Ritter S, Bugarith K, Dinh T T
Programs in Neuroscience, Washington State University, Pullman, WA 99164-6520, USA.
J Comp Neurol. 2001 Apr 2;432(2):197-216. doi: 10.1002/cne.1097.
The toxin-antibody complex anti-d(beta)h-saporin (DSAP) selectively destroys d(beta)h-containing catecholamine neurons. To test the role of specific catecholamine neurons in glucoregulatory feeding and adrenal medullary secretion, we injected DSAP, unconjugated saporin (SAP), or saline bilaterally into the paraventricular nucleus of the hypothalamus (PVH) or spinal cord (T2-T4) and subsequently tested rats for 2-deoxy-D-glucose (2DG)-induced feeding and blood glucose responses. Injections of DSAP into the PVH abolished 2DG-induced feeding, but not hyperglycemia. 2DG-induced Fos expression was profoundly reduced or abolished in the PVH, but not in the adrenal medulla. The PVH DSAP injections caused a nearly complete loss of tyrosine hydroxylase immunoreactive (TH-ir) neurons in the area of A1/C1 overlap and severe reduction of A2, C2, C3 (primarily the periventricular portion), and A6 cell groups. Spinal cord DSAP blocked 2DG-induced hyperglycemia but not feeding. 2DG-induced Fos-ir was abolished in the adrenal medulla but not in the PVH. Spinal cord DSAP caused a nearly complete loss of TH-ir in cell groups A5, A7, subcoeruleus, and retrofacial C1 and a partial destruction of C3 (primarily the ventral portion) and A6. Saline and SAP control injections did not cause deficits in 2DG-induced feeding, hyperglycemia, or Fos expression and did not damage catecholamine neurons. DSAP eliminated d(beta)h immunoreactivity but did not cause significant nonspecific damage at injection sites. The results demonstrate that hindbrain catecholamine neurons are essential components of the circuitry for glucoprivic control of feeding and adrenal medullary secretion and indicate that these responses are mediated by different subpopulations of catecholamine neurons.
毒素 - 抗体复合物抗 - d（β）h - 皂草素（DSAP）可选择性地破坏含d（β）h的儿茶酚胺能神经元。为了测试特定儿茶酚胺能神经元在糖调节性摄食和肾上腺髓质分泌中的作用，我们将DSAP、未结合的皂草素（SAP）或生理盐水双侧注射到下丘脑室旁核（PVH）或脊髓（T2 - T4）中，随后检测大鼠对2 - 脱氧 - D - 葡萄糖（2DG）诱导的摄食和血糖反应。向PVH注射DSAP可消除2DG诱导的摄食，但不会消除高血糖。2DG诱导的Fos表达在PVH中显著降低或消除，但在肾上腺髓质中未出现这种情况。向PVH注射DSAP导致A1/C1重叠区域酪氨酸羟化酶免疫反应性（TH - ir）神经元几乎完全丧失，以及A2、C2、C3（主要是室周部分）和A6细胞群严重减少。脊髓注射DSAP可阻断2DG诱导的高血糖，但不会阻断摄食。2DG诱导的Fos免疫反应性在肾上腺髓质中消除，但在PVH中未消除。脊髓注射DSAP导致A5、A7、蓝斑下核和延髓尾端C1细胞群中TH - ir几乎完全丧失，以及C3（主要是腹侧部分）和A6部分破坏。生理盐水和SAP对照注射不会导致2DG诱导的摄食、高血糖或Fos表达出现缺陷，也不会损伤儿茶酚胺能神经元。DSAP消除了d（β）h免疫反应性，但在注射部位未造成明显的非特异性损伤。结果表明，后脑儿茶酚胺能神经元是摄食和肾上腺髓质分泌的糖缺乏性控制回路的重要组成部分，并表明这些反应是由不同亚群的儿茶酚胺能神经元介导的。
