Expression and Region-Specific Regulation of the Oxytocin Receptor Gene in Rat Brain¹

May 1, 1997Endocrinology

Patterns and brain area–specific control of the oxytocin receptor gene in rats

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Abstract

An 8-fold increase in oxytocin receptor mRNA levels was observed following estrogen treatment in specific brain regions.

Oxytocin receptors are localized to distinct brain regions, including the hypothalamus and amygdala.
Two specific mRNA bands for oxytocin receptors were identified in these brain regions, corresponding to those found in the rat uterus.
Estrogen treatment resulted in an 8-fold increase in oxytocin receptor mRNA levels in estrogen-sensitive areas.
Progesterone did not affect oxytocin receptor mRNA levels when administered alone or influence the estrogen-induced increase.
Tamoxifen acted as a partial agonist, raising oxytocin receptor mRNA levels in the hypothalamus, but suppressed the estrogen-induced increase in some brain regions.
The findings suggest region-specific regulation of oxytocin receptor gene expression related to steroid hormone levels.

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The neuropeptide oxytocin (OT) exerts its various neurotransmitter functions via specific OT receptors (OTRs) that have been localized to distinct brain regions, including the ventromedial hypothalamus, the bed nucleus of stria terminalis, the amygdala, the subiculum, the hippocampus, and the olfactory nuclei. In the present study, we have characterized OTR gene expression by Northern blot and by semiquantitative RT-PCR in these brain regions and studied its regulation in response to estrogen (E2), progesterone, and the antiestrogen tamoxifen. We find that all regions analyzed express two messenger RNA (mRNA) bands (6.7 and 4.8 kb) that hybridize to a rat OTR complementary DNA probe and that correspond in size to two of the three OTR mRNA bands expressed in rat uterus. Analysis by RT-PCR, with two different primer pairs, did not reveal any structural differences between the coding regions of uterine and brain OTR mRNA. E2 treatment and gestation led to an 8-fold and a 6.5-fold increase in OTR mRNA levels, respectively. Progesterone was without effect, if administered alone, and did not influence the E2-induced rise in OTR mRNA. The E2 effect was restricted to E2-sensitive regions, such as the hypothalamus, and was not observed in the subiculum or the olfactory nuclei. Tamoxifen had a dual effect: on the one hand, it acted as a partial agonist in raising OTR mRNA levels in the hypothalamus of ovariectomized animals; on the other hand, it suppressed the E2-induced OTR mRNA rise in E2-sensitive brain regions. Although the present data do not exclude the possible existence of OTR subtype(s) in brain, they show that the uterine-type OTR gene is expressed in all major OTR-containing brain regions. Moreover, they show that region-specific regulation of OTR gene expression underlies the previously observed region-specific steroid regulation of central OT binding sites.

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Expression and Region-Specific Regulation of the Oxytocin Receptor Gene in Rat Brain¹

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