Effects of reserpine and monoamine oxidase inhibition on the levels of amino acids in sensory ganglia, sympathetic ganglia and spinal cord.
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Alanine↗
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Contribution of enzyme histochemistry as to the nature and differences among mantle cells (satellite cells), amphicytes, and Schwann cells in remak fiber bundles and of myelinated fibers in dorsal root ganglia, sympathetic ganglia and in peripheral nerves of various animals.
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Animals↗
Receptor binding sites for cholecystokinin, galanin, somatostatin, substance P and vasoactive intestinal polypeptide in sympathetic ganglia.
Sympathetic ganglia are innervated by neuropeptide-containing fibers originating from pre- and postganglionic sympathetic neurons, dorsal root ganglion neurons, and in some cases, myenteric neurons. In the present report receptor autoradiography was used to determine whether sympathetic ganglia express receptor binding sites for several of these neuropeptides including bombesin, calcitonin gene-related peptide-alpha, cholecystokinin, galanin, neurokinin A, somatostatin, substance P, and vasoactive intestinal polypeptide. The sympathetic ganglia examined included the rat and rabbit superior cervical ganglia and the rabbit superior mesenteric ganglion. High levels of receptor binding sites for cholecystokinin, galanin, somatostatin, substance P, and vasoactive intestinal polypeptide were observed in all sympathetic ganglia examined, although only discrete neuronal populations within each ganglion appeared to express receptor binding sites for any particular neuropeptide. These data suggest that discrete populations of postganglionic sympathetic neurons may be regulated by neuropeptides released from pre- and postganglionic sympathetic neurons, dorsal root ganglion neurons, and myenteric neurons.
Animals↗
RU38486 blocks the steroid regulation of transmitter choice in cultured rat sympathetic ganglia.
Sympathetic neurones grown in tissue culture change phenotype from adrenergic to cholinergic due to a factor released by non-neuronal cells. Glucocorticosteroids prevent the production of this factor by non-neuronal cells and hence prevent the change in phenotype. Conventional steroid antagonists, however, fail to block this effect. We report here that the steroid antagonist RU38486 is effective in preventing the action of corticosterone on cultured sympathetic ganglia and hence may be a useful in vivo tool to study the steroid regulation of development.
Animals↗
Imaging neural crest cell dynamics during formation of dorsal root ganglia and sympathetic ganglia.
The neural crest is a migratory population of cells that produces many diverse structures within the embryo. Trunk neural crest cells give rise to such structures as the dorsal root ganglia (DRG) and sympathetic ganglia (SG), which form in a metameric pattern along the anterior-posterior axis of the embryo. While static analyses have provided invaluable information concerning the development of these structures, time-lapse imaging of neural crest cells navigating through their normal environment could potentially reveal previously unidentified cellular and molecular interactions integral to DRG and SG development. In this study, we follow fluorescently labeled trunk neural crest cells using a novel sagittal explant and time-lapse confocal microscopy. We show that along their dorsoventral migratory route, trunk neural crest cells are highly motile and interact extensively with neighboring cells and the environment, with many cells migrating in chain-like formations. Surprisingly, the segregated pattern of crest cell streams through the rostral somite is not maintained once these cells arrive alongside the dorsal aorta. Instead, neural crest cells disperse along the ventral outer border of the somite, interacting extensively with each other and their environment via dynamic extension and retraction of filopodia. Discrete sympathetic ganglia arise as a consequence of intermixing and selective reorganization of neural crest cells at the target site. The diverse cell migratory behaviors and active reorganization at the target suggest that cell-cell and cell-environment interactions are coordinated with dynamic molecular processes.
Animals↗
The effect of hydrocortisone and adrenocorticotrophic hormone on monoamine oxidase and tyrosine hydroxylase in explant cultures of embryonic chick sympathetic ganglia.
Sympathetic ganglia from 13- to 15-day-old embryonic chicks were cultured for up to 2 days in Leighton tubes. The influence of hydrocortisone and ACTH added to the culture medium on the enzymes monoamine oxidase (MAO) and tyrosine hydroxylase was studied. Hydrocortisone (5 times 10(-5)M) had no effect on tyrosine hydroxylase but increased MAO activity by up to 46 percent over control values under conditions of low or zero nerve growth factor (NGF) concentration. ACTH also increased ganglionic MAO activity, the effect again depending on NGF concentration. This time the maximal response (an increase of 50 percent over controls) was seen at high NGF concentrations. This response was similar to the effect of 1 mM dibutyryl cyclic AMP, and was blocked by 1 times 10-5 M propranolol and 10 muM prostaglandin E(1). ACTH only slightly increased tyrosine hydroxylase activity and this effect was due to a small (18 percent) increase in sympathetic neurone number. Guanosine 5-diphosphate (0.5 mM) was found to increase tyrosine hydroxylase activity by 57 percent and this effect was blocked by the presence of ACTH.
Adrenocorticotropic Hormone↗
Region- and stage-specific patterns of melanocortin receptor ontogeny in rat central nervous system, cranial nerve ganglia and sympathetic ganglia.
Observations on developmental actions of melanotropic peptides in nervous system have been difficult to interpret in the absence of data on receptor ontogeny. We investigated binding of [125I]Nle4,D-Phe7-alpha-MSH ([125I]NDP) in developing Long Evans rats from gestational day (E) 13 by quantitative autoradiography. Regional [125I]NDP binding characteristics were assessed by competition experiments in early postnatal brain. The study revealed region- and stage-specific, often transient ontogenetic patterns. Sympathetic ganglia exhibit high [125I]NDP binding from E13, with a peak in superior cervical ganglion at E16-E18. The first central [125I]NDP binding sites transiently appear in parts of thalamus between E13 and E15. The early fetal period is characterized by prominent peaks of receptor density in somatosensory and viscerosensory nuclei (trigeminal sensory nuclei, solitary tract nucleus), paralleled by receptor expression in 5th, 7th, 9th and 10th cranial nerve ganglia. During late fetal life, receptor density peaks in dorsal motor nucleus of vagus and inferior olive; binding sites transiently appear in cerebellum. Caudate-putamen, nucleus accumbens, olfactory tubercle and septohippocampal nucleus show a high perinatal maximum. Starting with late fetal piriform cortex, [125I]NDP binding peaks sequentially in cerebral cortical areas, with highest levels in entorhinal cortex. Preoptic, septal, hypothalamic and amygdaloid areas known for elevated receptor densities in adulthood, exhibit a slow, peri- and postnatal receptor ontogeny. Temporal relations to regional developmental processes support the idea of a role of melanocortins during ontogeny.
Affinity Labels↗
Development of differential preganglionic projections to pre- and paravertebral sympathetic ganglia.
Sympathetic preganglionic axons project to spatially distinct targets in the periphery. A precise topographic pattern exists within the thoracic preganglionic cell column relative to the direction of axonal projections within the sympathetic chain. In this study, the time course and pattern of axonal outgrowth from different populations of preganglionic neurons in the chicken embryo is examined in detail to clarify the origin of the topography in this system. Projections to prevertebral targets are established by development of the splanchnic nerves by stage 25, well after the earliest somatic motor projections at stage 19 but at least two stages before the reported onset of paravertebral projections. Further, preganglionic axons that project rostrally into the sympathetic chain may do so earlier than those that project caudally in the chain. The separation of preganglionic axons into prevertebral, rostral paravertebral or caudal paravertebral directions occurs at a common site in the ventral mesenchyme, established by the initial ventromedial projection of the splanchnic nerves. Analysis of the axonal trajectories of rostrally and caudally projecting cells reveals that preganglionic axons are not selectively fasciculated before their point of separation at the sympathetic chain. The patterning of the preganglionic cell column is specified before the establishment of functional connections within the chain, indicating that target contact is not a determinant of the segmental pattern. We suggest that the differential outgrowth of preganglionic axons to peripheral targets is determined by the unique identities of underlying subpopulations of preganglionic axons.
Acetylcholinesterase↗
Expression of nerve growth factor in vivo from a defective herpes simplex virus 1 vector prevents effects of axotomy on sympathetic ganglia.
Sympathetic neurons in the superior cervical ganglion (SCG) of adult rats depend on target-derived nerve growth factor (NGF) for maintenance of tyrosine hydroxylase (TH) levels and the noradrenergic neurotransmitter system. Axotomy of a SCG results in NGF deprivation, causing a decline in TH activity; continuous local application of NGF can prevent this decline in TH activity. We now report that injection of a defective herpes simplex virus 1 vector that expresses NGF (pHSVngf) into a SCG can prevent the decline in TH activity that follows axotomy. SCG of adult rats were injected with either pHSVngf virus or pNFlac virus, which expresses Escherichia coli beta-galactosidase. Analysis of RNA from pHSVngf-infected SCG indicated that the NGF gene was efficiently transcribed and processed. Furthermore, 4 days after pHSVngf injection animals underwent axotomy of the virus-injected SCG. After another 10 days, animals were sacrificed and both the injected-axotomized and contralateral control ganglia were assayed for TH activity. Axotomy of SCG injected with pNFlac virus produced a 50% decline in TH activity relative to control ganglia (P = 0.02). In contrast, SCG injected with pHSVngf virus did not show a decline in TH activity following axotomy; instead, these ganglia manifested an 18% increase in TH levels relative to control ganglia. These data demonstrate that herpes simplex virus 1 vectors can be used to modify neuronal physiology in vivo; specifically, expression of a critical gene product by neural cells that do not normally produce it has potential applications for gene therapy.
Base Sequence↗
[Neural circuit of the cervical sympathetic nervous system with special reference to input and output of the cervical sympathetic ganglia: relationship between spinal cord and cervical sympathetic ganglia and that between cervical sympathetic ganglia and their target organs].
Using anterograde labeling technique with Phaseolus vulgaris leucoagglutinin (PHA-L), we demonstrated the arborization pattern of a single preganglionic axon in the superior cervical ganglion (SCG) and stellate ganglion (STG). These axons expanded in the longitudinal direction, but not for transverse direction. Segmental relationship was identified between the spinal cord and STG, as seen between spinal cord and sympathetic ganglia in the thoraco-lumbar region, but we did not find any segmental relationship between the spinal cord and SCG. Some sympathetic preganglionic neurons in the lateral horn of the thoracic cord, especially in the intermediolateral nucleus (IML) have nitric oxide synthase (NOS) activity. We demonstrated that SCG neurons, which were heavily innervated by these NOS-positive neurons, tended to innervate organs that have some secretory functional tissues. Finally, we showed that the size of neuronal somata does not correlate with the size of target organs, as has been reported in previous studies. We should consider that there are other factors determining the size of neuronal somata, such as the size of dendritic field or volumes of NGF secretory from target tissues.
Animals↗
Does failed natural opioid modulation in regional sympathetic ganglia cause reflex sympathetic dystrophy?
Early features of reflex sympathetic dystrophy in a limb resemble the general effects of autonomic arousal associated with opioid withdrawal. It is suggested that natural opioid peptide modulation in regional sympathetic ganglia normally rises to prevent excessive autonomic activity in an injured limb. After an injury (especially a trivial one) to a susceptible subject, this localised increase in opioid modulation may fail or may rapidly wane so that autonomic features of opioid withdrawal appear in the affected limb. Florid dystrophic changes may then occur because of passive complications of disuse associated with pain, or as a result of more active processes. Preservation of an appropriate opioid bias in the regional sympathetic ganglia might be an important factor in the successful management and prevention of reflex sympathetic dystrophy.
Autonomic Nerve Block↗
Peptidergic transmitters in synaptic boutons of sympathetic ganglia.
In sympathetic ganglia of the bullfrog, a slow synaptic potential lasting for minutes--the late slow excitatory postsynaptic potential (e.p.s.p.)--was discovered. This slow response, unlike other previously known synaptic potentials in the autonomic nervous system, is not mediated by acetylcholine or monoamines. Similar non-cholinergic, non-adrenergic slow synaptic potentials have since been found in several other vertebrate autonomic ganglia. We found that the late slow e.p.s.p. is probably mediated by a peptide that is identical to, or closely resembles, mammalian luteinizing hormone releasing hormone (LHRH), because (1) when applied directly to sympathetic neurones, LHRH and its agonists elicit a slow depolarization, associated with similar changes in membrane conductance and excitability as those occurring during the late slow e.p.s.p. Furthermore, both peptide-induced and nerve-evoked responses are blocked by antagonists of LHRH; and (2) radioimmunoassays indicate that a chain of sympathetic ganglia contains 100-800 pg of a LHRH-like peptide. Its distribution among spinal nerves, the great reduction of this substance following denervation, and its release from ganglia following isotonic KCl treatment or nerve stimulation suggest that the LHRH-like material is contained in preganglionic nerve fibres. Here we report that immunohistochemical staining of sympathetic ganglia shows that LHRH-like immunoreactivity is indeed present in synaptic boutons. We also show that the two types of ganglion cells (B cells and C cells) receive strikingly different patterns of peptidergic innervation.
Animals↗
Effects of ageing on the histochemically demonstrable catecholamines and acetylcholinesterase of human sympathetic ganglia.
The sympathetic ganglia of adult and aged humans were obtained during vascular, gynaecological and urological surgery, and studied using the formaldehyde-induced fluorescence (FIF) method for histochemical demonstration of catecholamines. Microspectrofluorimetry was applied to characterize the emission spectra of the flurophores. The sympathetic ganglia contained two types of cells exhibiting FIF: the adrenergic neurons and the small, intensely fluorescent (SIF) cells. The adrenergic neurons contained pigment granules exhibiting autofluorescence with emission maximum at 530---540 nm. The number of these granules increased with age while the FIF of the neurons decreased. In the oldest patients, most of the neurons in the sympathetic ganglia showed only pigment fluorescence but not FIF. The decrease of the perikaryonal catecholamine stores is interpreted as a degenerative change leading to impaired function of the neurons. The patterns of AChE did not change with age. The SIF cells were sparse and were mostly observed near the ganglia, forming paraganglia of varying size. Because of the rarity of the SIF cells, the effect of ageing could not be judged reliably.
Acetylcholinesterase↗
NAD(P)H oxidase-induced oxidative stress in sympathetic ganglia of apolipoprotein E deficient mice.
Superoxide anion (O2*-) is increased throughout the arterial wall in atherosclerosis. The oxidative stress contributes to lesion formation and vascular dysfunction. In the present study, we tested the hypothesis that NAD(P)H oxidase-derived O2*- is increased in nodose sensory ganglia and sympathetic ganglia of apolipoprotein E deficient (apoE-/-) mice, an established animal model of atherosclerosis. O2*- measured ex vivo by L-012-enhanced chemiluminescence was increased by 79+/-17% in whole sympathetic ganglia from apoE-/- mice (n=5) compared with sympathetic ganglia from control mice (n=5) (P<0.05). In contrast, O2*- was not elevated in nodose ganglia from apoE-/- mice. Dihydroethidium staining confirmed the selective increase in O2*- in sympathetic ganglia of apoE-/- mice, and revealed the contribution of both neurons and non-neuronal cells to the O2*- generation. We investigated the enzymatic source of increased O2*- in sympathetic ganglia of apoE-/- mice. The mRNA expression of gp91phox, p22phox, p67phox, and p47phox subunits of NAD(P)H oxidase measured by real time RT-PCR was increased approximately 3-4 fold in sympathetic ganglia of apoE-/- mice (n=5) compared with control ganglia (n=5). NADPH oxidase activity measured by lucigenin chemiluminescence was increased by 68+/-12% in homogenates of sympathetic ganglia from apoE-/- mice (n=7) compared with control ganglia (n=7) (P<0.05). The results identify sympathetic ganglia as a novel site of oxidative stress in atherosclerosis, and suggest that upregulation of NAD(P)H oxidase is the source of increased O2*- generation. We speculate that oxidative stress in sympathetic ganglia may contribute to impaired baroreflex control of sympathetic nerve activity.
Analysis of Variance↗
Localization, regulation and functions of neurotransmitters and neuromodulators in cervical sympathetic ganglia.
Cervical sympathetic ganglia represent a suitable model for studying the establishment and plasticity of neurochemical organization in the nervous system since sympathetic postganglionic neurons: (1) express several neuromediators, i.e., short acting transmitters, neuropeptide modulators and radicals, in different combinations; (2) receive synaptic input from a limited number of morphologically and neurochemically well-defined neuron populations in the central and peripheral nervous systems (anterograde influence on phenotype); (3) can be classified morphologically and neurochemically by the target they innervate (retrograde influence on phenotype); (4) regenerate readily, making it possible to study changes in neuromediator content after axonal lesion and their possible influence on peripheral nerve regeneration; (5) can be maintained in vitro in order to investigate effects of soluble factors as well as of membrane bound molecules on neuromediator expression; and (6) are easily accessible. Acetylcholine and noradrenaline, as well as neuropeptides and the recently discovered radical, nitric oxide, are discussed with respect to their localization and possible functions in the mammalian superior cervical and cervicothoracic (stellate) paravertebral ganglia. Furthermore, mechanisms regulating transmitter synthesis in sympathetic neurons in vivo and in vitro, such as soluble factors, cell contact or electrical activity, are summarized, since modulation of transmitter synthesis, release and metabolism plays a key role in the neuronal response to environmental influences.
Acetylcholine↗
Changes of the phosphatidylcholine content and the number of synaptic vesicles in relation to the neurohumoral transmission in sympathetic ganglia.
In sympathetic ganglia stimulated in the presence of HC-3, the reduction in number of synaptic vesicles was observed to be accompanied by a significant decrease of the ganglionic phosphatidylcholine content.
Animals↗
Small, intensely fluorescent cells of human sympathetic ganglia.
Human sympathetic ganglia obtained from sympathectomies were studied using the formaldehyde-induced fluorescence (FIF) method and electron microscopy to identify the small, intensely fluorescent (Sif) cells. Microspectrofluorimetry was used to study the intensity of the emitted FIF and the emission spectra. The SIF cells were found in every ganglion studied, but they were very sparce. They occurred alone or in small clusters and were mostly situated close to the blood vessels. The SIF cells contained high amounts of catecholamines, as indicated by microspectrofluorimetry. Electron microscopy revealed granule-containing cells (GC) enveloped by satellite cells; the former cells contained osmiophilic granules 300--400 nm in diameter and synapses of the cholinergic type were frequently found on their surface.
Dopamine↗
Immunopathology and microvascular lesions in human sympathetic ganglia.
Lumbar sympathetic ganglia surgically removed from adult patients affected by obstructive peripheral arteriopathies are investigated with traditional histology and fluorescent antibody technique. The presence of various pictures of microangiopathy is confirmed, mainly haemodynamic (hyaline-oedematous perivascular thickening) phenomena. Since specific fluorescence is absent from any lesion, the autoimmune pathogenic hypothesis may be discarded.
Adult↗