Involvement of oxytocin and its receptor in nociceptive modulation in the central nucleus of amygdala of rats

Studies have demonstrated that oxytocin plays important roles in pain modulation in the central nervous system. Oxytocin-ergic neurons are found in paraventricular nucleus and supraoptic nucleus of the hypothalamus. The oxytocin-ergic neurons send fibers from hypothalamus to amygdala and high density of oxytocin receptors are found in the central nucleus of amygdala (CeA). The present study was performed to investigate the influences of oxytocin and its receptors on nociceptive responses in the CeA of rats. Intra-CeA injection of 0.1, 0.5 or 1 nmol of oxytocin induced dose-dependent increases in the handpaw withdrawal latency induced by noxious thermal and mechanical stimulation in rats. The oxytocin-induced anti-nociception could be blocked by the selective oxytocin antagonist 1-deamino-2-d-Tyr-(Oet)-4-Thr-8-Orn-oxytocin. The present study demonstrated that oxytocin and its receptors are involved in nociceptive modulation in the CeA of rats.     

Light and electron microscopic studies of calcitonin gene-related peptide-like immunoreactive terminals in the central nucleus of the amygdala and the bed nucleus of the stria terminalis of the rat

Summary Light and electron microscopic analysis of calcitonin gene-related peptide (CGRP)-like immunoreactive (LI) terminals in the bed nucleus of the stria terminalis (BST) and the central nucleus of the amygdala (Ce) was carried out using the peroxidase-antiperoxidase method. CGRP-LI fibers were densely distributed in the dorsal subdivision of the lateral BST (BSTL) and the lateral and lateral capsular subdivisions of the Ce, where the CGRP-LI terminals formed symmetrical and asymmetrical axo-dendritic, and symmetrical axosomatic synapses. One of the most characteristic features of the CGRP-LI terminals was the presence of large, long boutons, each of which surrounded a cell soma and made many synaptic contacts. These findings suggest that CGRP exerts a significant influence on neurons in the BSTL and Ce.     

Localization of DARPP-32 immunoreactive neurons in the bed nucleus of the stria terminalis and central nucleus of the amygdala: co-distribution with axons containing tyrosine hydroxylase,vasoactive intestinal polypeptide,and calcitonin gene-related peptide

Summary The distribution and morphology of neurons containing the dopamine- and cyclic AMP-regulated phosphoprotein, DARPP-32, were investigated in the bed nucleus of the stria terminalis (BST) and the central nucleus of the amygdala (CeA). DARPP-32 immunoreactive neurons are numerous in both regions, but are restricted to the lateral dorsal and the lateral juxtacapsular subdivisions of the BST, and the central lateral and lateral capsular subdivisions of the CeA. Immunoreactive neurons in the lateral dorsal BST, and the central lateral and lateral capsular CeA are similar morphologically, while those in the juxtacapsular BST appear to be a subpopulation of striatal mediumsized spiny neurons. The distribution of DARPP-32 immunoreactive neurons in the BST and CeA overlaps considerably with axonal plexuses containing tyrosine hydroxylase (TH), vasoactive intestinal polypeptide (VIP), and calcitonin gene-related peptide (CGRP). These studies provide further evidence of the close relationship between the CeA and BST, and also provide anatomical evidence for possible interactions between neurotransmitters, neuropeptides, and phosphoproteins.Abbreviations ac anterior commissure - BLA basolateral amygdaloid nucleus - BST bed nucleus of the stria terminalis - BSTL bed nucleus of the stria terminalis, lateral - BSTLD bed nucleus of the stria terminalis, lateral dorsal - BSTLJ bed nucleus of the stria terminalis, juxtacapsular - BSTM bed nucleus of the stria terminalis, medial - BSTV bed nucleus of the stria terminalis, ventral - CeA central nucleus of the amygdala - CGRP calcitonin gene-related peptide - CL central amygdaloid nucleus, lateral central - CLC central amygdaloid nucleus, lateral capsular - CM central amygdaloid nucleus, medial - CPu caudate-putamen - DARPP-32 dopamine- and cyclic AMP-regulated phosphoprotein with an apparent molecular weight of 32000 Daltons - GP globus pallidus - ic internal capsule - I intercalated mass of the amygdala - IMG intramedullary gray - LA lateral amygdaloid nucleus - LV lateral ventricle - LS lateral septal nucleus - Me medial amygdaloid nucleus - ot optic tract - SHy septohypothalamic nucleus - st stria terminalis - TH tyrosine hydroxylase - VIP vasoactive intestinal polypeptide     

Lateral parabrachial nucleus and central amygdala in the control of sodium intake

The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important areas for the control of sodium appetite. In the present study we investigated the effects of bilateral lesions of the CeA on the facilitation of water and 0.3 M NaCl intake produced by the blockade of serotonergic mechanisms or activation of α₂-adrenoceptors with bilateral injections of methysergide or moxonidine, respectively, into the LPBN. Male Holtzman rats (n=5–8) with bilateral sham or electrolytic lesions of the CeA (2 mA; 10 s) and stainless steel cannulas implanted bilaterally in the LPBN were used. In sham rats treated with the diuretic furosemide (10 mg/kg b.w.) combined with the angiotensin converting enzyme inhibitor captopril (5 mg/kg b.w) subcutaneously, bilateral injections of moxonidine (0.5 nmol) or methysergide (4 μg) into the LPBN increased 0.3 M NaCl intake (29.8±5.1 and 19.5±3.7 ml/2 h, respectively, versus vehicle: 8.3±1.4 ml/2 h) and water intake (17.9±3.7 and 23.3±2.8 ml/2 h, respectively, versus vehicle: 11.5±1.6 ml/2 h). Lesions of the CeA (5–18 days) abolished the increase in 0.3 M NaCl and water intake produced by bilateral injections of moxonidine (10.3±2.8 and 6.8±2.3 ml/2 h, respectively) and reduced the increase produced by methysergide (13.6±2.5 and 14.5±3.2 ml/2 h, respectively) into the LPBN. The present results show that the increase in water and 0.3 M NaCl intake produced by serotonergic blockade and α₂-adrenergic activation in the LPBN depends on the integrity of the CeA, suggesting that facilitatory mechanisms present in the CeA are essential for the increase of water and hypertonic NaCl intake produced by the blockade of the inhibitory mechanisms of the LPBN.     

中央杏仁核内CGRP能阳性突触的超微结构研究

目的:观察降钙素基因相关肽(calcitonin-gene-related peptide,CGRP)样阳性终末在中央杏仁核(cen-tral nucleus of amygdala,CeA)内形成的突触的超微结构。方法:应用免疫荧光组织化学和包埋前免疫电镜等方法,观察CGRP样阳性终末在CeA内所形成的突触分布形式及结构特点。结果:CGRP样阳性终末在中央杏仁核内可以与细胞体、树突干和树突棘等结构形成突触;轴-体突触几乎全为对称性突触,而轴-树突触和轴-棘突触则多为非对称性突触。在所有的非对称性突触里,轴-树突触占84.9%,而轴-棘突触占15.1%。CGRP样阳性轴-树的突触后致密带的平均长度为(790.77±313.55)nm,而轴-棘突触的突触后致密带的平均长度为(723.34±357.20)nm,两者之间没有显著性差异。结论:CGPR样阳性的兴奋性突触尤其是轴-树突触在伤害性信息传递以及痛相关情绪的产生中发挥了重要作用。     

Influence of ascending noradrenergic fibers on the neurotensin-like immunoreactive perikarya and evidence of direct projection of ascending neurotensin-like immunoreactive fibers in the rat central nucleus of the amygdala

The influence of ascending noradrenergic neuronal input on the neurotensin (NT)-like immunoreactive neuronal perikarya located in the dorsal part of the central nucleus of the amygdala (CNA) was examined using fluorescence histochemistry and peroxidase-antiperoxidase (PAP) immunocytochemistry. Unilateral hemitransection of the ascending noradrenergic pathway by injection of 6-hydroxydopamine into the caudal mesencephalon just rostral to the locus coeruleus caused a marked depletion of immunoreactivity in NT-like immunoreactive neuronal perikarya in the CNA. Ascending noradrenergic neuronal input, therefore, is considered to facilitate production of NT-like immunoreactive substances in neuronal perikarya and to influence on the functional role of the amygdaloid complex. In addition, we obtained evidence of unilateral direct ascending projections of NT-like immunoreactive neurons into the CNA since the disappearance of NT-like immunoreactive processes occurred mainly in the ventral part of the CNA after surgical hemitransection of the ascending neuronal pathway that interrupts the ascending NT-like immunoreactive pathway arising from the neurons in the brain stem.     

The participation of a neurocircuit from the paraventricular thalamus to amygdala in the depressive like behavior

Depression is a neuropsychological disease derived from genetic, biochemical, environmental, and psychological factors. However the neurocircuits involved in it are not clear. We introduced the forced swimming test (FST) as a model of the depressive like behavior. In our study, the participation of projections from paraventricular nucleus of the thalamus (PVT) in FST was detected. The retrograde tracing combined with immunofluorescent detection of c-fos was used. Our results showed that the FST greatly increased the c-fos level in PVT and the central amygdale (CE) neurons. These populations of activated neurons in the PVT and the CE were also labeled by the retrograde tracer FG injected in the CE, suggesting that the activation of PVT was involved in this depressive like behavior by relaying information to the CE.     

神经病理性痛大鼠中央杏仁核内磷酸化ERK的过表达参与负性情绪的产生

目的:观察神经病理性痛条件下细胞外信号调节激酶(extracellular singal-regulated kinase,ERK)对疼痛引起的负性情绪反应的影响。方法:应用Western blot和行为药理学方法,观察腰5脊神经结扎(L5 spinalnerve ligation,SNL)大鼠中央杏仁核外侧囊状部(latero-capsular division of central nucleus of amygdala,CeC)内ERK及磷酸化-ERK(phosphorylated-ERK,p-ERK)的表达情况及ERK磷酸化抑制剂对疼痛引起的负性情绪反应的影响。结果:SNL模型大鼠CeC内p-ERK的表达水平明显升高,与对照组相比,有统计学差异(P<0.05),而总ERK的表达水平则未见组间差异;用超声波检测仪可以检测到SNL大鼠超声发声明显增多,但腹膜腔注射ERK磷酸化的抑制剂U0126后其超声发声被显著抑制。结论:中央杏仁核外侧囊状部内ERK的激活参与了神经病理性痛引起的突触可塑性,在痛相关情绪的产生中发挥了重要作用。     

Systemic blockade of complement C5a receptors reduces lipopolysacharride-induced responses in the paraventricular nucleus and the central amygdala

The complement anaphylatoxin C5a is a potent mediator of the innate immune response to infection. Recent evidence also reveals that C5a contributes to central nervous system effects in addition to its well-known peripheral functions. However, it is not known if C5a has a role in the activation of the hypothalamic–pituitary–adrenal (HPA) axis; a critical cascade that exemplifies neuroimmune interactions between the periphery and the brain. In the present study we examined if systemic pre-treatment with a C5a receptor antagonist, PMX53, can affect lipopolysaccharide-induced (LPS; 1 mg/kg, i.p.) activation of the HPA axis in the rat. Using Fos protein as a marker of neuronal activation, we found that systemic administration of PMX53 reduced the LPS-induced activation of paraventricular corticotropin-releasing factor (PVN CRF) and central amygdala cells. However, PMX53 did not alter LPS-induced responses in the bed nucleus of the stria terminalis, nucleus tractus solitarius and ventrolateral medulla. Our findings demonstrate that C5a may have a role in the activation of the HPA axis in response to systemic LPS.     

Adaptation of the cardiovascular system to weightlessness: Surprises,paradoxes and implications for deep space missions

Weightlessness in space induces a fluid shift from the dependent to the cephalad parts of the body leading to distension of the cardiac chambers and an accumulation of blood in the veins of the head and neck. Surprisingly, central venous pressure (CVP) during the initial hours of spaceflight decreases compared to being horizontal supine on the ground. The explanation is that the thorax is expanded by weightlessness leading to a decrease in inter‐pleural pressure (IPP), which exceeds the measured decrease in CVP. Thus, transmural CVP (TCVP = CVP ? IPP) is increased indicating an augmented cardiac preload. Simultaneously, stroke volume and cardiac output (CO) are increased by 18%‐26% within the initial weeks and more so by 35%‐56% during the subsequent months of flight relative to in the upright posture on the ground. Mean arterial pressure (MAP) is decreased indicating a lower systemic vascular resistance (MAP/CO). It is therefore a surprise that sympathetic nerve activity is not suppressed in space and thus cannot be a mechanism for the systemic vasodilation, which still needs to be explored. Recent observations indicate that the fluid shift during long duration (months) flights is associated with increased retinal thickness that sometimes leads to optical disc oedema. Ocular and cerebral structural changes, increases in left atrial size and decreased flows with thrombi formation in the left internal jugular vein have also been observed. This is of concern for future long duration deep space missions because the health implications are unknown.     

Nitric oxide and GABA mediate bi-directional cardiovascular effects of orexin in the nucleus tractus solitarii of rats

The present study investigated the cardiovascular effects of orexin (OX)-A and OX-B in the nucleus tractus solitarii (NTS) and delineated the engagement of nitric oxide (NO) and GABA in OX-induced cardiovascular responses. In adult male Sprague-Dawley rats maintained under propofol anesthesia, microinjection bilaterally into the NTS of OX-A or OX-B evoked bi-directional cardiovascular effects in a dose-dependent manner. At a lower dose (5 pmol), OX-A or OX-B decreased systemic arterial pressure (SAP), heart rate (HR), and power density of the vasomotor components of SAP signals, our experimental index for sympathetic neurogenic vasomotor tone. At higher doses (>20 pmol), these two compounds elicited cardiovascular excitatory responses. These bi-directional cardiovascular effects of OX were abolished by co-injection of an OX(1) receptor antagonist, 1-(2-methylbenzoxazol-6-yl)-3-[1,5]naphthyridin-4-yl-urea hydrochloride (SB-334867, 0.75 nmol) or the OX(2) receptor antiserum (1:20). In addition, the vasodepressor effects of low dose (5 pmol) OX-A or OX-B in the NTS were attenuated by a nitric oxide synthase (NOS) inhibitor, N(G)-nitro-l-arginine methyl ester (l-NAME, 5 nmol), a neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (2.5 pmol) or the soluble guanylate cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazole[4,3-alpha]quinoxalin-1-one (250 pmol). The vasopressor effects of high dose (200 pmol) OX were reversed by co-administration with GABA(A) or GABA(B) receptor antagonist, bicuculline methiodine (10 pmol) or 2-hydroxy saclofen (100 pmol), or l-NAME (5 nmol). Our results indicate that OX-A or OX-B elicited bi-directional cardiovascular effects via OX receptor-dependent mechanisms. The vasodepressor effects of OX were induced by the nNOS-derived NO and activation of sGC-associated signaling pathway, whereas the vasopressor effects were mediated by interaction with GABAergic or nitrergic neurotransmission in the NTS.     

Intermittent activation of peripheral chemoreceptors in awake rats induces Fos expression in rostral ventrolateral medulla-projecting neurons in the paraventricular nucleus of the hypothalamus

Despite the well-established sympathoexcitation evoked by chemoreflex activation, the specific sub-regions of the CNS underlying such sympathetic responses remain to be fully characterized. In the present study we examined the effects of intermittent chemoreflex activation in awake rats on Fos-immunoreactivity (Fos-ir) in various subnuclei of the paraventricular nucleus of the hypothalamus (PVN), as well as in identified neurosecretory preautonomic PVN neurons. In response to intermittent chemoreflex activation, a significant increase in the number of Fos-ir cells was found in autonomic-related PVN subnuclei, including the posterior parvocellular, ventromedial parvocellular and dorsal-cap, but not in the neurosecretory magnocellular-containing lateral magnocellular subnucleus. No changes in Fos-ir following chemoreflex activation were observed in the anterior PVN subnucleus. Experiments combining Fos immunohistochemistry and neuronal tract tracing techniques showed a significant increase in Fos-ir in rostral ventrolateral medulla (RVLM)-projecting (PVN-RVLM), but not in nucleus of solitarii tract (NTS)-projecting PVN neurons. In summary, our results support the involvement of the PVN in the central neuronal circuitry activated in response to chemoreflex activation, and indicate that PVN-RVLM neurons constitute a neuronal substrate contributing to the sympathoexcitatory component of the chemoreflex.     

Projections of the bed nucleus of the stria terminalis to the mesencephalon,pons, and medulla oblongata in the cat

Summary Injections of HRP in the nucleus raphe magnus and adjoining medial reticular formation in the cat resulted in many labeled neurons in the lateral part of the bed nucleus of the stria terminalis (BNST) but not in the medial part of this nucleus. HRP injections in the nucleus raphe pallidus and in the C2 segment of the spinal cord did not result in labeled neurons in the BNST. Injections of ³H-leucine in the BNST resulted in many labeled fibers in the brain stem. Labeled fiber bundles descended by way of the medial forebrain bundle and the central tegmental field to the lateral tegmental field of pons and medulla. Dense BNST projections could be observed to the substantia nigra pars compacta, the ventral tegmental area, the nucleus of the posterior commissure, the PAG (except its dorsolateral part), the cuneiform nucleus, the nucleus raphe dorsalis, the locus coeruleus, the nucleus subcoeruleus, the medial and lateral parabrachial nuclei, the lateral tegmental field of caudal pons and medulla and the nucleus raphe magnus and adjoining medial reticular formation. Furthermore many labeled fibers were present in the solitary nucleus, and in especially the peripheral parts of the dorsal vagal nucleus. Finally some fibers could be traced in the marginal layer of the rostral part of the caudal spinal trigeminal nucleus. These projections appear to be virtually identical to the ones derived from the medial part of the central nucleus of the amygdala (Hopkins and Holstege 1978). The possibility that the BNST and the medial and central amygdaloid nuclei must be considered as one anatomical entity is discussed.Abbreviations AA anterior amygdaloid nucleus - AC anterior commissure - ACN nucleus of the anterior commissure - ACO cortical amygdaloid nucleus - AL lateral amygdaloid nucleus - AM medial amygdaloid nucleus - APN anterior paraventricular thalamic nucleus - AQ cerebral aqueduct - BC brachium conjunctivum - BIC brachium of the inferior colliculus - BL basolateral amygdaloid nucleus - BNSTL lateral part of the bed nucleus of the stria terminalis - BNSTM medial part of the bed nucleus of the stria terminalis - BP brachium pontis - CA central nucleus of the amygdala - Cd caudate nucleus - CI inferior colliculus - CL claustrum - CN cochlear nucleus - CP posterior commissure - CR corpus restiforme - CSN superior central nucleus - CTF central tegmental field - CU cuneate nucleus - D nucleus of Darkschewitsch - EC external cuneate nucleus - F fornix - G gracile nucleus - GP globus pallidus - HL lateral habenular nucleus - IC interstitial nucleus of Cajal - ICA internal capsule - IO inferior olive - IP interpeduncular nucleus - LC locus coeruleus - LGN lateral geniculate nucleus - LP lateral posterior complex - LRN lateral reticular nucleus - MGN medial geniculate nucleus - MLF medial longitudinal fascicle - NAdg dorsal group of nucleus ambiguus - NPC nucleus of the posterior commissure - nV trigeminal nerve - nVII facial nerve - OC optic chiasm - OR optic radiation - OT optic tract - P pyramidal tract - PAG periaqueductal grey - PC cerebral peduncle - PO posterior complex of the thalamus - POA preoptic area - prV principal trigeminal nucleus - PTA pretectal area - Pu putamen - PUL pulvinar nucleus - R red nucleus - RF reticular formation - RM nucleus raphe magnus - RP nucleus raphe pallidus - RST rubrospinal tract - S solitary nucleus - SC suprachiasmatic nucleus - SCN nucleus subcoeruleus - SI substantia innominata - SM stria medullaris - SN substantia nigra - SO superior olive - SOL solitary nucleus - SON supraoptic nucleus - spV spinal trigeminal nucleus - spVcd spinal trigeminal nucleus pars caudalis - ST stria terminalis - TRF retroflex tract - VC vestibular complex - VTA ventral tegmental area of Tsai - III oculomotor nucleus - Vm motor trigeminal nucleus - VI abducens nucleus - VII facial nucleus - Xd dorsal vagal nucleus - XII hypoglossal nucleus     

Gross anatomical study of the sympathetic cardiac nerves in the house musk shrew (Suncus murinus)

The sympathetic cardiac nerves originating from the cervical and upper thoracic sympathetic ganglia in the house musk shrew (Suncus murinus) were examined using macroscopic and whole‐mount immunohistochemical methods. Based on the results, the nerves were macroscopically classified into the following three groups: nerves innervating the cervical sympathetic ganglia mainly to the arterial porta of the heart; nerves supplying the stellate and thoracic sympathetic ganglia at the level of T2–T5 or T6 for both the arterial and venous portae of the heart; and nerves innervating the thoracic sympathetic ganglia at the level of T4–T9 to the esophagus and lung and then the heart via the blood vessels within the mediastinal pleura. These findings in the house musk shrew suggest a possible primitive morphological pattern of the cervical and thoracic sympathetic nervous system that may be related to those in other mammals, including humans. Anat Rec, 2007. © 2007 Wiley‐Liss, Inc.     

Antinociceptive effects induced by injection of the galanin receptor 1 agonist M617 into central nucleus of amygdala in rats

The present study was performed to explore the antinociceptive effects of M617, a selective galanin receptor 1 agonist, in the central nucleus of amygdala (CeA) of rats. Intra-CeA injection of 0.1 nmol, 0.5 nmol and 1 nmol of M617 induced dose-dependent increases in hindpaw withdrawal latencies (HWLs) to noxious thermal and mechanical stimulations in rats. Furthermore, rats received intra-CeA administration of M617 and galanin. The HWL to noxious thermal and mechanical stimulations increased markedly, and there were no significant differences in HWLs of rats received intra-CeA administration of M617 and galanin. The results demonstrated that intra-CeA injection of M617 induced significant antinociceptive effects in CeA of rats, indicating that galanin receptor 1 may be involved in M617-induced antinociception in the CeA of rats.     

Amygdala projections to central amygdaloid nucleus subdivisions and transition zones in the primate

In rats and primates, the central nucleus of the amygdala (CeN) is most known for its role in responses to fear stimuli. Recent evidence also shows that the CeN is required for directing attention and behaviors when the salience of competing stimuli is in flux. To examine how information flows through this key output region of the primate amygdala, we first placed small injections of retrograde tracers into the subdivisions of the central nucleus in Old world primates, and examined inputs from specific amygdaloid nuclei. The amygdalostriatal area and interstitial nucleus of the posterior limb of the anterior commissure (IPAC) were distinguished from the CeN using histochemical markers, and projections to these regions were also described. As expected, the basal nucleus and accessory basal nucleus are the main afferent connections of the central nucleus and transition zones. The medial subdivision of the central nucleus (CeM) receives a significantly stronger input from all regions compared to the lateral core subdivision (CeLcn). The corticoamygdaloid transition zone (a zone of confluence of the medial parvicellular basal nucleus, paralaminar nucleus, and the sulcal periamygdaloid cortex) provides the main input to the CeLcn. The IPAC and amygdalostriatal area can be divided in medial and lateral subregions, and receive input from the basal and accessory basal nucleus, with differential inputs according to subdivision. The piriform cortex and lateral nucleus, two important sensory interfaces, send projections to the transition zones. In sum, the CeM receives broad inputs from the entire amygdala, whereas the CeLcn receives more restricted inputs from the relatively undifferentiated corticoamygdaloid transition region. Like the CeN, the transition zones receive most of their input from the basal nucleus and accessory basal nucleus, however, inputs from the piriform cortex and lateral nucleus, and a lack of input from the parvicellular accessory basal nucleus, are distinguishing afferent features.     

Projections from the central nucleus of the amygdala to the nucleus pontis oralis in the rat: An anterograde labeling study

The present study was designed to elucidate the neuronal projections from the amygdala to the nucleus pontis oralis (NPO). We propose that glutamatergic cells in the central nucleus of the amygdala (CNA) activate neurons in the NPO, which is the critical brainstem site that is responsible for the generation and maintenance of active (REM) sleep. Phaseolus vulgaris-leucoagglutinin (PHA-L), an anterograde transported neuronal tracer, was iontophoresed into the CNA of adult male Sprague-Dawley rats. After a survival time of 7-8 days, the animals were perfused with a fixative and brain tissue was prepared for histological analysis. Sections of the NPO and CNA, which were immunostained with an antibody against PHA-L, were examined with light microscopy. In addition, in order to identify the phenotype of PHA-L-labeled fibers and terminals in the NPO, a double immunohistochemical technique was employed with antibodies against PHA-L and the vesicular glutamate transporter type 2 (VGluT2). Numerous PHA-L-labeled axons and terminals were found in the NPO ipsilateral to the injection site in the CNA. Within the NPO, the majority of labeled fibers were located in the dorsolateral portion of the caudal part of the nucleus. Double-labeling immunostaining studies revealed that PHA-L-labeled axons and terminals in the NPO were glutamatergic. The present demonstration of direct, excitatory (glutamatergic) projections from the CNA to the NPO provide an anatomical basis for the amygdalar control of active sleep.     

去除窦弓神经引起下丘脑室旁核小细胞部氮能神经元持续激活(英文)

目的:旨在研究去除窦弓神经是否导致下丘脑室旁核(PVN)氮能神经元处于持续激活状态。方法:成年大鼠行窦弓神经去除术,1周后制备下丘脑脑片,进行还原型尼克酰胺腺嘌呤二核苷酸脱氢酶(NADPH-d)组织化学结合Fos免疫组织化学染色。结果:在PVN的内侧、背侧和外侧小细胞部有大量Fos阳性神经元分布,并与NADPH-d部分共存,但在PVN的室周和前小细胞部以及大细胞仅观察到弱阳性的Fos信号,偶尔观察到双标记神经元。结论:去窦弓神经大鼠下丘脑室旁核小细胞部氮能神经元处于持续激活状态,可能起代偿性抑制中枢交感活性的作用。     

Cardiovascular function of a glutamatergic projection from the hypothalamic paraventricular nucleus to the nucleus tractus solitarius in the rat

Experiments were done in urethane-anesthetized, barodenervated, male Wistar rats. Chemical stimulation of the hypothalamic paraventricular nucleus (PVN) by unilateral microinjections of N-methyl-d-aspartic acid (NMDA) elicited increases in mean arterial pressure (MAP) and greater splanchnic nerve activity (GSNA). The increases in the MAP and GSNA induced by chemical stimulation of the PVN were significantly exaggerated by bilateral microinjections of d(−)-2-amino-7-phosphono-heptanoic acid (d-AP7) and 2,3-dioxo-6-nitro-1,2,3,4-tetrahydro-benzo[f]quinoxaline-7-sulfonamide disodium (NBQX) (ionotropic glutamate receptor antagonists) into the medial subnucleus of the nucleus tractus solitarius (mNTS). These results were confirmed by single unit recordings; i.e. excitation of mNTS barosensitive neurons caused by chemical stimulation of the ipsilateral PVN was blocked by application of d-AP7 and NBQX to these neurons. Bilateral microinjections of d-AP7 and NBQX into the mNTS elicited pressor responses which were significantly attenuated by inhibition of PVN neurons by bilateral microinjections of muscimol. Unilateral microinjections of fluorogold into the mNTS resulted in bilateral retrograde labeling of the PVN neurons. Unilateral microinjections of biotinylated dextran amine into the PVN resulted in anterograde labeling of axons and terminals in the mNTS bilaterally and the labeled terminals exhibited vesicular glutamate transporter-2 immunoreactivity. These results indicated that 1) a tonically active glutamatergic bilateral projection from the PVN to the mNTS exists; 2) bilateral blockade of ionotropic glutamate receptors in the mNTS exaggerates the increases in MAP and GSNA, but not heart rate, to the chemical stimulation of the PVN; and 3) this projection may serve as a restraint mechanism for excitatory cardiovascular effects of PVN stimulation.