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Superior Cervical Ganglion (superior + cervical_ganglion)
Selected AbstractsThe Developing Left Superior Cervical Ganglion of Pacas (Agouti paca)THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 7 2009Samanta Rios Melo Abstract In this study the main question investigated was the number and size of both binucleate and mononucleate superior cervical ganglion (SCG) neurons and, whether post-natal development would affect these parameters. Twenty left SCGs from 20 male pacas were used. Four different ages were investigated, that is newborn (4 days), young (45 days), adult (2 years), and aged animals (7 years). By using design-based stereological methods, that is the Cavalieri principle and a physical disector combined with serial sectioning, the total volume of ganglion and total number of mononucleate and binucleate neurons were estimated. Furthermore, the mean perikaryal (somal) volume of mononucleate and binucleate neurons was estimated using the vertical nucleator. The main findings of this study were a 154% increase in the SCG volume, a 95% increase in the total number of mononucleate SCG neurons and a 50% increase in the total volume of SCG neurons. In conclusion, apart from neuron number, different adaptive mechanisms may coexist in the autonomic nervous system to guarantee a functional homeostasis during ageing, which is not always associated with neuron losses. Anat Rec, 2009. © 2009 Wiley-Liss, Inc. [source] High-frequency stimuli preferentially release large dense-core vesicles located in the proximity of nonspecialized zones of the presynaptic membrane in sympathetic gangliaDEVELOPMENTAL NEUROBIOLOGY, Issue 4 2008F. Cifuentes Abstract We characterized the effect of a brief high-frequency stimulus on the number, distribution, and optical density of large dense-core vesicles (LDCVs) in the nerve terminals of the rat superior cervical ganglia. From 4.21 ± 0.37 LDCVs/bouton detected in control nerve terminals, a stimulus of 40 Hz for 1 min released 41% of LDCVs, decreasing their number to 2.48 ± 0.14 LDCVs/bouton (p = 0.0009). In control ganglia, most dense vesicles were located close to the plasma membrane (at ,100 nm); in contrast, in stimulated ganglia they were broadly distributed with respect to the active zone. The mean distance of LDCVs to membrane and active zones was 95 ± 8 nm and 473 ± 15 nm, respectively. The analysis of the core density showed that both groups had a similar asymmetric distribution with the same average. Stimulation preferentially released those vesicles located ,100 nm from the plasma membrane that had no apparent relationship with the active zone. After the stimulus, the average distances of LDCVs to the plasma membrane and active zone did not change, suggesting that the stimulus also caused the relocation of inner LDCVs. Interestingly, optical density analysis showed that the released vesicles had low range densities, and suggested that LDCVs release their entire content. We conclude that LDCV exocytosis mainly involves those vesicles located ,100 nm from the plasma membrane and occurs in regions of synaptic boutons presumed to be nonspecialized. These results agree with the characteristics of the classical model that proposes full content release. © 2008 Wiley Periodicals, Inc. Develop Neurobiol, 2008. [source] Nerve growth factor expression in parasympathetic neurons: regulation by sympathetic innervationEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2000Wohaib Hasan Abstract Interactions between sympathetic and parasympathetic nerves are important in regulating visceral target function. Sympathetic nerves are closely apposed to, and form functional synapses with, parasympathetic axons in many effector organs. The molecular mechanisms responsible for these structural and functional interactions are unknown. We explored the possibility that Nerve Growth Factor (NGF) synthesis by parasympathetic neurons provides a mechanism by which sympathetic,parasympathetic interactions are established. Parasympathetic pterygopalatine ganglia NGF-gene expression was examined by in situ hybridization and protein content assessed by immunohistochemistry. Under control conditions, NGF mRNA was present in ,,60% and NGF protein was in 40% of pterygopalatine parasympathetic neurons. Peripheral parasympathetic axons identified by vesicular acetylcholine transporter-immunoreactivity also displayed NGF immunoreactivity. To determine if sympathetic innervation regulates parasympathetic NGF expression, the ipsilateral superior cervical ganglion was excised. Thirty days postsympathectomy, the numbers of NGF mRNA-positive neurons were decreased to 38% and NGF immunoreactive neurons to 15%. This reduction was due to a loss of sympathetic nerve impulse activity, as similar reductions were achieved when superior cervical ganglia were deprived of preganglionic afferent input for 40 days. These findings provide evidence that normally NGF is synthesized by parasympathetic neurons and transported anterogradely to fibre terminals, where it may be available to sympathetic axons. Parasympathetic NGF expression, in turn, is augmented by impulse activity within (and presumably transmitter release from) sympathetic axons. It is suggested that parasympathetic NGF synthesis and its modulation by sympathetic innervation provides a molecular basis for establishment and maintenance of autonomic axo-axonal synaptic interactions. [source] How important is stimulation of ,-adrenoceptors for melatonin production in rat pineal glands?JOURNAL OF PINEAL RESEARCH, Issue 4 2002V. A. Tobin The objective of this study was to determine the role of , -adrenoceptors in melatonin production by rat pineal gland. Pineal glands were isolated from adult male rats and maintained in organ baths. The perfusate was sampled every 5 min, stored, and later assayed for melatonin. Exposure to norepinephrine (10 ,M) or the , -adrenoceptor agonist orciprenaline (2,10 ,M) increased the glands' production of melatonin. The time courses of melatonin production in response to these agonists were unaffected by the rats' pretreatment in vivo with the , -adrenoceptor antagonist prazosin (2 mg/kg i.p., three times). Rats that had had their superior cervical ganglia removed were primed with either orciprenaline (2 mg/kg i.p) or both orciprenaline and phenylephrine (1 mg/kg i.p) 1 hr before decapitation. Exposure of the pineal glands from these rats to orciprenaline evoked melatonin release that was similar in each group. These results lend weight to the suggestion that the marked potentiation by , -adrenoceptor agonists of the stimulation of cAMP and N-acetyltransferase (NAT) by , -adrenoceptor agonists, demonstrated most readily in cultured glands or dispersed rat pinealocytes, does not carry over into significant augmentation of melatonin production in intact pineal glands. [source] Age-Related Sympathetic Ganglionic Neuropathology: Human Pathology And Animal ModelsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2002RE. Schmidt Systematic studies of the autonomic nervous system of human subjects and development of well-defined animal models have begun to substantially improve our understanding of the pathogenesis of autonomic dysfunction in aging and may eventually provide strategies for intervention. Neuropathological studies of the sympathetic ganglia of aged human subjects and rodent models have demonstrated that neuroaxonal dystrophy involving intraganglionic terminal axons and synapses is a robust, unequivocal and consistent neuropathological finding in the aged sympathetic nervous system of man and animals. Quantitative studies have demonstrated that markedly swollen argyrophilic dystrophic axon terminals develop in the prevertebral superior mesenteric (SMG) and coeliac, but to a much lesser degree in the superior cervical ganglia (SCG) as a function of age, sex (males more than females) and diabetes. Dystrophic axons were immunoreactive for neuropeptide Y, tyrosine hydroxylase, dopamine-beta-hydroxylase, trkA and p75(NTR), an immunophenotype consistent with their origin from postganglionic sympathetic neurons, and contained large numbers of highly phosphorylated neurofilaments or tubulovesicular elements. The sympathetic ganglia of aged rodents also showed the hallmark changes of neuroaxonal dystrophy as a function of age and location (many more in the SMG than in the SCG). Plasticity-related synaptic remodeling could represent a highly vulnerable target of the aging process. The fidelity of animal models to the neuropathology of aged humans suggests that similar pathogenetic mechanisms may be involved in both and that therapeutic advances in animal studies may have human application. [source] Distribution and Cytoarchitecture of Sympathetic Neurons Innervating the Pineal Gland in Chick: A CTB-HRP StudyANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 1 2009L. Jia Summary The neurons in bilateral superior cervical ganglia (SCG) innervating the chick pineal gland were labelled by using the technique of retrograde axonal labelling with cholera toxin B subunit linked to horseradish peroxidase (CTB-HRP). To our results, perikarya of these sympathetic neurons distributed from rostral to caudal in the SCG, and mainly localized in the opposite side of the paravertebral trunk. The fibres of these neurons were collected by the cephalic carotid nerve. According to the sizes of somal area and dendritic field, these sympathetic neurons projecting to the pineal gland were classified into four major groups: group I cells (52.4%) with a small somal area (303.5 ,m2 on average) and narrow dendritic field (3767.8 ,m2 on average), group II cells (39.0%) with a middle-sized somal area (473.3 ,m2) and middle-sized dendritic field (7522.2 ,m2), group III cells (6.4%) with a middle-sized somal area (473.4 ,m2) and wide dendritic field (13 104.4 ,m2), and group IV cells (2.2%) with a large somal area (940.7 ,m2) and wide dendritic field (14 553.2 ,m2). Of these pineal projecting neurons, most took on a lesser dendritic field. The neurons with small or middle-sized dendritic field from group I and II were about 91.4% of the total neurons labelled with CTB-HRP, and the neurons with wide dendritic field from group III and IV were less with 8.6%. [source] The Anticonvulsant SGB-017 (ADCI) Blocks Voltage-Gated Sodium Channels in Rat and Human Neurons: Comparison with CarbamazepineEPILEPSIA, Issue 3 2000Lucy Sun Summary: Purpose: SGB-017 (ADCI) is a novel anticonvul-sant that blocks both voltage-activated sodium channels and N -methyl- d -aspartate (NMDA)-receptor-gated channels. Results by Rogawski et al. suggested that SGB-017 produces its anticonvulsant action primarily by inhibition of NMDA-receptor channels. However, SGB-017 is effective in several animal models of epilepsy that are unresponsive to NMDA antagonists. These results indicate that block of NMDA-receptor channels is not the only mechanism contributing to its anticonvulsant activity. Thus the effects of SGB-017 on neu-ronal sodium channels were investigated. Methods: Whole cell voltage-clamp techniques were used to record sodium currents in freshly dissociated rat superior cervical ganglion (SCG) and hippocampal neurons and cultured human NT2 neurons. The effects of SGB-017 on the amplitude of sodium currents, elicited by a depolarizing pulse to 0 mV from different holding potentials, were measured and compared with those of carbamazepine (CBZ). Results: SGB-017 inhibited sodium currents in rat SCG and hippocampal neurons with a similar potency to CBZ. Like CBZ, the inhibition of sodium channels by SGB-017 was voltage dependent. Its median inhibitory concentration (IC50) for inhibition of sodium channels at depolarized holding potentials is similar to that for its inhibition of NMDA receptor channels. In human hNT2 neurons, SGB-017 was more potent than CBZ at inhibiting sodium currents. Conclusions: SGB-017 produces its anticonvulsant activity by blocking both sodium- and NMDA-receptor channels in a voltage- and use-dependent manner. The combination of these two mechanisms of action makes SGB-017 an effective AED in several different animal models of epilepsy. [source] The role of NGF uptake in selective vulnerability to cell death in ageing sympathetic neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2004Kliment P. Gatzinsky Abstract We have examined the hypothesis that differences in nerve growth factor (NGF) uptake and transport determine vulnerability to age-related neurodegeneration. Neurons projecting to cerebral blood vessels (CV) in aged rats are more vulnerable to age-related degeneration than those projecting to the iris. Uptake of NGF was therefore examined in sympathetic neurons projecting from the superior cervical ganglion (SCG) to CV and iris in young and old rats by treating the peripheral processes of these neurons with different doses of I125 -NGF. Total uptake of I125 -NGF was reduced in old CV-projecting, but not iris-projecting, neurons. Numbers of radiolabelled neurons projecting to each target were counted in sectioned ganglia. The data showed age-related reductions in numbers of labelled neurons projecting to CV, but no change in numbers of neurons projecting to the iris. Calculation of uptake of I125 -NGF per neuron unexpectedly showed no major age-related differences in either of the two neuron populations. However, uptake per neuron was considerably lower for young and old CV-projecting, compared to iris-projecting, SCG neurons. We hypothesized that variations in NGF uptake might affect neuronal survival in old age. Counts of SCG neurons using a physical disector following retrograde tracing with Fluorogold confirmed the selective vulnerability of CV-projecting neurons by showing a significant 37% loss of these neurons in the period between 15 and 24 months. In contrast, there was no significant loss of iris-projecting neurons. We conclude that vulnerability to, or protection from, age-related neurodegeneration and neuronal cell death are associated with life-long low, or high, levels of NGF uptake, respectively. [source] Nerve growth factor expression in parasympathetic neurons: regulation by sympathetic innervationEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2000Wohaib Hasan Abstract Interactions between sympathetic and parasympathetic nerves are important in regulating visceral target function. Sympathetic nerves are closely apposed to, and form functional synapses with, parasympathetic axons in many effector organs. The molecular mechanisms responsible for these structural and functional interactions are unknown. We explored the possibility that Nerve Growth Factor (NGF) synthesis by parasympathetic neurons provides a mechanism by which sympathetic,parasympathetic interactions are established. Parasympathetic pterygopalatine ganglia NGF-gene expression was examined by in situ hybridization and protein content assessed by immunohistochemistry. Under control conditions, NGF mRNA was present in ,,60% and NGF protein was in 40% of pterygopalatine parasympathetic neurons. Peripheral parasympathetic axons identified by vesicular acetylcholine transporter-immunoreactivity also displayed NGF immunoreactivity. To determine if sympathetic innervation regulates parasympathetic NGF expression, the ipsilateral superior cervical ganglion was excised. Thirty days postsympathectomy, the numbers of NGF mRNA-positive neurons were decreased to 38% and NGF immunoreactive neurons to 15%. This reduction was due to a loss of sympathetic nerve impulse activity, as similar reductions were achieved when superior cervical ganglia were deprived of preganglionic afferent input for 40 days. These findings provide evidence that normally NGF is synthesized by parasympathetic neurons and transported anterogradely to fibre terminals, where it may be available to sympathetic axons. Parasympathetic NGF expression, in turn, is augmented by impulse activity within (and presumably transmitter release from) sympathetic axons. It is suggested that parasympathetic NGF synthesis and its modulation by sympathetic innervation provides a molecular basis for establishment and maintenance of autonomic axo-axonal synaptic interactions. [source] Nicotinic acetylcholine receptor-subunit mRNAs in the mouse superior cervical ganglion are regulated by development but not by deletion of distinct subunit genesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2008G. Putz Abstract Mice with deletions of nicotinic ACh receptor (nAChR) subunit genes are valuable models for studying nAChR functions. We could previously show in the mouse superior cervical ganglion (SCG) that the absence of distinct subunits affects the functional properties of receptors. Here, we have addressed the question of whether deletions of the subunits ,5, ,7, or ,2 are compensated at the mRNA level, monitored by reverse transcription and quantitative real-time polymerase chain reaction. Relative to our reference gene, ,3, which is expressed in all SCG nAChRs, mRNA levels of ,4 showed little change from birth until adult ages in intact ganglia of wild-type mice. In contrast, ,4 declined sharply after birth and was barely detectable in adult animals. ,5, ,7, and ,2 subunit message levels also declined, though more slowly and less completely than ,4. The subunits ,6 and ,3 were detected by conventional polymerase chain reaction at very low levels, if at all, whereas ,2 was never seen in any of our samples. The developmental profile of nAChR mRNA levels in the three knockout strains did not differ markedly from that of wild-type mice. Likewise, message levels of nAChR subunits were similar in cultures prepared from either wild-type or knockout animals. Our observations indicate a developmental regulation of nAChR subunit mRNAs in the SCG of mice after birth that was not affected by the three knockouts under investigation. © 2007 Wiley-Liss, Inc. [source] BDNF activated TrkB/IRR receptor chimera promotes survival of sympathetic neurons through Ras and PI-3 kinase signalingJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2002Karen S. Kelly-Spratt Insulin receptor-related receptor (IRR) expression is tightly coupled to the nerve growth factor (NGF) receptor, TrkA, throughout development. Expression of both receptors is primarily localized to neural crest derived sensory and sympathetic neurons. In contrast to TrkA, however, the physiological ligand for IRR is unknown. To analyze the intracellular signaling and potential function of the orphan IRR in neurons, an adenovirus expressing a TrkB/IRR chimeric receptor was used to infect cultured mouse superior cervical ganglion neurons that normally require NGF for survival. Brain derived neurotrophic factor (BDNF)-activated TrkB/IRR induced neuronal survival. We utilized numerous receptor mutants in order to identify the intracellular domains of IRR necessary for signaling and neuron survival. Finally, we employed adenovirus encoding dominant negative forms of the extracellular signal-regulated kinase (ERK) signaling cascade to demonstrate that IRR, like TrkA, requires ras activation to promote neuron survival. Therefore, by use of the chimeric TrkB/IRR receptor, we have demonstrated the ability of IRR to elicit activation of signaling cascades resulting in a biological response in superior cervical ganglion (SCG) neurons. © 2002 Wiley-Liss, Inc. [source] Natriuretic peptides in relation to the cardiac innervation and conduction systemMICROSCOPY RESEARCH AND TECHNIQUE, Issue 5 2002Magnus HanssonArticle first published online: 10 SEP 200 Abstract During the past two decades, the heart has been known to undergo endocrine action, harbouring peptides with hormonal activities. These, termed "atrial natriuretic peptide (ANP)," "brain natriuretic peptide (BNP)," and "C-type natriuretic peptide (CNP)," are polypeptides mainly produced in the cardiac myocardium, where they are released into the circulation, producing profound hypotensive effects due to their diuretic, natriuretic, and vascular dilatory properties. It is, furthermore, well established that cardiac disorders such as congestive heart failure and different forms of cardiomyopathy are combined with increased expression of ANP and BNP, leading to elevated levels of these peptides in the plasma. Besides the occurrence of natriuretic peptides (NPs) in the ordinary myocardium, the presence of ANP in the cardiac conduction system has been described. There is also evidence of ANP gene expression in nervous tissue such as the nodose ganglion and the superior cervical ganglion of the rat, ganglia known to be involved in the neuronal regulation of the heart. Furthermore, in the mammalian heart, ANP appears to affect the cardiac autonomic nervous system by sympathoinhibitory and vagoexcitatory actions. This article provides an overview of the relationship between the cardiac conduction system, the cardiac innervation and NPs in the mammalian heart and provides data for the concept that ANP is also involved in neuronal cardiac regulation. Microsc. Res. Tech. 58:378,386, 2002. © 2002 Wiley-Liss, Inc. [source] Histopathological basis of Horner's syndrome in obstetric brachial plexus palsy differs from that in adult brachial plexus injuryMUSCLE AND NERVE, Issue 5 2008Yi-Gang Huang MD Abstract Although Horner's syndrome is usually taken as an absolute indicator of avulsions of the C8 and T1 ventral roots in adult brachial plexus injury, its pathological basis in obstetric brachial plexus palsy (OBPP) is unclear. We therefore examined the morphological mechanism for the presence of Horner's syndrome in brachial plexus injury in infants and adults. Some axons of sympathetic preganglionic neurons in T1 innervate the superior cervical ganglion via the C7 ventral root in infants but not in adults. Therefore, the presence of Horner's syndrome may relate in part to avulsion of the C7 root in OBPP. These findings suggest that Horner's syndrome in OBPP is not necessarily indicative of avulsions of the C8 and T1 roots, as it can occur with avulsion of the C7 root. Muscle Nerve, 2008 [source] The Developing Left Superior Cervical Ganglion of Pacas (Agouti paca)THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 7 2009Samanta Rios Melo Abstract In this study the main question investigated was the number and size of both binucleate and mononucleate superior cervical ganglion (SCG) neurons and, whether post-natal development would affect these parameters. Twenty left SCGs from 20 male pacas were used. Four different ages were investigated, that is newborn (4 days), young (45 days), adult (2 years), and aged animals (7 years). By using design-based stereological methods, that is the Cavalieri principle and a physical disector combined with serial sectioning, the total volume of ganglion and total number of mononucleate and binucleate neurons were estimated. Furthermore, the mean perikaryal (somal) volume of mononucleate and binucleate neurons was estimated using the vertical nucleator. The main findings of this study were a 154% increase in the SCG volume, a 95% increase in the total number of mononucleate SCG neurons and a 50% increase in the total volume of SCG neurons. In conclusion, apart from neuron number, different adaptive mechanisms may coexist in the autonomic nervous system to guarantee a functional homeostasis during ageing, which is not always associated with neuron losses. Anat Rec, 2009. © 2009 Wiley-Liss, Inc. [source] SERCA function declines with age in adrenergic nerves from the superior cervical ganglionAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 5-6 2000W. J. Pottorf 1 Intracellular calcium is a universal second messenger integrating numerous cellular pathways. An age-related breakdown in the mechanisms controlling [Ca2+]i homeostasis could contribute to neuronal degeneration. One component of neuronal calcium regulation believed to decline with age is the function of sarco/endoplasmic reticulum calcium ATPase (SERCA) pumps. 2 Therefore we investigated the impact of age on the capacity of SERCA pumps to control high (68 m M) [K+]-evoked [Ca2+]i -transients in acutely dissociated superior cervical ganglion (SCG) cells from 6- and 20-month-old Fisher-344 rats. Calcium transients were measured by fura-2 microfluorometry in the presence of vanadate (0.1 ,M) to selectively block plasma membrane calcium ATPase (PMCA) pumps, dinitrophenol (100 ,M) to block mitochondrial calcium uptake and extracellular sodium replaced with tetraethylammonium to block Na+/Ca2+ -exchanger, thus forcing the neuronal cells to rely on SERCA uptake to control [Ca2+]i homeostasis. 3 In the presence of these calcium buffering blockers, the rate of recovery of [Ca2+]i was significantly slower and time to recover to approximately 90% of resting [Ca2+]i was significantly greater in SCG cells from old (20 months) compared with young (6 months) animals. 4 This age-related change in the recovery phase of [K+]-evoked [Ca2+]i -transients could not be explained by differences in the sensitivity of SCG cells to the calcium buffering blockers, as no age-related difference in basal [Ca2+]i was observed. 5 These studies illustrate that when rat SCG cells are forced to rely on SERCAs to buffer [K+]-evoked [Ca2+]i -transients, an age-related decline in SERCA function is revealed. Such age-related declines in calcium regulation coupled with neuronal sensitivity to calcium overload underscore the importance of understanding the components of [Ca2+]i homeostasis and the functional compensation that may occur with advancing age. [source] 2215: Animal models of herpetic retinitisACTA OPHTHALMOLOGICA, Issue 2010M LABETOULLE The Herpes simplex virus (HSV) is characterized its ability to replicate in the nervous system, before inducing a latent infection with potential reactivation. Most frequent ocular complications of recurrent HSV infection are keratitis and conjunctivitis. Less frequently, the iris and the ciliary body may also be involved (anterior uveitis). The most severe HSV ocular infection is retinitis, a rare but potentially blinding disease, due to frequent bilateral involvement. Studies on human post-mortem tissues showed that HSV is widely distributed in the population, with a preferential location within the trigeminal ganglions (innervating the cornea), but also in the superior cervical ganglions (innervating the iris) or in brain/medullar tissues (innervating the retina). Animal models have been developed to understand the pathogenic processes that lead to this rare but devastating retinal disease. Since human is the only natural host of HSV, it is difficult to obtain a perfect animal model that perfectly mimics the disease. Several animal models, based on different inoculation procedures, are thus necessary to circumscribe the anatomical, cellular and molecular aspects that lead to retinal infection. Finally, HSV retinitis appears as a clinical condition that is highly constrained by the relationships between the strain of the virus and the immune response of the host. [source] | |||||||||||||||||||||||||