By O. Hornykiewicz (auth.), Professor Gaetano Di Chiara (eds.)
Dopamine was once before everything considered as a trifling precursor of noradrenaline, yet has steadily won its current prestige of a typical goal for significant drug sessions and a substrate for a few easy services and dysfunctions of the primary apprehensive procedure. The medical curiosity has shifted from in general motor parts of the striatum to typically limbic ones because the nucleus accumbens and its afferent components, the prefrontal cortex, the hippocampal formation and the basolateral amygdala. This double quantity offers a scientific account of the anatomy, body structure, neurochemistry, molecular biology and behavioural pharmacology of dopamine within the CNS. - the 1st quantity offers with the historical past of dopamine, the anatomy of dopamine neurons, the biochemistry and molecular biology of dopamine uptake websites and of dopamine receptors.
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Extra info for Dopamine in the CNS I
Dopamine and Striatal Neurotransmitter Interactions Until the introduction of the L-dopa treatment of PD, the only (moderately) effective anti-Parkinson's drugs were the anticholinergics. Immediately after the discovery of DA's pivotal role in PD, the concept of a brain DA-acetylcholine interrelationship was developed (MCGEER et al. 1961b; BARBEAU 1962). In PD, the reduction of striatal DA (corrected with L-dopa) was proposed to result in a cholinergic overactivity (responding to anticholinergics).
Brain Dopamine: A Historical Perspective 11 PD the striatum developed a denervation supersensitivity to DA. This required the existence of specific DA receptors and their up-regulation after dopaminergic denervation. For the idea of a specific DA receptor, as for DA itself, the first difficulty was to free itself conceptually from the near-reflex connection, and confusion, with NA. The possibility of DA acting (in the crayfish preparation) on "a type of [inhibitory] receptor for catecholamines" different from the inhibitory receptor for y-aminobutyric acid (GABA), was first raised in print in 1961 (MCGEER et a1.
Rather, our results suggested that at least the hypotensive action was due to an effect on catecholamines and that this effect was caused by depletion rather than release. Unfortunately, this divergence of opinion was to place my mentors and myself in different "camps" for many years to come and led to a large number of sometimes very intense debates, in writing as well as at various meetings. This was especially unfortunate, because we, despite these divergences, were much more on common ground than a great number of other workers in this field, as will be apparent in the following.