Ferris C F, Delville Y, Brewer J A, Mansour K, Yules B, Melloni R H
Psychiatry Department, University of Massachusetts Medical Center, Worcester 01655, USA.
J Neurobiol. 1996 Jun;30(2):192-204. doi: 10.1002/(SICI)1097-4695(199606)30:2<192::AID-NEU2>3.0.CO;2-0.
Golden hamsters start displaying flank marking behavior (a form of scent marking) around postnatal day 20 (P-20). Because the behavior is dependent upon the central activity of arginine vasopressin (AVP), the present study was conducted to correlate this activation with changes in the vasopressinergic system. A first set of experiments was performed to compare flank marking activity between P-18 and P-22. A second set of experiments was performed to compare the density of AVP receptors between the age periods and assess responsiveness to AVP microinjection. Finally, a third set of experiments incorporated immunocytochemistry, radioimmunoassay, in situ hybridization, and Northern blot analysis to determine the location and numbers of AVP immunoreactive neurons and the level of mRNA correlating with the developmental onset of flank marking behavior. Our results show that flank marking develops between P-18 and P-22. Male and female hamsters do not display odor-induced flank marking anytime before P-19. However, all animals show odor-induced flank marking by P-22. The onset of flank marking does not appear to be associated with any change in AVP receptor binding in the anterior hypothalamus. Indeed, flank marking can be triggered in hamsters on P-18 by the microinjection of AVP in the anterior hypothalamus. This would suggest that the postsynaptic mechanisms contributing to the transduction of the AVP signal and the motor control of flank marking are intact prior to the onset of odor-induced flank marking. In contrast, AVP levels in the hypothalamus and pituitary increase by two to threefold between P-18 and P-22, suggesting that changes in AVP synthesis and release from presynaptic sites may contribute to the onset of flank marking. Interestingly, there is no change in AVP mRNA between P-18 and P-22, which raises questions about posttranslational processing during this developmental period. These results suggest that heightened synthesis and release of AVP between P-18 and P-22 may contribute to the developmental onset of flank marking.
金黄地鼠在出生后第20天（P-20）左右开始表现出胁腹标记行为（一种气味标记形式）。由于该行为依赖于精氨酸加压素（AVP）的中枢活性，因此进行了本研究以将这种激活与加压素能系统的变化相关联。进行了第一组实验以比较P-18和P-22之间的胁腹标记活动。进行了第二组实验以比较不同年龄段之间AVP受体的密度，并评估对AVP微量注射的反应性。最后，第三组实验采用免疫细胞化学、放射免疫测定、原位杂交和Northern印迹分析来确定AVP免疫反应性神经元的位置和数量以及与胁腹标记行为发育起始相关的mRNA水平。我们的结果表明，胁腹标记行为在P-18和P-22之间发育。雄性和雌性地鼠在P-19之前的任何时候都不会表现出气味诱导的胁腹标记行为。然而，到P-22时，所有动物都表现出气味诱导的胁腹标记行为。胁腹标记行为的起始似乎与下丘脑前部AVP受体结合的任何变化无关。事实上，通过在下丘脑前部微量注射AVP，可以在P-18的地鼠中触发胁腹标记行为。这表明在气味诱导的胁腹标记行为起始之前，有助于AVP信号转导和胁腹标记运动控制的突触后机制是完整的。相比之下，下丘脑和垂体中的AVP水平在P-18和P-22之间增加了两到三倍，这表明突触前部位AVP合成和释放的变化可能有助于胁腹标记行为的起始。有趣的是，P-18和P-22之间AVP mRNA没有变化，这引发了关于这个发育时期翻译后加工的问题。这些结果表明，P-18和P-22之间AVP合成和释放的增加可能有助于胁腹标记行为的发育起始。
