Hormonal regulation of diencephalic DA neurons

The TIDA neurons are activated by prolactin. This was first shown by Hokfelt and Fuxe (1972) when they demonstrated that systemic administration of this hormone to rats increased the a-methyltyrosine-induced decline in DA histofluorescence exclusively in the median eminence. Subsequent investigators using quantitative biochemical procedures have demonstrated that systemic and ventricular injections of prolactin increase the activity of TIDA, but not other DA neurons (Moore, 1987b). There is a delay of 12-16 h before the actions of prolactin became evident and at least part of the delay appears to be secondary to processes that involved alterations in gene expression and protein synthesis. 

The two phases of prolactin activation of TIDA neurons (rapid tonic and delayed induction components) suggest that the level of activity of these DA neurons reflects both amount of circulating prolactin at the time of measurement (tonic component) and the past history of blood levels of this hormone (induction component). That is, animals treated chronically in such a way as to maintain high circulating concentrations of prolactin exhibit an exaggerated stimulatory response to acute injections of prolactin. Conversely, chronic hypoprolactinemia causes a reduced response to the acute administration of this hormone (Demarest et al., 1985a). 

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