Hileman S M, Kuehl D E, Jackson G L
Department of Veterinary Biosciences, University of Illinois, Urbana 61802, USA.
J Neuroendocrinol. 1998 Aug;10(8):587-92. doi: 10.1046/j.1365-2826.1998.00243.x.
This study tested the hypothesis that photoperiod affects the ability of testosterone to reduce proopiomelanocortin (POMC) mRNA levels in the arcuate nucleus and luteinizing hormone-releasing hormone (LHRH) mRNA levels in both the preoptic area (POA) or medial basal hypothalamus (MBH). Twenty castrated male sheep were assigned to one of four treatment groups (i): short days (SD; n=5) (ii), short days with testosterone (SD+T; n=5) (iii), long days (LD; n=5), or (iii) long days with testosterone (LD+T; n=5). Blood samples were collected twice weekly for the last 3 weeks of photoperiod treatment and assessed for LH to validate the response to photoperiod. After evaluating LH levels, one animal each from the LD+T and SD+T groups was excluded from the analyses. Mean concentrations of LH were lower (P<0.01) in the LD+T group than in the other treatment groups, which did not differ (P>0.10) from each other. Neither POA nor MBH LHRH mRNA levels were affected (P>0.10) by treatment. Conversely, POMC mRNA levels were suppressed (P<0.01) in the LD+T males compared with the other treatment groups which did not differ (P>0.10) from each other. These observations suggest that photoperiod specific, testosterone-induced alterations in LHRH mRNA levels are not a mechanism whereby testosterone suppresses LHRH release, and that increased beta-endorphin synthesis and release do not mediate testosterone-induced seasonal suppression of LHRH release.
光周期会影响睾酮降低弓状核中阿片-促黑素皮质素原(POMC)mRNA水平以及视前区(POA)或内侧基底下丘脑(MBH)中促黄体生成素释放激素(LHRH)mRNA水平的能力。将20只去势雄羊分配到四个治疗组之一:(i)短日照(SD;n = 5);(ii)短日照加睾酮(SD+T;n = 5);(iii)长日照(LD;n = 5);或(iii)长日照加睾酮(LD+T;n = 5)。在光周期治疗的最后3周,每周采集两次血样,检测促黄体生成素(LH)以验证对光周期的反应。评估LH水平后,将LD+T组和SD+T组中的各一只动物排除在分析之外。LD+T组的LH平均浓度低于其他治疗组(P<0.01),其他治疗组之间无差异(P>0.10)。治疗对POA和MBH的LHRH mRNA水平均无影响(P>0.10)。相反,与其他治疗组相比,LD+T组雄性的POMC mRNA水平受到抑制(P<0.01),其他治疗组之间无差异(P>0.10)。这些观察结果表明,光周期特异性的、睾酮诱导的LHRH mRNA水平变化不是睾酮抑制LHRH释放的机制,并且β-内啡肽合成和释放的增加不会介导睾酮诱导的LHRH释放的季节性抑制。