Department of Physiology, University of Massachusetts Medical Center, Worcester, Massachusetts, USA.
J Neuroendocrinol. 1990 Apr 1;2(2):123-9. doi: 10.1111/j.1365-2826.1990.tb00841.x.
Abstract It is well established that flank marking behavior in the Golden hamster is controlled by vasopressin-sensitive neurons localized to the anterior hypothalamus; however, the source(s) of vasopressinergic innervation to this area is unknown. Previous analysis by immunocytochemistry showed distinct populations of vasopressinergic magnocellular neurons localized to the supraoptic nucleus, paraventricular nucleus and the nucleus circularis that did not project to the neurohypophysis. In the present study, these same hypothalamic nuclei were lesioned by microinjection of kainic acid to determine which, if any, of these populations of vasopressin neurons are involved in the control of flank marking. Unilateral lesions in the areas of the nucleus circularis and supraoptic nucleus at the rostro-caudal plane of the anterior hypothalamus abolished odor-induced flank marking behavior. Lesions in the paraventricular nucleus at the level of the anterior hypothalamus did not consistently inhibit flank marking, while lesions of magnocellular neurons rostral or caudal to the anterior hypothalamus were ineffective. The microinjection of vasopressin into the anterior hypothalamus following lesion of the paraventricular and supraoptic nuclei stimulated flank marking, evidence that treatment with kainic acid did not damage the efferent component of this behavior. However, animals with lesions in the nucleus circularis did not respond to the microinjection of vasopressin; hence, it is uncertain whether lesions in this area disrupt vasopressinergic innervation to the anterior hypothalamus or simply destroy the motor neurons controlling flank marking. In summary, the data clearly demonstrate that vasopressin neurons localized primarily to the medial aspect of the supraoptic nucleus are necessary for sensory integration of odor-induced flank marking, and as such, may be one possible source of neurotransmitter controlling this behavior.
众所周知，金黄仓鼠的侧腹斑纹行为是由位于下丘脑前部的血管加压素敏感神经元控制的；然而，该区域的血管加压素能神经支配的来源尚不清楚。免疫细胞化学分析先前显示，定位于视上核、室旁核和环状核的血管加压素大细胞神经元有明显的群体，但这些神经元不投射到神经垂体。在本研究中，通过微注射海人酸对这些下丘脑核进行了损伤，以确定这些血管加压素神经元群体中，是否有任何一个参与了侧腹斑纹的控制。在前下丘脑的头尾部平面处，对环状核和视上核区域的单侧损伤消除了气味诱导的侧腹斑纹行为。在前下丘脑水平的室旁核损伤并不一致地抑制侧腹斑纹，而在前下丘脑的头侧或尾侧的大细胞神经元损伤则无效。在损伤室旁核和视上核后，将血管加压素微注射到前下丘脑会刺激侧腹斑纹，这表明用海人酸处理不会损害该行为的传出成分。然而，在环状核损伤的动物对血管加压素的微注射没有反应；因此，尚不确定该区域的损伤是否破坏了对前下丘脑的血管加压素能神经支配，还是仅仅破坏了控制侧腹斑纹的运动神经元。总之，这些数据清楚地表明，主要位于视上核内侧的血管加压素神经元是气味诱导的侧腹斑纹感觉整合所必需的，因此，它们可能是控制这种行为的神经递质的一个可能来源。
