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Abstract
THE catecholaminergic neurones of the mammalian brain are generally believed to be important in the control of voluntary behaviour and affect. The evidence for this comes from work with pharmacological agents which enhance or block the post-synaptic effects of noradrenergic or dopaminergic neurones1–3. This has led to speculations implicating central catecholaminergic dysfunction in affective disorders such as depression1,4,5 and in other disorders such as Parkinson's disease6 and schizophrenia7,8. But research on the behavioural effects in animals of pharmacological interference with the normal functions of central catecholamines has been hindered by the fact that the sudden withdrawal of either noradrenaline or dopamine leads to behavioural sedation and inactivity9–14, which precludes any fine analysis of behavioural deficits.
Published Version
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