Corticosteroid Actions on Neurotransmission

Publication Type:

Book Chapter

Source:

Handbook of Neuroendocrinology, Academic Press, San Diego, p.415-431 (2012)

ISBN:

978-0-12-375097-6

DOI Name (links to online publication)

10.1016/B978-0-12-375097-6.10018-6

Abstract:

Publisher Summary Neural communication mediated by corticosteroid hormones is essentially different from signal transduction through classical neurotransmitters. The second is the glucocorticoid receptor (GR), with an approximately 10-fold lower affinity for corticosterone and cortisol. This receptor is quite ubiquitous in its distribution, although particularly high expression levels are seen in the hippocampal CA1 area and dentate gyrus, and in the main feedback site, the paraventricular nucleus (PVN) of the hypothalamus. Functional read-outs of all of these in vivo experiments are the firing rate of single neurons, or the amplitude and slope of field potentials. In many cases, these parameters are linked to the functionality of glutamatergic synapses, but the exact mechanism of action is hard to determine from these indirect measures. The enhanced influx of calcium is probably coupled to a decreased extrusion. A high dose of glucocorticoids was found to significantly reduce expression of the plasma membrane calcium pump isoform 1 (PMCA1), a plasma membrane calcium ATPase.

18/01/2013