Autonomic-affective dysfunctions

Abstract

As we have repeatedly emphasised, the right balance between the various systems of neurotransmitter amines and neuropeptides is the essential precondition for our normal state of mind, and this balance is maintained by a variety of feedback mechanisms. As a clinical example we might mention the striatonigral GABA system. The neurotransmitter GABA travels to the substantia nigra via GABA-ergic nerve tracts. There GABA blocks the activity of DA in the nerve cells of the substantia nigra, and therefore the transport of DA to the striatum. If the level of DA is too low, then there is a negative feedback control mechanism which inhibits GABA-ergic activity. The resulting fall in the concentration of GABA in the cells of the substantia nigra increases the availability of DA in the striatum. In Parkinson’s disease the stimulation of DA synthesis in the cells of the substantia nigra improves the patient’s akinesia. Conversely, too great an activity in the striatum similarly causes a feedback-regulation of GABA-ergic activity.