Glucoprivation increases expression of neuropeptide Y mRNA in hindbrain neurons that innervate the hypothalamus
Glucoprivation increases expression of neuropeptide Y mRNA in hindbrain neurons that innervate the hypothalamus
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DOI：
10.1111/j.1460-9568.2004.03287.x
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发表时间：
2004-04-01
影响因子：
3.4
通讯作者：
Ritter, S
中科院分区：
文献类型：
--
作者：
Li, AJ;Ritter, S
下丘脑由后脑和下丘脑神经肽Y（NPY）细胞体共同支配。虽然这些不同来源的神经支配的具体作用是未知的，下丘脑内的神经肽Y神经传递似乎有助于葡萄糖调节喂养。在这里，我们研究参与后脑神经肽Y神经元的葡萄糖调节使用原位杂交，以评估其对葡萄糖的反应。下丘脑的后脑神经肽Y神经支配来源于共表达去甲肾上腺素或肾上腺素的细胞体。因此，我们定量的神经肽Y mRNA杂交信号在后脑儿茶酚胺细胞组90分钟后，皮下注射糖酵解抑制剂2-脱氧-D-葡萄糖（2DG，250毫克/公斤）的雄性大鼠。儿茶酚胺细胞组A1，A1/C1和C2（提供下丘脑的主要神经肽Y神经支配）显示了一个基础水平的神经肽Y mRNA杂交信号，显着增加了2DG。在C1和C3中，基础NPY mRNA表达接近或低于我们的检测阈值，2DG也显著增加了杂交信号。在A2、A5、A6和A7细胞组中，未检测到基础或2DG刺激的NPY mRNA表达。下丘脑微量注射逆行转运的儿茶酚胺免疫毒素皂草素结合抗多巴胺-β-羟化酶破坏后脑儿茶酚胺/NPY神经元和取消基础和2DG刺激的增加，在后脑细胞群中的NPY表达。后脑神经肽Y神经元对葡萄糖缺乏的反应性表明，这些神经元参与葡萄糖消耗或其他葡萄糖调节反应。
The hypothalamus is jointly innervated by hindbrain and hypothalamic neuropeptide Y (NPY) cell bodies. While the specific roles of these distinct sources of innervation are not known, NPY neurotransmission within the hypothalamus appears to contribute to glucoregulatory feeding. Here we examine the involvement of hindbrain NPY neurons in glucoregulation using in situ hybridization to assess their responsiveness to glucoprivation. The hindbrain NPY innervation of the hypothalamus is derived from cell bodies that coexpress norepinephrine or epinephrine. Therefore, we quantified NPY mRNA hybridization signal in hindbrain catecholamine cell groups 90 min after subcutaneous administration of the glycolytic inhibitor 2-deoxy-D-glucose (2DG, 250 mg/kg) to male rats. Catecholamine cell groups A1, A1/C1 and C2 (that provide the major NPY innervation of the hypothalamus) showed a basal level of NPY mRNA hybridization signal that was dramatically increased by 2DG. In C1 and C3, where basal NPY mRNA expression was close to or below our detection threshold, the hybridization signal was also significantly increased by 2DG. In cell groups A2, A5, A6 and A7, neither basal nor 2DG-stimulated NPY mRNA expression was detected. Hypothalamic microinjection of the retrogradely transported catecholamine immunotoxin saporin conjugated to anti-dopamine-beta-hydroxylase destroyed hindbrain catecholamine/NPY neurons and abolished basal and 2DG-stimulated increases in NPYexpression in hindbrain cell groups. The responsiveness of hindbrain NPY neurons to glucose deficit suggests that these neurons participate in glucoprivic feeding or other glucoregulatory responses.