Systematic review of gamma-aminobutyric-acid inhibitory deficits across the reproductive life cycle.

Deficiencies in the inhibitory functioning of gamma-aminobutyric acid (GABA) have been implicated in the pathophysiology of depressive disorders. Reproductive life cycle events, including menstruation, pregnancy, and menopause, are consistently associated with increased psychopathology, in particular mood disorders. Given that GABA-inhibitory activity may be modulated directly or indirectly by estrogen, progesterone, and their metabolites receptors, it has been hypothesized that GABA deficits may be evident during these reproductive periods.

Variable sensitivity to noxious heat is mediated by differential expression of the CGRP gene.

Heat sensitivity shows considerable functional variability in humans and laboratory animals, and is fundamental to inflammatory and possibly neuropathic pain. In the mouse, at least, much of this variability is genetic because inbred strains differ robustly in their behavioral sensitivity to noxious heat. These strain differences are shown here to reflect differential responsiveness of primary afferent thermal nociceptors to heat stimuli.

The heritability of antinociception: common pharmacogenetic mediation of five neurochemically distinct analgesics.

The heritability of nociception and antinociception has been well established in the mouse. The pharmacogenetics of morphine analgesia are fairly well characterized, but far less is known about other analgesics. The purpose of this work was to begin the systematic genetic study of non-mu-opioid analgesics.