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PubMed1999

Neuronal messengers and peptide receptors in the human sphenopalatine and otic ganglia.

A majority of the parasympathetic nerve fibers to cranial structures derive from the sphenopalatine and otic ganglia. In particular, blood vessels are invested with a rich supply of dilator fibers of parasympathetic origin. In the present study, we have examined the occurrence of noncholinergic neuromessengers and neuropeptide receptors in the human sphenopalatine and otic ganglia. Vasoactive intestinal peptide (VIP)-immunoreactive (ir) nerve cell bodies occurred in high numbers in the sphenopalatine and otic ganglia. Likewise, high numbers of NOS- and PACAP-containing nerve cell bodies were seen in both ganglia. Autofluorescent lipofuscin, characteristic of adult human nervous tissue, was present within many nerve cell bodies in both ganglia. Receptor mRNA was studied with reverse transcriptase-polymerase chain reaction (RT-PCR). Total RNA from the sphenopalatine and otic ganglia was successfully extracted. By using appropriate sense and antisense primers, oligonucleotides were designed from the human sequences derived from GenBank, corresponding to human NPY Y1, CGRP1 and VIP1 receptors. In the sphenopalatine ganglion, we revealed the presence of mRNA for the human NPY Y1 and VIP1 receptors but not the CGRP1 receptor. The otic ganglion was found to react positively only for primers to mRNA for VIP1 but not for CGRP1 or NPY Y1 receptors.

Aged↗

PubMed2000

Lesch-Nyhan disease and the basal ganglia.

The purpose of this review is to summarize emerging evidence that the neurobehavioral features of Lesch-Nyhan disease (LND), a developmental disorder caused by congenital deficiency of the purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT), may be attributable to dysfunction of the basal ganglia. Affected individuals have severe motor disability described by prominent extrapyramidal features that are characteristic of dysfunction of the motor circuits of the basal ganglia. They also display disturbances of ocular motility, cognition, and behavioral control that may reflect disruption of other circuits of the basal ganglia. Though neuropathologic studies of autopsy specimens have revealed no obvious neuroanatomical abnormalities in LND, neurochemical studies have demonstrated 60-90% reductions in the dopamine content of the basal ganglia. In addition, recent PET studies have documented significant reductions in dopamine transporters and [18F]fluorodopa uptake in the basal ganglia. These findings support the proposal that many of the neurobehavioral features of LND might be related to dysfunction of the basal ganglia.

Animals↗

PubMed1997

Selective disruption of neurotransmission by acetylcholinesterase antibodies in sympathetic ganglia examined with intracellular microelectrodes.

Antibodies to acetylcholinesterase (AChE) induce adrenergic dysfunction in rats by selective, complement-mediated destruction of preganglionic sympathetic nerve terminals. To analyze this phenomenon at the neuronal level, monoclonal antibodies to AChE (1.6 mg) were injected via the tail vein, and superior cervical ganglia (SCG) or inferior mesenteric ganglia (IMG) were studied in vitro. In control SCG, all impaled neurons generated action potentials during direct injection of depolarizing current or indirect stimulation through the preganglionic nerve. Current injection remained effective in ganglia from treated rats, but preganglionic stimulation was greatly impaired: at 12 h and 3 d, less than 10% of the neurons responded, even to a maximal stimulus (150 V); at 9 d, only 25% responded. By contrast, in IMG, synaptic transmission was much less affected by antibody exposure: 60% or more of examined neurons responded to preganglionic stimulation. Differences in antibody access did not explain differing sensitivities of SCG and IMG since immunohistochemistry showed rapid accumulation of IgG deposits in both ganglia. These results are believed to reflect widespread but subtotal preganglionic sympathectomy by AChE antibodies. Current information indicates that paravertebral ganglia are all antibody-sensitive, but some prevertebral ganglia are resistant, suggesting immunochemical differences between them.

Acetylcholinesterase↗

PubMed1997

Quantitative analysis of mu and delta opioid receptor gene expression in rat brain and peripheral ganglia using competitive polymerase chain reaction.

Competitive polymerase chain reaction assays following reverse transcription have been developed for quantitative analysis of delta and mu opioid receptor gene expression. The assay was used to obtain quantitative measurements of mu and delta opioid receptor expression levels in different brain regions and sensory and sympathetic ganglia in the rat. The assays provide accurate estimates of the relative levels of receptor messenger RNAs by the inclusion in the assays of known amounts of internal standards with the same sequence, except for a small deletion, as the target complementary DNA. The amplification products of target and competitor can be distinguished by size, and their amounts measured by densitometry. Expression of mu and delta opioid receptor messenger RNAs in different regions of the rat brain, somatic and visceral sensory and sympathetic ganglia was investigated using this method. In the brain the highest density of delta receptor messenger RNA was detected in the olfactory bulb, followed by the striatum. The mu receptor was expressed at highest levels in the midbrain-hypothalamic region. All the sensory ganglia studied expressed both mu and delta opioid receptor messenger RNAs. In the nodose ganglion we observed the highest level of mu receptor messenger RNA of any structure studied; in the trigeminal ganglion the level was about 10 times lower than that in the nodose ganglion. Among the dorsal root ganglia, mu receptor messenger RNA density was highest in the lumbar region, followed by the thoracic and cervical regions. The sympathetic superior cervical ganglion expressed a very low level of mu message. Delta receptor messenger RNA was detected only in the sensory ganglia, at levels that were considerably lower than in the striatum. The reverse transcription polymerase chain reaction assay is quantitatively reliable for comparison of messenger RNA levels between different RNA extracts, and sensitive enough to permit the detection and assay of mu and delta opioid receptor gene expression in a single pair of sensory or autonomic ganglia from the rat.

Animals↗

PubMed2001

Expression of immediate early genes in sensory ganglia.

C-Jun and c-Fos belong to the family of immediate early genes. Apart from their role as transcription factors, a basal expression was shown for them in central nervous system tissues. The expression of c-Jun and c-Fos in sensory ganglia of guinea pig, rat and murine sensory ganglia was examined under normal, unstimulated conditions by quantitative double-immunohistochemistry. 4.6 +/- 2.8% of neuron-specific protein gene-product 9.5 -positive cells in nodose ganglia, 51.6 +/- 2.1% in jugular ganglia, 46.4 +/- 3.0% in trigeminal ganglia and 42.5 +/- 1.3% of cervical dorsal root ganglia neurons were positive for c-Jun in the guinea pig (less than 1% for c-Fos). In rat and mouse, less than 1% of the sensory neurons exhibited c-Jun and c-Fos-immunoreactivity. The high basal expression of c-Jun in guinea pig sensory neurons suggests that in this species the presence of c-Jun does not only depend on specific stimulation and is not exclusively associated with neuronal plasticity of gene expression and functional changes.

Animals↗

PubMed1985

Differentiation of catecholaminergic cells in cultures of embryonic avian sensory ganglia.

From the results of previous studies in which developing peripheral ganglia from quail embryos were transplanted into younger chicken embryo hosts, we concluded that spinal and cranial sensory ganglia contain dormant precursors with autonomic potentialities. Here we describe the differentiation of these precursors in vitro, from dorsal root and nodose ganglion cell suspensions. Dorsal root ganglia were removed from quail embryos at 9 to 15 days of incubation, dissociated to single cells, and grown in tissue culture. The differentiation of cells with autonomic features was followed by monitoring properties associated with the adrenergic phenotype (absent from quail sensory ganglia during normal embryonic development). Provided that the medium was supplemented with chicken embryo extract, numerous cells displaying tyrosine hydroxylase immunoreactivity could be detected from day 4 onward. They possessed long, multiple processes but appeared morphologically distinct from primary sensory neurons. The catalytic activity of tyrosine hydroxylase and of other enzymes required for catecholamine production was demonstrated in the cultures by glyoxylic acid-induced histofluorescence and by radiochemical measurement of the conversion of exogenous tyrosine to norepinephrine. A large proportion of tyrosine hydroxylase-positive cells were found to incorporate [3H]thymidine before and after differentiating. In contrast, recognizable sensory neurons never exhibited adrenergic properties and did not divide. Qualitatively similar results were obtained with cultures of dissociated nodose ganglia. These findings lend further weight to the assumption that latent autonomic precursors are included in the non-neuronal compartment of sensory ganglia.

Adrenergic Fibers↗

PubMed1981

Physiology of mammalian prevertebral ganglia.

When assessing the physiological role of the prevertebral ganglia, the following should be considered. Ganglion cells in these ganglia receive continuous excitatory synaptic input from peripheral sensory mechanoreceptors and central preganglionic neurons. The latter may result from sensory afferents projecting from the gastrointestinal tract to spinal preganglionic neurons or as a result of endogenous oscillator activity located in the spinal cord (18) or within the ganglion (45). Peripheral and spinal reflex pathways probably do not operate as separate, independent pathways. Rather, they must be considered functionally integrated in the prevertebral ganglia. Because of continuous synaptic input, the prevertebral neuron operates at some level of "neurogenic tone" that provides capabilities for bi-directional responses. An increase in spinal or peripheral synaptic input will be matched by a proportional increase in output firing. The functional effect of spatial summation of peripheral and central input is to prime the prevertebral neuron so that adjustments in its firing frequency can be made without the lag inherent in building up a response in a quiescent system. Not all prevertebral ganglia participate in reflex activity. It may be that reflex activity between prevertebral ganglia and visceral smooth muscle depends upon the nature of the mechanical activity of the muscle. For example, the mechanical activity of smooth muscle of the vas deferens is not characterized by spontaneous, myogenic, regularly occurring contractions. Mechanical activity in this organ occurs in bursts. There is no evidence to suggest that sensory fibers project from the wall of the vas deferens to the hypogastric plexus thereby forming a peripheral reflex arc. Contraction of th smooth muscle of the vas deferens is brought about by bursts of nerve impulses through simple relay connections in the pelvic plexus. Smooth muscles supplied by this ganglion have a direct line to the central nervous system and are secured by a "fail-safe" system. In contrast, the mechanical activity of the gastrointestinal system is characterized by slow spontaneous myogenic activity. Pattern formation of motor activity is achieved by reflex activity within the enteric plexuses. Extrinsic alteration of the nature and pattern of contraction of smooth muscle of the gastrointestinal tract would be best served by prevertebral ganglia that modulate and adjust motor function by continuous integration of convergent weak synaptic input emanating from the peripheral and central nervous systems. When a prevertebral neuron is part of a peripheral reflex loop, its physiological role may be to modulate end organ activity; when it does not participate in a peripheral reflex loop, its role may be to relay CNS input and initiate end organ activity.

Animals↗

PubMed2005

Role of the basal ganglia in balance control.

In this review paper, we summarize the important contributions of the basal ganglia to the regulation of postural control. After a brief overview of basal ganglia circuitries, the emphasis is on clinical observations in patients with focal lesions in parts of the basal ganglia, as the impairments seen here can serve to highlight the normal functions of the basal ganglia nuclei in postural control. Two particularly relevant functions are discussed in detail: first, the contribution of the basal ganglia to flexibility and to gaining control of balance-correcting responses, including the ability to lend priority to the elements of a postural task; and second, processing afferent information by the basal ganglia, which is increasingly recognized as being highly relevant for postural control.

Adaptation, Physiological↗

PubMed2006

[Basal ganglia calcification: clinical manifestations and diagnostic evaluation].

Physiological intracranial calcification occurs in about 0,3-1,5% of cases. It is asymptomatic and is detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases and other. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Such parkinsonism doesn't respond to drugs containing levodopha. Infections (toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders (blood calcium level and other), those are: Cockayne syndrome, tuberous sclerosis, Fahr's syndrome, Down syndrome and other. We observed some cases of basal ganglia calcification and studied clinical manifestations and treatment tolerance of this pathological condition. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, serum concentration of calcium, phosphorus, and parathyreoid hormone is suggested to be determined in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism. Basal ganglia calcification in young patient with acute hepatitis may be result of Wilson disease.

Adolescent↗

PubMed1985

How do the migratory and adhesive properties of the neural crest govern ganglia formation in the avian peripheral nervous system?

The peripheral nervous system derives mainly from the neural crest both in the head and trunk. Using markers such as fibronectin (FN), neural cell-adhesion molecule (NCAM), the nucleolar marker for quail cells in chimaeric embryos, and NC-1, a monoclonal antibody specific to crest cells and their neural derivatives, we have attempted to reconstruct the processes that lead to the formation of peripheral ganglia. Our observations allow us to propose a model of the formation of ganglia based on morphogenetic movements and on variations of crest cell adhesiveness. In most cases, crest cells migrate in morphologically defined and transient pathways that lead them to their final site of arrest; these pathways are always associated with FN, which appears necessary for crest cell attachment and movement in vitro. The directionality of crest cell migration is probably dictated by the cells' motile properties and population pressure in restricted areas suitable for cell movement. The disappearance of the pathways and of the substrate necessary for migration while the population is rapidly dividing may be responsible for the aggregation of crest cells in the case of the sensory ganglia. To the contrary, the aggregation of crest cells into autonomic ganglia (sympathetic, enteric, and ciliary ganglia) does not seem to obey the same rules, no disappearance of the substratum or of the pathways being obvious; rather, their formation seems correlated with the de novo synthesis of adhesive molecules such as NCAM.

Animals↗

PubMed1996

Basal ganglia volume and proximity to onset in presymptomatic Huntington disease.

OBJECTIVE: To determine in presymptomatic individuals who carry the gene mutation for Huntington disease whether proximity to estimated age at onset is associated with volume of basal ganglia, as measured on magnetic resonance imaging scans. DESIGN: Survey study involving correlations between basal ganglia volume, measured blind to subject status, and estimation of subjects' age at onset. SETTING: Huntington's Disease Presymptomatic Testing Program at The Johns Hopkins University School of Medicine, Baltimore, Md. PATIENTS AND OTHER PARTICIPANTS: Subjects included 47 individuals at risk for Huntington disease (ie, off-spring of patients with Huntington disease). Twenty subjects tested positive for the gene mutation but were not symptomatic. Twenty-seven subjects tested negative. MAIN OUTCOME MEASURES: Estimated age at onset was calculated for each of 20 gene-positive individuals using an empirically derived formula based on the subject's trinucleotide repeat length and parental age at onset. Each subject's age at the time of the magnetic resonance imaging scan was subtracted from his or her estimated age at onset, yielding estimated years to onset. Volumes of caudate, putamen, and globus pallidus were measured on magnetic resonance imaging scans. RESULTS: After controlling for the subject's age at the time of the scan, significant correlations were found between volumes of all basal ganglia structures and years to onset. Gene-positive subjects who were far from onset had smaller basal ganglia volumes than gene-negative subjects for all structures except globus pallidus. Gene-positive subjects who were close to onset had smaller volumes than gene-negative subjects for all basal ganglia structures and had smaller volumes than subjects far from onset for all structures except caudate. CONCLUSIONS: The results suggest that atrophy of the basal ganglia occurs gradually, beginning years before symptom onset.

Adult↗

PubMed1977

Herpesvirus in sensory and autonomic ganglia after eye infection.

In herpesvirus hominis (HVH) infections, virus harbored in the sensory ganglia is now thought to be the main source of recurrent infection at peripheral sites. Experimental HVH infection of the external eye in rabbits produces an acute infection and then latent infection of the trigeminal ganglion. In this study, acute infection of the automatic ganglia serving the eye (superior cervical and ciliary) as well as trigeminal ganglia occurred after HVH inoculation of rabbits' corneas with a herpes type 1 strain (RE). Latent virus infection was detected in the trigeminal ganglion of one of five animals tested six months after initial infection. Since the superior cervical and other autonomic ganglia serving the eye become infected during acute herpes simplex virus infection of the external eye in rabbits, it is possible that these ganglia are also sources of reinfection in recurrent herpetic disease of the eye. Following the initial eye disease with this virus strain, HVH shedding could not be demonstrated even after induction attempts by topically applied epinephrine or systemic use of cyclophosphamide. Thus, establishment of latent HVH infection in the ganglia and chronic shedding of virus into the external eye is not a constant feature of this animal model, but may depend on the specific strain of herpesvirus used.

Animals↗

PubMed1997

Detection of latent varicella-zoster virus infection in human vestibular and spiral ganglia.

Varicella-zoster virus (VZV) becomes latent in the sensory ganglia after primary infection and VZV DNA has been found in human trigeminal, thoracic, and geniculate ganglia. In this study, human vestibular and spiral ganglia, which do not received innervation from the skin, were examined for VZV DNA using the polymerase chain reaction. VZV DNA was detected in 2 of 10 (20%) vestibular ganglia and in 2 of 10 (20%) spiral ganglia from five adults. VZV DNA was undetectable in either type of ganglion from a newborn and from two of the five adults. These two adults were VZV seronegative. The results indicate that VZV becomes latent in several types of sensory ganglion after primary infection and suggest the possibility that reactivation of the virus from the vestibular and spiral ganglia may cause disorders in the labyrinth.

Adult↗

PubMed1996

Growth, proliferation, and cell death in the ontogeny of transient DRG (Froriep's ganglia) of chick embryos.

A striking example of axial patterning in nervous system development is the unusual fate of dorsal root ganglia (DRG) that develop in the most rostral somites, the Froriep's ganglia. In amniotes, the DRG that develop adjacent to the occipital (cranial) and the first cervical segments of the CNS "disappear" early in embryonic development. In contrast, all other DRG are present throughout the animal's life. We here reexamine in greater detail the ontogeny of the longest surviving Froriep's ganglion of the chick embryo, DRG C-2. By 50 h of development (stage, st. 15), an anlagen of a DRG had formed in C-2 that was indistinguishable from those of adjacent "permanent" ganglia. At st. 18 [embryonic day (E) 2.5+], the C-2 DRG had the same shape and volume as permanent ganglia C-5 and C-6. C-2's development first diverged from that of normal DRG at st. 19 (E3-), when C-2 was observed to be half the size and shaped differently from its neighbors, and its peripheral nerve root began to degenerate. Two cellular mechanisms appear to contribute to the reduced size of C-2 compared to normal DRG at st. 20 at this early stage: lower proliferation and higher apoptosis rates. One-third fewer C-2 cells were found to be in the S phase when compared to neighboring ganglia, and apoptotic cells were more than three times more abundant in C-2 than in conventional DRG at this stage. The C-2 DRG continued to grow, but at a slower pace than neighboring ganglia through st. 32 (E7). At the height of the normal programmed DRG cell death in normal cervical DRG at st. 28 (E6), even more massive apoptosis occurred in C-2, which resulted in the absence of this ganglion in 80% of st. 36 (E10) embryos. A recent study demonstrated that the overexpression of a single Hox gene can "rescue" the C-2 DRG in transgenic mice. We speculate that Hox genes may produce the difference in fate between C-2 and normal DRG by modulating proliferation and apoptosis via modified neurotrophic factor and/or receptor expression.

Animals↗

PubMed1999

Distribution of herpes simplex virus type 1 in human geniculate and vestibular ganglia: implications for vestibular neuritis.

Vestibular neuritis is a common cause of partial unilateral vestibular paralysis, which usually spares posterior semicircular canal function. The cause is assumed to be a viral reactivation of latent herpes simplex virus type 1 (HSV-1) in human vestibular ganglia. The existence of an anastomosis between the intermediate nerve and the superior vestibular nerve suggests the question of whether selective affliction of the superior vestibular nerve is the result of migration of HSV-1 from the geniculate ganglion along this faciovestibular anastomosis. We determined the distribution of HSV-1 among geniculate ganglia, vestibular ganglia, and within Scarpa's ganglion by examining 35 human temporal bones by polymerase chain reaction. HSV-1 was found in 66% of geniculate ganglia and 60% of vestibular ganglia; all examined parts of vestibular ganglia were almost equally HSV-1 infected. Our data provided no support for viral migration along this anastomosis or for a preferential latency of HSV-1 in the superior vestibular nerve. We suggest that the common double innervation of the posterior ampulla by two nerves running in two separate bony canals could offer an alternative explanation for the regular sparing of posterior canal function in vestibular neuritis.

Adolescent↗

PubMed2000

Computational models of the basal ganglia.

Computer simulation studies and mathematical analysis of models of the basal ganglia are being used increasingly to explore theories of basal ganglia function. We review the implications of these new models for a general understanding of basal ganglia function in normal as well as in diseased brains. The focus is on their functional similarities rather than on the details of mathematical methodologies and simulation techniques. Most of the models suggest a vital role for the basal ganglia in learning. Although this interest in learning is partly driven by experimental results associating the acute firing of dopamine cells with reward prediction in monkeys, some of the models have preceded the electrophysiological results. Another common theme of the models is selection. In this case, the striatum is seen as detecting and selecting cortical contexts for access to basal ganglia output. Although the behavioral consequences of this selection are hard to define, the models provide frameworks within which to explore these ideas empirically. This provides a means of refining our understanding of basal ganglia function and to consider dysfunction within the new logical frameworks.

Animals↗

PubMed2004

An electron microscope immunocytochemical study of GABA(B) R2 receptors in the monkey basal ganglia: a comparative analysis with GABA(B) R1 receptor distribution.

Functional gamma-aminobutyric acid (GABA)(B) receptors are heterodimers made up of GABA(B) R1 and GABA(B) R2 subunits. The subcellular localization of GABA(B) R2 receptors remains poorly known in the central nervous system. Therefore, we performed an ultrastructural analysis of the localization of GABA(B) R2 receptor immunoreactivity in the monkey basal ganglia. Furthermore, to characterize better the neuronal sites at which GABA(B) R1 and GABA(B) R2 may interact to form functional receptors, we compared the relative distribution of immunoreactivity of the two GABA(B) receptors in various basal ganglia nuclei. Light to moderate GABA(B) R2 immunoreactivity was found in cell bodies and neuropil elements in all basal ganglia nuclei. At the electron microscope level, GABA(B) R2 immunoreactivity was commonly expressed postsynaptically, although immunoreactive preterminal axonal segments were also frequently encountered, particularly in the globus pallidus and substantia nigra, where they accounted for the third of the total number of GABA(B) R2-containing elements. A few labeled terminals that displayed the ultrastructural features of glutamatergic boutons were occasionally found in most basal ganglia nuclei, except for the subthalamic nucleus, which was devoid of GABA(B) R2-immunoreactive boutons. The relative distribution of GABA(B) R2 immunoreactivity in the monkey basal ganglia was largely consistent with that of GABA(B) R1, but some exceptions were found, most noticeably in the globus pallidus and substantia nigra, which contained a significantly larger proportion of presynaptic elements labeled for GABA(B) R1 than GABA(B) R2. These findings suggest the possible coexistence and heterodimerization of GABA(B) R1 and GABA(B) R2 at various pre- and postsynaptic sites, but also raise the possibility that the formation of functional GABA(B) receptors in specific compartments of basal ganglia neurons relies on mechanisms other than GABA(B) R1/R2 heterodimerization.

Animals↗

PubMed1980

Development of chick paravertebral sympathetic ganglia. I. Fine structure and correlative histofluorescence of catecholaminergic cells.

Paravertebral sympathetic ganglia from the lumbosacral region of a series of chick embryos have been studied with electron microscopic methods, including aldehyde-osmium and permanganate fixatives, and correlative histofluorescence (Grillo et al, '74). Our purpose was to assess the differentiation of catecholaminergic (CA) cells during histogenesis in ovo. Examination of comparable adult ganglia as a baseline for differentiating stages confirmed that the principal sympathetic neuron (PN) is similar to those of other species in that it contains predominately small dense-cored vesicles (SDCV) preserved only by permanganate, and does not histofluoresce following the method of Grillo et al. ('74). At embryonic day (E) 7--8, when ganglia have just formed, areas fluorescing bright yellow-green are correlated with two types of cells: 1) Neuroblasts with vesicular nuclei and large dense-cored vesicles (LDCV) are common. As the neuroblasts grow and differentiate, LDCV move away from perikaryal cytoplasm into developing processes. Around E13-15, LDCV appear in the neuroblasts which continue to develop until they resemble miniature adult PN in late embryos and hatchlings. 2) Granule (GR) cells with clumped chromatin and sparse cytoplasm are clustered in te ganglionic periphery at E7-8, but are rare. The GR cells increase somewhat in size and numbers by E11, but retail essentially the same characteristics as at earlier stages. Neither bright fluorescence nor GR cells appear later than stages E13-15. These results are interpreted to mean that when chick sympathetic stem cells have migrated from the primary ganglia into the paravertebral ganglia, they give rise to two separate lines of CA cells, one of which is not maintained and subsequently disappears. The results are significant as a basis for understanding how a mixed population of CA cells might arise within sympathetic ganglia in situ.

Animals↗