Rinaman L, Hoffman G E, Dohanics J, Le W W, Stricker E M, Verbalis J G
Department of Neuroscience, University of Pittsburgh, Pennsylvania 15260, USA.
J Comp Neurol. 1995 Sep 18;360(2):246-56. doi: 10.1002/cne.903600204.
Stimulation of gastric vagal afferents by systemic administration of cholecystokinin octapeptide (CCK) inhibits gastric motility, reduces food intake, and stimulates pituitary secretion of oxytocin and adrenocorticotropic hormone in rats. To characterize further the central neural circuits responsible for these effects, the present study used triple-labeling immunocytochemical methods to determine whether or not exogenous CCK activates cFos expression in catecholaminergic neurons in the caudal medulla that project to the paraventricular nucleus of the hypothalamus (PVN). To identify these neurons, the retrograde tracer fluorogold (FG) was iontophoresed into the PVN of anesthetized rats under stereotaxic guidance. After 2 weeks, rats were injected with CCK (100 micrograms/kg, i.p.) and then anesthetized and killed 1 hour later by perfusion fixation. Medullary sections were processed for triple immunocytochemical localization of cFos, retrogradely transported FG, and tyrosine hydroxylase (TH). In rats with FG injections centered in the PVN (n = 10), approximately 70% of the FG-labeled neurons in the caudal nucleus of the solitary tract (NST) and ventrolateral medulla (VLM) expressed cFos. Of these activated PVN-projecting neurons, approximately 78% in the NST and 89% in the VLM were catecholaminergic (TH positive). These results indicate that PVN-projecting catecholaminergic neurons within the caudal medulla are activated by peripheral administration of CCK, further implicating these ascending catecholaminergic pathways in the neuroendocrine, physiological, and behavioral effects produced by gastric vagal stimulation.
通过全身给予八肽胆囊收缩素（CCK）刺激大鼠胃迷走神经传入纤维，可抑制胃动力、减少食物摄入，并刺激垂体分泌催产素和促肾上腺皮质激素。为了进一步明确介导这些作用的中枢神经回路，本研究采用三重标记免疫细胞化学方法，以确定外源性CCK是否能激活延髓尾部投射至下丘脑室旁核（PVN）的儿茶酚胺能神经元中cFos的表达。为了识别这些神经元，在立体定位引导下，将逆行示踪剂荧光金（FG）离子导入麻醉大鼠的PVN。2周后，给大鼠注射CCK（100微克/千克，腹腔注射），然后在1小时后将其麻醉并通过灌注固定处死。对延髓切片进行处理，用于cFos、逆行转运的FG和酪氨酸羟化酶（TH）的三重免疫细胞化学定位。在FG注射集中于PVN的大鼠（n = 10）中，孤束核（NST）和延髓腹外侧（VLM）中约70%的FG标记神经元表达cFos。在这些被激活的投射至PVN的神经元中，NST中约78%以及VLM中约89%为儿茶酚胺能神经元（TH阳性）。这些结果表明，延髓尾部投射至PVN的儿茶酚胺能神经元可被外周给予的CCK激活，进一步表明这些上行儿茶酚胺能通路参与了胃迷走神经刺激所产生的神经内分泌、生理和行为效应。
