By M. Diana, J. M. Tepper (auth.), Professor Gaetano Di Chiara (eds.)
Dopamine was once in the beginning considered as an insignificant precursor of noradrenaline, yet has steadily won its current prestige of a standard goal for significant drug sessions and a substrate for a few easy services and dysfunctions of the critical frightened procedure. The medical curiosity has shifted from quite often motor components of the striatum to often 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 second one quantity offers with practical and behavioural features because the electrophysiology of dopamine neurons and of dopamine activities, the interplay with different transmitters and its position in behaviour and within the motion of centrally appearing medicinal drugs.
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Extra info for Dopamine in the CNS II
1995; PALADINI and TEpPER 1999). This latter effect appears due to increased GABA release as a result of blockade of the presynaptic GABAB receptors discussed above. This results in increased stimulation of postsynaptic GABA A receptors on dopaminergic neurons and decreased burst firing, probably due to the GABAA-mediated decrease in input resistance (CANAVIER 1999; PALADINI et al. 1999b). Subsequent experiments revealed that a significant source of the GABAergic input that was blocked by bicuculline or picrotoxin resulting in burst firing was the pars reticulata, and that the reticulata efferents could be effectively modulated by output from the globus pallidus (CELADA et al.
1979; GARIANO and GROVES 1988). No attempts to block the bursts with glutamate antagonists were made and given the long latency, mediation by a monosynaptic glutamatergic input from cortex seemed unlikely. Soon after, inactivating the prefrontal cortex by local cooling was shown to abolish bursting and induce pacemaker-like firing in dopami- 16 M. DIANA and 1M. TEPPER nergic neurons (SVENSSON and TUNG 1989). On the other hand, lesions of medial prefrontal cortex were largely without effect on the spontaneous activity of substantia nigra dopaminergic neurons, although there was a significant reduction in the number of VTA neurons encountered per track (SHIM et al.
1982) and VTA dopaminergic neurons (MEREU et al. 1987) together with an increment in burst firing of dopaminergic neurons (GRENHOFF et al. 1986). It is interesting to note that the increase in firing rate and increase in burst firing were only poorly correlated, suggesting a possible nicotinic effect on firing pattern independent of its effect on firing rate (GRENHOFF et al. 1986). Dopaminergic neurons also express muscarinic receptors, and are depolarized by muscarinic agonists in vitro with a pharmacological profile resembling that of the M J receptor, although the mechanism of the response appears different from that of the classic m-current closure of potassium channels (LACEY 1993).