Department of Pharmacology of the School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil,
Department of Pharmacology of the School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil.
Neuroendocrinology. 2020;110(1-2):10-22. doi: 10.1159/000500160. Epub 2019 Jun 18.
Acute restraint stress (RS) has been reported to cause neuronal activation in the supraoptic nucleus of the hypothalamus (SON). The aim of the study was to evaluate the role of SON on autonomic (mean arterial pressure [MAP], heart rate [HR], and tail temperature), neuroendocrine (corticosterone, oxytocin, and vasopressin plasma levels), and behavioral responses to RS.
Guide cannulas were implanted bilaterally in the SON of male Wistar rats for microinjection of the unspecific synaptic blocker cobalt chloride (CoCl2, 1 mM) or vehicle (artificial cerebrospinal fluid, 100 nL). A catheter was introduced into the femoral artery for MAP and HR recording. Rats were subjected to RS, and it was studied the effect of microinjection of CoCl2 or vehicle into the SON on pressor and tachycardic responses, drop in tail temperature, plasma oxytocin, vasopressin, and corticosterone levels, and anxiogenic-like effect induced by RS.
SON pretreatment with CoCl2 reduced the RS-induced MAP and HR increase, without affecting the RS-evoked tail temperature decrease. Microinjection of CoCl2 into areas surrounding the SON did not affect RS-induced increase in MAP and HR, reinforcing the idea that SON influences RS-evoked cardiovascular responses. Also, SON pretreatment with CoCl2 reduced RS-induced increase in corticosterone and oxytocin, without affecting vasopressin plasma levels, suggesting its involvement in RS-induced neuroendocrine responses. Finally, the CoCl2 microinjection into SON inhibited the RS-caused delayed anxiogenic-like effect.
The results indicate that SON is an important component of the neural pathway that controls autonomic, neuroendocrine, and behavioral responses induced by RS.
急性束缚应激（RS）已被报道会导致下丘脑视上核（SON）中的神经元激活。本研究旨在评估 SON 在自主神经（平均动脉压 [MAP]、心率 [HR] 和尾巴温度）、神经内分泌（皮质酮、催产素和血管加压素血浆水平）和行为对 RS 的反应中的作用。
雄性 Wistar 大鼠双侧视上核内植入引导套管，用于微量注射非特异性突触阻滞剂氯化钴（CoCl2，1mM）或载体（人工脑脊液，100nL）。将导管插入股动脉以记录 MAP 和 HR。大鼠接受 RS，研究 CoCl2 或载体微注射到 SON 对加压和心动过速反应、尾巴温度下降、血浆催产素、血管加压素和皮质酮水平以及 RS 引起的焦虑样效应的影响。
SON 用 CoCl2 预处理可减少 RS 引起的 MAP 和 HR 增加，而不影响 RS 引起的尾巴温度下降。将 CoCl2 注射到 SON 周围区域不会影响 RS 引起的 MAP 和 HR 增加，这进一步证实了 SON 影响 RS 诱导的心血管反应。此外，SON 用 CoCl2 预处理可减少 RS 引起的皮质酮和催产素增加，而不影响血管加压素血浆水平，表明其参与了 RS 诱导的神经内分泌反应。最后，SON 内 CoCl2 微注射抑制了 RS 引起的延迟焦虑样效应。
这些结果表明，SON 是控制 RS 诱导的自主神经、神经内分泌和行为反应的神经通路的重要组成部分。
