Carithers J, Bealer S L, Johnson A K
Brain Res. 1984 Jul 9;305(2):247-57. doi: 10.1016/0006-8993(84)90431-1.
Electrolytic lesions of tissue surrounding the preoptic recess (AV3V region) appear to cause loss of stimulatory input to the supraoptic nuclei from angiotensin receptors and osmoreceptors. To investigate the pathways affected by AV3V lesions, we observed the ultrastructural effects of coronal cuts in a plane caudal to the organum vasculosum lamina terminalis upon supraoptic nuclei and neural lobes of rats. Like AV3V lesions, these cuts caused degeneration of axons and terminals in the supraoptic nuclei. Degenerating terminals lay in axodendritic synapses and in axosomatic synapses on neurosecretory cells. Unlike AV3V lesions, the cuts did not result in an appearance of decreased secretory activity in the supraoptic nuclei or decreased release of hormone from the neural lobe. On the contrary, terminals in the neural lobe tended to be depleted of neurosecretory material, and glial cell processes tended to be withdrawn from the secretory interface at the basal lamina surrounding fenestrated capillaries; both are changes which have been associated with enhanced hormone release. We suggest that inhibitory input to the supraoptic nuclei is lost as a result of these cuts.
视前隐窝（AV3V区域）周围组织的电解损伤似乎会导致来自血管紧张素受体和渗透压感受器的对视上核的刺激输入丧失。为了研究受AV3V损伤影响的通路，我们观察了终板血管器尾侧平面的冠状切口对大鼠视上核和神经叶的超微结构影响。与AV3V损伤一样，这些切口导致视上核中的轴突和终末发生变性。变性终末位于神经分泌细胞的轴树突触和轴体突触中。与AV3V损伤不同，这些切口并未导致视上核中分泌活动减少或神经叶中激素释放减少。相反，神经叶中的终末往往缺乏神经分泌物质，并且神经胶质细胞突起往往从有孔毛细血管周围基膜处的分泌界面退缩；这两种变化都与激素释放增强有关。我们认为，这些切口导致对视上核的抑制性输入丧失。
