ACI患者治疗前后血浆ET-1和血清NSE、NPY联检的临床意义

目的:评估了急性脑梗死(ACI)患者治疗前后血浆内皮素-1(ET-1)和血清神经元特异性烯醇化酶(NSE)、神经肽-Y(NPY)水平的变化及临床意义.方法:应用放射免疫分析对32例ACI患者进行了治疗前后血浆ET-1和血清NSE、NPY检测,并与35名正常健康人作比较.结果:在治疗前血浆ET-1和血清NSE、NPY水平...     

急性脑梗死患者治疗前后血清NSE、血浆NPY水平检测的临床意义

目的：探讨了急性脑梗死患者血清神经元特异性烯醇化酶（NSE）和血浆神经肽Y（NPY）水平的变化及临床意义。方法：应用放射免疫分析对38例急性脑梗死患者进行了血清NSE和血浆NPY水平测定,并以35名正常健康人作比较。结果：急性脑梗死患者血清NSE和血浆NPY水平非常显著地高于正常人组（P〈0．01）,经治疗3个月后血清NSE和血浆NPY仍有差异（P〈0．05）。结论：急性脑梗死患者血清NSE和血浆NPY水平的变化与急性脑梗死的发病机理有密切的关系。     

Influence of fasting and neuropeptide Y on the suppressive food intake induced by intracerebroventricular injection of glucagon-like peptide-1 in the neonatal chick

Recently, we have reported that central administration of glucagon-like peptide-1 (GLP-1) strongly decreased food intake of chicks. The aim of the present study was to elucidate whether suppressed food intake by central injection of GLP-1 would be modified by an appetite stimulant such as fasting and neuropeptide Y (NPY). Birds (2 days old) were starved for 3 or 6 h and then GLP-1 (0.03 μg/10 μl) or saline was injected by the intracerebroventricular (i.c.v.) route. Birds starved for 6 h ate significantly more food than those starved for 3 h, while irrespective of the time for fasting GLP-1 strongly inhibited food intake as rapidly as 10 min after i.c.v injection. The suppressive effect on food intake continued until 4 h after injection. Central administration of NPY (2.5 μg/10 μl) greatly enhanced food intake, but co-injection of GLP-1 (0.01, 0.02 or 0.03 μg/10 μl) decreased food intake in a dose-dependent fashion. Under GLP-1 (0.03 μg/10 μl) treatment, whether NPY modifies food intake of chicks in a dose-dependent manner was investigated by co-injection of graded levels of NPY (0.4, 1.0 and 2.5 μg/10 μl). GLP-1 completely inhibited the effect of NPY on food intake without a dose response. These results suggest that central GLP-1 may interact with NPY and may be the most potent inhibitor of food intake in the chicken.     

Neuropeptide tyrosine-like immunoreactive nerve fibers in the carotid body chemoreceptor of rats

Abundant NPY-immunoreactive nerve fibers were found throughout the parenchyma of the rat carotid body. They were in close proximity to smooth muscle cells and pericytes of small blood vessels intervening a narrow interstitial space of 80-150 nm. No immunoreactive nerve fibers were associated with chief or sustentacular cells. After removing the superior cervical ganglion, no immunoreactive nerve fibers were seen in the ipsilateral carotid body and the immunoreactive nerve fibers remained intact in the carotid body after cutting the ipsilateral superior cervical sympathetic trunk. The NPY-immunoreactive nerve fibers are therefore considered to be postganglionic sympathetic noradrenergic nerves.     

冠心病并焦虑患者血浆神经肽Y和心率变异性的相关研究

目的探讨冠心病（CHD）合并焦虑障碍患者血浆神经肽Y（NPY）与心率变异性（HRV）的相关性。方法66例经选择性冠状动脉造影确诊为CHD的住院病人，通过Zung焦虑自评量表问卷调查分为焦虑障碍组（焦虑组，41例）和对照组（不伴焦虑障碍，30例）。运用放射免疫法检测患者血浆NPY含量，运用动态心电图系统采集患者的心电信号进行HRV分析。结果（1）与CHD患者比较，合并焦虑障碍的CHD患者血浆NPY水平均明显增高，具有统计学差异（P〈0．05）；（2）与CHD患者比较，合并焦虑障碍的CHD患者HRV指标SDNN、rMSSD、PNN50明显降低，具有统计学差异（P〈0．05）；（3）CHO并焦虑障碍患者血NPY与HRV呈负相关。结论CHD并焦虑障碍患者血NPY增高与HRV降低密切相关。     

冠心病并抑郁患者血浆NPY、NE、DA、5-HT的变化及其临床意义

目的探讨冠心病合并抑郁障碍患者血浆神经肽Y、去甲肾上腺素、多巴胺、5-羟色胺水平的变化及其临床意义。方法66例经选择性冠状动脉造影确诊为CHD的住院病人，通过Zung抑郁自评量表问卷调查分为抑郁障碍组（抑郁组，36例）和对照组（不伴抑郁障碍，30例）。统计其年住院次数及年住院天数，并分别运用放射免疫法和免疫荧光法检测患者血浆NPY和NE、DA、5-HT的含量。结果①与CHD患者比较，合并抑郁障碍的CHD患者年住院次数及年住院天数均明显增多，具有统计学差异（P〈0．05）；②与CHD患者比较，合并抑郁障碍的CHD患者血浆NPY、NE、DA水平均显著增高，具有统计学差异（P〈0．05）；血浆5-HT水平均显著降低，具有统计学差异（P〈0．05）。结论①合并抑郁障碍的CHD患者年住院次数及天数明显增加，应引起临床医生尤其是心血管医师的高度重视；②血NPY、NE、DA、5-HT的异常增加可能参与了改变CHD患者抑郁障碍的发生发展过程。     

ＰＧＰ９．５和ＮＰＹ肽能神经在成人睾丸组织中的分布

目的:研究蛋白基因产物9.5(protein gene product 9.5,PGP9.5)肽能神经和神经肽Y(neuropeptide Y,NPY)肽能神经在成人睾丸组织中的分布情况.方法:成年男性睾丸标本4例,将其制成5μm厚冰冻切片,运用ABC免疫组织化学方法检测睾丸组织中PGP9.5与NPY肽能神经纤维的分布.结果:PGP9.5肽能神经纤维主要分布于睾丸间质中.其与曲细精管及Leydig细胞存在较为紧密的联系;NPY肽能神经纤维主要分布于睾丸血管周嗣,生精小管管周也可见部分分布,NPY神经纤维分布密度低于PGP9.5神经纤维.结论:人睾丸组织内分布着PGP9.5和NPY肽能神经纤维,精索神经通过这些神经纤维实现其对精子发生过程的调控.     

Biomarkers of adult and developmental neurotoxicity

Neurotoxicity may be defined as any adverse effect on the structure or function of the central and/or peripheral nervous system by a biological, chemical, or physical agent. A multidisciplinary approach is necessary to assess adult and developmental neurotoxicity due to the complex and diverse functions of the nervous system. The overall strategy for understanding developmental neurotoxicity is based on two assumptions: (1) significant differences in the adult versus the developing nervous system susceptibility to neurotoxicity exist and they are often developmental stage dependent; (2) a multidisciplinary approach using neurobiological, including gene expression assays, neurophysiological, neuropathological, and behavioral function is necessary for a precise assessment of neurotoxicity. Application of genomic approaches to developmental studies must use the same criteria for evaluating microarray studies as those in adults including consideration of reproducibility, statistical analysis, homogenous cell populations, and confirmation with non-array methods. A study using amphetamine to induce neurotoxicity supports the following: (1) gene expression data can help define neurotoxic mechanism(s), (2) gene expression changes can be useful biomarkers of effect, and (3) the site-selective nature of gene expression in the nervous system may mandate assessment of selective cell populations.     

The melanocortin agonist Melanotan-II reduces the orexigenic and adipogenic effects of neuropeptide Y (NPY) but does not affect the NPY-driven suppressive effects on the gonadotropic and somatotropic axes in the male rat

Neuropeptide Y (NPY) is a strong orexigenic neurotransmitter also known to modulate several neuroendocrine axes. alpha-Melanocyte-stimulating hormone (MSH) is an essential anorectic neuropeptide, acting on hypothalamic MC3/4 receptor subtypes. When given as an intracerebroventricular bolus injection, Melanotan-II (MT-II), a non selective MC receptor agonist, inhibits feeding, suppresses the NPY orexigenic action, and reduces basal insulinaemia. We evaluated the effects of a 7-day central infusion of MT-II (15 nmol/day) given either alone or in association with NPY (5 nmol/day) in male Sprague-Dawley rats. MT-II produced almost full anorexia for 1-2 days but then feeding gradually returned to normal despite continued MT-II infusion. When coinfused with NPY, MT-II also produced the same initial anorectic episode but then maintained feeding to upper normal levels, thus cancelling the hyperphagia driven by NPY. Whereas NPY infusion produced a doubling of fat pad weight, MT-II reduced adiposity by a factor of two compared to pair-fed rats, and vastly curtailed the NPY-driven increase in fat pad weight. MT-II infusion also significantly curtailed the NPY-induced rise in insulin and leptin secretions. NPY infusion significantly inhibited hypothalamic pro-opiomelanocortin mRNA expression, most likely cancelling the alpha-MSH anorectic activity. As expected from previous studies, chronic NPY infusion strongly inhibited both the gonadotropic and somatotropic axes, and coinfusion of MT-II did not reverse these NPY-driven effects, in sharp contrast with that seen for the metabolic data. MT-II infusion alone had little effect on these axes. In conclusion, chronic MT-II infusion generated a severe but transient reduction in feeding, suggesting an escape phenomenon, and clearly reduced fat pad size. When coinfused with NPY, MT-II was able to cancel most of the NPY effects on feeding, but not those on the neuroendocrine axes. It appears therefore that, as expected, NPY and alpha-MSH closely interact in the control of feeding, whereas the neural pathways by which NPY affects growth and reproduction are distinct and not sensitive to MC peptide modulation.     

Orexin-induced food intake involves neuropeptide Y pathway

Orexins (orexin-A and -B) are recently identified neuropeptides, which are thought to be implicated in the regulation of feeding behavior. We used a NPY-Y1 receptor specific antagonist, BIBO3304, to examine whether NPY is involved in orexin-induced feeding behavior. Intracerebroventricular administration of orexin-A (10 nmol) induced food intake in rats (food intake for 3 h; vehicle 0.3+/-0.2 g vs. orexin-A 10 nmol, 4.0+/-0.5 g, n=4). Orexin-induced feeding behavior was partially inhibited by prior administration of BIBO3304 (3 h food intake: orexin-A 10 nmol, 4.0+/-0.5 g vs. BIBO3304 (60 microgram) + orexin-A 10 nmol, 2.2+/-0.2 g, n=4). A low dose of BIBO3304 (30 microgram) did not show a significant inhibitory effect. BIBO3457, an inactive enantiomer, used as a negative control, did not show any inhibitory effect on orexin-A-induced feeding behavior. Fos expression was observed in NPY-containing neurons in the arcuate nucleus 1 h after orexin-A (10 nmol) was administered intracerebroventricularly (control 0.3+/-0.08%, orexin-A 10.2+/-0.8%, n=5 rats/group). These observations suggest that NPY is involved in orexin-induced feeding behavior. However, BIBO3304 did not completely abolish the effect of orexin-A. These results suggest that orexin-A elicits feeding behavior partially via the NPY pathway. The NPY system could be the one of downstream pathways by which orexin-A induces feeding behavior. Another pathway may also be involved in orexin-A-induced feeding behavior, because BIBO3304 did not completely abolish orexin-A-induced feeding behavior.