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Biomedical subjects

A Longden

Publications and source records attributed to A Longden.

22 records · Page 2Linked to original sources

Dopamine and schizophrenia.

The antipsychotic actions and extra-pyramidal side-effects of neuroleptic drugs are strongly correlated with their ability to block central dopaminergic transmission. It is argued that the former are more closely related to actions on dopaminergic mechanisms in the "mesolimbic dopamine" system, and the latter to similar actions in the striatum. Although the amphetamine psychosis closely resembles paranoid schizophrenia and may be due to excess dopamine release, clinical, biochemical, and endocrine studies suggest that dopaminergic overactivity is not a necessary concomitant of schizophrenic illnesses. It is suggested that the primary defect in schizophrenia does not lie in the dopamine neuron. It remains to be excluded that the receptors, particularly in the mesolimbic dopamine areas, become supersensitive, or that there is a deficit in a system which normally acts in antiagonism to the to the mesolimbic dopamine system.

Animals↗

Effects of nicotine on plasma corticosterone and brain amines in stressed and unstressed rats.

The administration of nicotine (0.4 mg/kh) to unstressed rats caused a rise in plasma corticosterone which persisted for 60 minutes and a fall in hippocampal 5-hydroxytryptamine (5-HT) at 45 minutes followed by a rise at 60 minutes. In rats which were stressed by being placed on an elevated platform, nicotine caused a reduction in hippocampal 5-HT at 45 and 75 minutes but did notaffect the plasma corticosterone concentration. Rats studied 16 hours after the last injection of a course of treatment with metypone had much reduced levels of plasma corticosterone and hippocampal 5-HT. Under the present conditions metyrapone also much diminished the effects of nicotine on plasma corticosterone levels in unstressed rats but had little effect on the response to stress.

Animals↗

Effects of bradykinin on PC-12 cell differentiation.

PC-12 cells are used as a model for neuronal differentiation because they assume a neuronal phenotype, including the extension of neurites, when exposed to nerve growth factor (NGF). The present results show that bradykinin (BK) also causes PC-12 cells to extend neurites. In addition, BK potentiates the neurite-extending effect of nerve growth factor (NGF), an action which is attenuated by a BK antagonist. The potentiation of neurite extension produced by the combination of BK and NGF may be mediated at the receptor level, as indicated by an NGF-induced alteration of BK binding.

Animals↗