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31.
The HSD2 (11-beta-hydroxysteroid dehydrogenase type 2-expressing) neurons in the nucleus of the solitary tract (NTS) of the rat are aldosterone-sensitive and have been implicated in sodium appetite. The central nucleus of the amygdala (CeA) has been shown to modulate salt intake in response to aldosterone, so we investigated the connections between these two sites. A prior retrograde tracing study revealed only a minor projection from the HSD2 neurons directly to the CeA, but these experiments suggested that a more substantial projection may be relayed through the parabrachial nucleus. Small injections of cholera toxin beta subunit (CTb) into the external lateral parabrachial subnucleus (PBel) produced both retrograde cell body labeling in the HSD2 neurons and anterograde axonal labeling in the lateral subdivision of the CeA. Also, injections of either CTb or Phaseolus vulgaris leucoagglutinin into the medial subdivision of the CeA labeled a descending projection from the amygdala to the medial NTS. Axons from the medial CeA formed numerous varicosities and terminals enveloping the HSD2 neurons. Complementary CTb injections, centered in the HSD2 subregion of the NTS, retrogradely labeled neurons in the medial CeA. These bidirectional projections could form a functional circuit between the HSD2 neurons and the CeA. The HSD2 neurons may represent one of the functional inputs to the lateral CeA, and their activity may be modulated by a return projection from the medial CeA. This circuit could provide a neuroanatomical basis for the modulation of salt intake by the CeA. 相似文献
32.
Adrenaline is a potent respiratory regulator. However, adrenergic contribution to the developing respiratory center has not been studied extensively. Adrenaline application on embryonic day 17 medulla-spinal cord block preparations abolished non-respiratory activity and enhanced respiratory frequency. Phentolamine application on neonatal blocks that produced stable neonatal respiration resulted in respiratory destabilization. These results suggest that central adrenergic modulation is involved in fetal respiratory development and maintenance of stable respiration. 相似文献
33.
34.
Carvalho AF Van Bockstaele EJ 《Progress in neuro-psychopharmacology & biological psychiatry》2012,38(1):59-67
The interaction between the endocannabinoid system and catecholaminergic circuits has gained increasing attention as it is recognized that the development of synthetic cannabinoid receptor agonists/antagonists or compounds targeting endocannabinoid synthesis/metabolism may hold some therapeutic potential for the treatment of psychiatric disorders. The noradrenergic system plays a critical role in the modulation of emotional state, primarily related to anxiety, arousal, and stress. Recent evidence suggests that the endocannabinoid system mediates stress responses and emotional homeostasis, in part, by targeting noradrenergic circuits. This review summarizes our current knowledge regarding the anatomical substrates underlying regulation of noradrenergic circuitry by the endocannabinoid system. It then presents biochemical evidence showing an important effect of cannabinoid modulation on adrenergic receptor signaling. Finally, new evidence from behavioral pharmacology studies is provided demonstrating that norepinephrine is a critical determinant of cannabinoid-induced aversion, adding another dimension to how central noradrenergic circuitry is regulated by the cannabinoid system. 相似文献
35.
为研究来自孤束核的内脏传导信息在臂旁核水平是否接受中央杏仁核的反馈调节及其递质性质,以及孤束核—臂旁核—中央杏仁核传导通路中,在臂旁核水平是否接受GABA的调节,本文将HRP注入中央杏仁核进行顺、逆行标记,同时将兴奋性氨基酸毒素海人酸注入孤束核进行损毁,观实其顺行溃变终末,取外侧臂旁核超薄切片后结合抗GABA的免疫电镜染色,观察发现有下列几种标记;(1)顺行溃变终末,所有的都与臂旁核神经元形成非对称性突触;(2)HRP标记终末有两类:第一类和臂旁核神经元形成对称性突触,占HRP标记终末总数的80%以上,第二类与臂旁核神经元形成非对称性突触,另外有大量的HRP标记的胞体和树突;(3)胶体金标记的GABA阳性终末,皆与突触后结构形成对称性突触;(4)GABA/HRP双标记终末,具有GABA免疫阳性终末和第一类HRP标记终末的共同特征。上述几种标记在臂旁核内有以下几种关系:(1)溃变终末和GABA阳性终末与同一个HRP标记或非标记的突形成轴-树突触;(2)溃变终末和第一类HRP标记终末共同终止于同一非标记讨突;(3)溃变终末与HRP标记树突或胞位形成非对称性突触;(4)GABA/HRP双标记终末与非标记树突或胞体? 相似文献
36.
Núñez C Castells MT Laorden ML Milanés MV 《Naunyn-Schmiedeberg's archives of pharmacology》2008,378(4):407-420
Our previous studies have shown that morphine withdrawal increases the hypothalamic–pituitary–adrenocortical axis activity,
which is dependent on a hyperactivity of noradrenergic pathways (nucleus tractus solitarius-A2) innervating the hypothalamic paraventricular nucleus. The extracellular signal-regulated kinase has been implicated in drug
addiction, but its role in activation of paraventricular nucleus and nucleus tractus solitarius during morphine dependence
remain poorly understood. We have determined the activation of extracellular signal-regulated kinase during morphine dependence
and withdrawal as well as its involvement in morphine withdrawal-induced gene expression. We show that naloxone-induced morphine
withdrawal activates extracellular signal-regulated kinases1/2 and increases c-Fos expression in rat paraventricular nucleus and nucleus tractus solitarius-A2 neurons. Activated extracellular signal-regulated kinases1/2 was colocalized with c-Fos in both nuclei, and this response was blocked by SL327, a drug that prevents extracellular signal-regulated
kinase activation. In the paraventricular nucleus from morphine-withdrawn rats, the number of neurons expressing CRF was increased.
Immunohistochemical study showed a dramatic increase in c-Fos immunoreactivity within CRF-positive cells. These results suggest
that extracellular signal-regulated kinases1/2 signaling pathway is necessary for morphine withdrawal-induced activation of
brain areas associated with the stress system. 相似文献
37.
The present study was conducted in order to observe the potential participation of the nitric oxide synthase-NO pathway in CO-mediated regulation of respiration of neonatal rats. An immunofluorescent histochemical technique was used to examine the existence of the neuronal nitric oxide synthase, a key enzyme of synthesizing NO, in medullary respiratory nuclei. The rhythmic respiratory-like discharges of hypoglossal rootlets of medullary slices were recorded to test the role of the nitric oxide synthase in CO-mediated respiratory effects. We observed neuronal nitric oxide synthase expressed in the medullary respiratory nuclei in conjunction with CO lengthened expiratory duration, decreased respiratory frequency, and increased inspiratory amplitude. These CO-mediated respiratory effects could be partially eliminated by prior treatment of the slices with Nω-nitro-l-arginine methyl ester, an inhibitor of nitric oxide synthase. The results suggest that nitric oxide synthase-NO pathway might be involved in the CO-mediated central regulation of respiration at the level of medulla oblongata in neonatal rats. 相似文献
38.
39.
Justin Doritchamou Pascal Bigey Morten Agertoug Nielsen Sédami Gnidehou Sem Ezinmegnon Aurore Burgain Achille Massougbodji Philippe Deloron Ali Salanti Nicaise Tuikue Ndam 《Vaccine》2013
Background
VAR2CSA is a large polymorphic Plasmodium falciparum protein expressed on infected erythrocytes (IE) that allows their binding in the placenta, thus precipitating placental malaria (PM). The N-terminal part of VAR2CSA that contains the binding site to placental chondroitin sulfate A (CSA) is currently recognized as the most attractive region for vaccine development. An ultimate challenge is to define epitopes in this region that induce a broad cross-reactive adhesion inhibitory antibody response.Methods
Based on phylogenetic data that identified a dimorphic sequence motif in the VAR2CSA DBL2X, we raised antibodies against the NTS-DBL2X constructs containing one sequence or the other (3D7 and FCR3) and tested their functional properties on P. falciparum isolates from pregnant women and on laboratory-adapted strains.Results
The CSA binding inhibitory capacity of the antibodies induced varied from one parasite isolate to another (range, 10%–100%), but the combined analysis of individual activity highlighted a broader functionality that increased the total number of isolates inhibited. Interestingly, the differential inhibitory effect of the antibodies observed on field isolates resulted in significant inhibition of all field isolates tested, suggesting that optimal inhibitory spectrum on field isolates from pregnant women might be achieved with antibodies targeting limited variants of the N-terminal VAR2CSA.Conclusions
Our findings indicate that the NTS-DBL2X region of VAR2CSA can elicit strain-transcending anti-adhesion antibodies and suggest that the combination of the two major variants used here could represent the basis for an effective bivalent VAR2CSA-based vaccine. 相似文献40.
Cherylea J. Browne Nidhi Sharma Karen A. Waters Rita Machaalani 《International journal of developmental neuroscience》2010
Exposure to cigarette smoke is a major risk factor for sudden infant death syndrome (SIDS). We tested the hypothesis that nicotine increases expression of the nicotinic acetylcholine receptor (nAChR) subunits α7 and β2 in a piglet model. Piglets exposed to 2 mg/kg/day nicotine for 14 days postnatally (n = 14) were compared to non-exposed controls (n = 14), (equal gender proportions). Immunohistochemistry was performed to identify and quantify changes in, α7 and β2 nAChR subunits in 8 nuclei of the medulla at both the rostral and caudal levels. Compared to controls, nicotine exposed piglets had decreased α7 in the rostral dorsal motor nucleus of the vagus (rDMNV) (p = 0.01), and increased β2 in the caudal DMNV (cDMNV) (p = 0.05), caudal nucleus of the spinal trigeminal tract (cNSTT) (p = 0.03) and caudal nucleus of the solitary tract (cNTS) (p = 0.04). Analysis by gender showed that in the control group, compared to males, females had higher β2 in the caudal hypoglossal (cXII) (p < 0.01) and caudal inferior olivary (p = 0.04) nuclei, while in the nicotine group females had higher β2 in the cDMNV (p = 0.02). Compared to control males, nicotine exposed males had lower β2 in the cXII (p < 0.01). Overall, changes in α7 were specific to nicotine exposure with no gender differentiation. Changes in β2 were more widespread but showed gender-specific effects. These findings provide evidence that early postnatal exposure to nicotine significantly affects nAChR subunit expressions in the developing brainstem. 相似文献