes or of their components and adding back the cytoplasm reduced the activity of the pellets. Noradrenaline did not affect the activity of the pellets but increased that of the synaptosomes in a dose-dependent fashion. It inhibited the activity of the membranes. Results indicate that synaptosomal Na+, K+-ATPase activity is low because of a factor in the cytoplasm and this factor is not present in synaptosome pellets. NA antagonises the activity of the factor.

Animals↗
PubMed1979

An investigation into the roles of synaptic vesicular Mg++-ATPase in neurotransmitter release, using benzhydryl piperazines.

A series of benzhydryl piperazines was found to inhibit synaptic vesicular Mg++-ATPase. These compounds were also found to increase basal and evoked release of noradrenaline from synaptosomes. A comparison was made between the concentrations effective in inhibiting the enzyme and promoting noradrenaline release. In general, as the degree of Mg++-ATPase inhibition increased, noradrenaline release was increased. The relevance of these findings to a possible role of Mg++-ATPase in noradrenaline release is discussed.

Acetylcholine↗
PubMed1977

Effects of delta9-tetrahydrocannabinol and cannabidiol on a Mg2+-ATPase of synaptic vesicles prepared from rat cerebral cortex.

1. delta9-Tetrahydrocannabinol and cannabidiol both exhibited a concentration-related inhibition of Mg2+-ATPase of vesicles prepared from synaptosomes isolated from rat cerebral cortex. Cannabidiol was about 3 times more potent than tetrahydrocannabinol. 2. These results were similar to those obtained previously using drugs with well established anticonvulsant activity. 3. Tetrahydrocannabinol at a sub-inhibitory concentration (1 micronM) increased the activity of the Mg2+-ATPase relative to values obtained with vehicle controls.

Adenosine Triphosphatases↗