The exact role and function of the CNS is extremely complex and, despite decades of research, still not clearly understood. Malfunction of the basal ganglia has been implicated in several diverse neurological disorders such as Alzheimer’s disease, hemiballism and of most interest to this study, Parkinson’s disease. The main topic of this thesis is the substantia nigra and, in particular, the apparent relationship between dopamine and acetylcholinesterase in this region. An understanding of the mechanisms that influence the development and regeneration of the dopaminergic neurons of the nigro-striatal pathway is of particular importance since it is the death of these neurons that causes Parkinson’s disease. Numerous neurotransmitter or neuromodulator substances are found in the CNS, the distribution, fibre connections and ultrastructure of the peptidergic system have been explored, though little is known about their function. Colocalisation of classical neurotransmitters and neuropeptides is a widely accepted feature of neurons in many parts of the CNS. The materials and methods chapter provides a detailed account of the experimental procedures used in this thesis. Particular reference is made to the on-line chemiluminescent system, as this procedure is not used outside Prof. Dr. S.A. Greenfield’s laboratory. The experimental chapters presented in this thesis fall into three main sections. The first set of experiments determine whether a relationship exists between dopamine, the regulation of AChE- release in the substantia nigra of the rat and concomitant behaviour following different drug stimulations in naive and 6-OHDA lesioned rats. The experiments indicated that different drug stimulations in naive animals and in 6-OHDA animals have an influential effect on the release of AChE and behaviour. In addition, the local or systemic application of amphetamine significantly increased the spontaneous release of AChE in the substantia nigra and concomitant behaviour in naive animals. Apomorphine, quinpirole and NMDA showed a lesser effect. Neurotoxin pre-treatment significantly reduced AChE-release in the substantia nigra and dopamine content of the ipslateral striatum. Amphetamine applied locally to lesioned animals showed no significant increase in the release of AchE, but did produce a significant return from robust basal circling to normal behaviour. In contrast to this, the systemic application of amphetamine increased the release of AChE and the level of both contraversive and ipsiversive circling behaviour. Sham-operated animals showed results similar to those achieved with the naive animals. In the second study, a new animal model was established using (E18) embryonic chicks (Gallus gallus domesticus), the aim of which was to determine the development of mid-brain dopaminergic neurons in organotypic slice culture and the development and regeneration of chick dopaminergic neurons of the ventral mesencephalon. It was possible to culture single ventral mesencephalon slices of the chick. Cultures were stained for tyrosine hydroxylase. When the culture medium was supplemented with AChE, the level of growth in tyrosine hydroxylase-immunoreactive neurites was not changed. Addition of a specific inhibitor of AChE, BW284c51, caused cell death. In the discussion chapter, the general findings and conclusions of this thesis are discussed in the light of previously published work. Furthermore, the possible role and function of the relationship between the dopaminergic and cholinergic systems are suggested, and future proposals are made regarding continued research which would both extend and clarify further the findings of this thesis.