杏仁中央核μ阿片受体参与蔗糖溶液摄入的调节

目的探讨杏仁中央核内μ阿片受体是否参与大鼠蔗糖溶液摄入的调节及其可能的机制。方法杏仁中央核内注入μ阿片受体激动剂DAMGO或生理盐水,测量大鼠在双瓶选择试验中对蔗糖溶液及蒸馏水的摄入量;利用荧光免疫组织化学方法,在大鼠摄入蔗糖溶液或蒸馏水后,观察杏仁中央核内μ阿片受体/Fos免疫阳性双标记神经元的数量。结果与生理盐水注射组相比,杏仁中央核内注入DAMGO增加了大鼠3 h内的蔗糖溶液摄入量;与蒸馏水摄入组相比,大鼠摄入蔗糖溶液后,杏仁中央核内c-Fos阳性神经元及μ阿片受体/Fos共表达神经元均显著增加(P<0.05)。结论杏仁中央核参与大鼠蔗糖溶液摄入的调节,该调节作用可能部分是由μ阿片受体介导的。     

不同饥饿刺激对下丘脑穹隆周区orexin-A神经元的影响

目的:通过观察下丘脑穹窿周区orexin-A神经元对不同刺激方式的反应特性探索能够激活该系统的高效而适宜的方法。方法:采用禁食、腹腔注射胰岛素和2-DG三种饥饿刺激方式,利用免疫组织化学染色及ELISA检测相结合的方法对大鼠穹隆周区orexin-A神经元的Fos的表达,脑脊液中orexin-A的浓度进行了对比分析。27只SD大鼠随机分为六组,分别进行禁食2 d,腹腔注射胰岛素或生理盐水存活5 h,腹腔注射2-脱氧-D-葡萄糖(2-DG)或生理盐水存活2 h和正常对照处理,动物的饮水量保持正常。结果:三种饥饿刺激引发的Fos表达比较类似,主要集中于下丘脑背内侧核,下丘脑外侧区和下丘脑后区,2-DG组的Fos表达最为浓密。三种刺激对orexin-A神经元的数量无明显影响,但orexin-A/Fos双标细胞数占所有orexin-A阳性细胞数的比例以2-DG组最高,为26%;禁食2 d组次之为21%;胰岛素组最低为14%。禁食组和2-DG组的双标细胞率与胰岛素组相比差异具有统计学意义(P<0.05)。ELISA检测结果显示禁食组脑脊液中orexin-A的含量显著高于对照组23%,而其它两组与对照组相比没有差别。结论:本研究提示orexin-A的功能状态与刺激方式密切相关:急性刺激如2-DG注射适于研究神经元的激活状态,而慢性刺激如禁食适于研究激活后导致的orexin-A表达变化。     

Activation of phenotypically distinct neuronal subpopulations in the anterior subdivision of the rat basolateral amygdala following acute and repeated stress

The effects of acute and repeated stress on expression of the early immediate gene c-fos in the basolateral amygdala have previously been reported; however, characterization of which neuronal subpopulations are activated by these stimuli has not been investigated. This question is of considerable relevance, insofar as the basolateral amygdala houses a heterogeneous population of neurons, including those of gamma-aminobutyric acid (GABA)-ergic and glutamatergic phenotypes that may be subcategorized based on their expression of various calcium-binding proteins, including parvalbumin, calbindin, calretinin, and the calcium-sensitive enzyme calcium/calmodulin-dependent kinase II. Characterization of these subpopulations has revealed unique differences in their physiology, synaptology, and morphology, suggesting that each distinct phenotype may have profound effects on the local circuitry of the amygdala. Therefore, we examined the effects of acute and repeated restraint stress on expression of the immediate early gene c-fos in neurons containing parvalbumin, calbindin, calretinin, or calcium/calmodulin-dependent kinase II in the basolateral amygdala. Double-label immunohistochemistry revealed that acute restraint stress activated a proportion of parvalbumin-, calbindin-, or calcium/calmodulin-dependent kinase II-positive neurons. Prior exposure to repeated restraint stress markedly attenuated acute-stress mediated activation of these neuronal populations, although not equally. Expression of c-Fos protein was not detected in calretinin-positive neurons in any experimental group. These results demonstrate that distinct neuronal phenotypes in the basolateral amygdala are activated by acute restraint stress and that prior repeated restraint stress differentially affects this response.     

Acute baroreceptor unloading evokes Fos expression in anesthetized rat brain

Functional organization of brain pathways subserving the baroreceptor reflex was investigated by mapping immunoreactivity of Fos protein, a neuronal activity marker, in response to acute baroreceptor unloading in anesthetized rats. Compared with normal control and sham operation, sinoaortic denervation (SAD) evoked a distinctive pattern of Fos expression in the nucleus tractus solitarii (NTS), the primary termination of baroreceptor afferents. The sinoaortic denervation also induced a prominent and reproducible Fos expression in specific regions of the brainstem and forebrain, which receive direct or indirect inputs from the nucleus tractus solitarii. These brain regions included the rostral ventrolateral medulla (RVLM), lateral parabrachial nucleus (LPBN), hypothalamic paraventricular nucleus (PVN), supraoptic nucleus (SON), and central amygdaloid nucleus (CeA). These findings help us to identify brain regions that are specifically responsive to decreased arterial baroreceptor activity, without the accompanying confounding variables of behavioral arousal or stress.     

Phosphodiesterase 4 inhibitors, rolipram and diazepam block the adaptive changes observed during morphine withdrawal in the heart

In this study, we investigated whether morphine dependence was inhibited by phosphodiesterase (PDE) 4 inhibitors rolipram and diazepam, since a role for the cyclic AMP systems in the development of morphine dependence was reported. Dependence of morphine was induced by a 7-day s.c. implantation of morphine pellets. Morphine withdrawal was precipitated on day 8 by an injection of naloxone. In order to determine the effect of rolipram or diazepam the animals were injected with these drugs for seven days and 30 min before the administration of naloxone. When opioid withdrawal was precipitated, enhancement of noradrenaline (NA) turnover in the heart was observed 30 min after naloxone administration. Moreover, morphine withdrawal induces Fos expression, increase in cyclic AMP and cyclic GMP levels. Co-administration of rolipram or diazepam with morphine during the pre-treatment period significantly reduces the signs of withdrawal symptoms, the enhancement of NA turnover, the increase in cyclic AMP and the Fos expression. However, these inhibitors did not modify the levels of cyclic GMP. These findings demonstrated that co-administration of rolipram or diazepam with morphine abolish the development of morphine dependence and suggest that these compounds prevent the up-regulation of the cyclic AMP pathway and the associated increase in cyclic AMP level after naloxone administration.     

Enhancer and super-enhancer landscape in polycystic kidney disease

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