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PubMed1983

Long-term effects of spinal transection on the development and function of sympathetic ganglia.

The long-term effect of interruption of descending central pathways on the biochemical development and function of sympathetic neurons was examined in the sixth lumbar (L6) sympathetic ganglia of the rat. Previous investigations had defined the normal maturation of presynaptic choline acetyltransferase (CAT) activity, postsynaptic tyrosine hydroxylase (T-OH) activity and total protein in L6 ganglia. Neonatal spinal cord transection prevented the normal ontogeny of CAT activity: enzyme activity was 40% of control one week and one year after surgery. Similarly, T-OH activity failed to develop normally after transection and was 22% of control one year postoperatively. Spinal transection at 30 days of age did not alter baseline CAT or T-OH activities in L6 ganglia when examined up to 6 months after surgery. Apparently during the first month of life descending central pathways exert critical facilitatory influences on sympathetic ganglia maturation; interruption of these influences results in long-lasting biochemical deficits. We also examined the role of central mechanisms in adult sympathetic function. Stressful stimuli, including reserpine treatment, normally induce adult T-OH through reflex sympathetic activation. This biochemical adaptability was studied by treating rats with reserpine after spinal transection. After motor and autonomic spinal reflexes returned in paraplegic animals, reserpine treatment was initiated. Spinal animals did not exhibit T-OH induction. These observations indicate that central rather than spinal mechanisms govern this biochemical adaptability of mature sympathetic neurons.

Aging↗
PubMed1992

Rolling mouse Nagoya as a mutant animal model of basal ganglia dysfunction: determination of absolute rates of local cerebral glucose utilization.

In order to elucidate the neuronal mechanism of the motor disturbances of the Rolling mouse Nagoya (rolling), a neurological mutant mouse (genotype rol/rol) showing frequent lurching and falling over on walking, we determined absolute rates of local cerebral glucose utilization (LCGU) with the [14C]deoxyglucose method. The rates were compared with those of heterozygote (+/rol) with normal behavior, and of normal mice (+/+) of the same strain (C3Hf/Nga). Rolling showed marked and significant increases in LCGU in the structures of the basal ganglia such as the globus pallidus, entopeduncular nucleus, substantia nigra pars compacta and pars reticulata, and subthalamic nucleus, confirming our previous finding with semiquantitative LCGU determination. Additional significant but much less marked increases in LCGU of rolling were found in some structures of the brainstem and limbic system, such as the pedunculopontine nucleus, red nucleus, ventral tegmental area, lateral habenula, and CA1 and CA3 of the hippocampus. Although rolling has been regarded as an animal model of cerebellar ataxia, rolling showed no alterations of LCGU in the cerebellum. The heterozygote showed intermediate increases in LCGU between rolling and normal mice in the basal ganglia structures such as the globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. Our findings indicate that rolling has a definite, genetically determined dysfunction of the basal ganglia. The primary site of the basal ganglia dysfunction might probably be in the striatum, involving both the neostriatum and limbic striatum, and resulting in secondary dysfunction in their target structures.

Animals↗
PubMed1995

Changes in preprotachykinin mRNA expression and substance P levels in dorsal root ganglia of monoarthritic rats: comparison with changes in synovial substance P levels.

We have measured changes in the expression of gamma-preprotachykinin mRNA and levels of the neuropeptide substance P in the lumbar 4 and 5 dorsal root ganglia at various time points following the induction of an antigenic monoarthritis in the rat knee. The results were compared with changes in substances P levels in the knee joint synovium during acute and chronic phases of the disease. On day 3 post-induction, there was a significant increase in the expression of gamma-preprotachykinin mRNA in the dorsal root ganglia. Concomitant with this increase in message was a rise in the levels of substance P in the dorsal root ganglia. On days 7, 10 and 21, mRNA expression had returned to control values whereas ganglion peptide levels were significantly below controls. In contrast there was little change in the total substance P levels in the synovium on days 1 and 3 despite the observed changes in the ganglia. By day 10, however, synovial levels had risen significantly above control values and remained elevated thereafter. Our results show a transitory increase in substance P synthesis after induction of an antigenic monoarthritis. This response is not mirrored in the periphery where there is no initial change in total substance P levels perhaps reflecting increased degradation be enzymes known to be present within inflamed tissue. Paradoxically synovial substance P levels are increased in the latter phases of the model which may serve to modify the inflammatory response.

Animals↗
PubMed1986

Requirement of a neural tube signal for the differentiation of neural crest cells into dorsal root ganglia.

The influence of the neural tube on early development of neural crest cells into sensory ganglia was studied in the chick embryo. Silastic membranes were implanted between the neural tube and the somites in 30-somite-stage embryos at the level of somites 21-24, thus separating the early migrated population of neural crest cells from the neural tube. Neural crest cells and peripheral ganglia were visualized by immunofluorescence using the HNK-1 monoclonal antibody and several histochemical techniques. Separation of crest cells from the neural tube caused the selective death of the neural crest cells from which dorsal root ganglia (DRG) would have developed. Complete disappearance of HNK-1 positive cells was evident already 10 hr after silastic implantation, before early differentiation sensory neurons could have reached their peripheral targets. In older embryos, DRG were absent at the level of implantation. In contrast, the development of ventral roots, sympathetic ganglia and adrenal gland was normal, and so was somitic differentiation into cartilage and muscle, while morphogenesis of the vertebrae was perturbed. To overcome the experimentally induced crest cell death, the silastic membranes were impregnated with a 3-day-old embryonic chick neural tube extract. Under these conditions, crest cells which were separated from the tube survived for a period of 30 hr after operation, compared to less than 10 hr in respective controls. The extract of another tissue, the liver, did not protract survival of DRG progenitor cells. Among the cells which survived with neural tube extract, some even succeeded in extending neurites; nevertheless, in absence of normal connections with the central nervous system (CNS) they finally died. Treatment of silastic implanted embryos with nerve growth factor (NGF) did not prevent the experimentally induced crest cell death. These results demonstrate that DRG develop from a population of neural crest cells which depends for its survival and probably for its differentiation upon a signal arising from the CNS, needed as early as the first hours after initiation of migration. Recovery experiments suggest that the subpopulation of crest cells which will develop along the sensory pathway probably depends for its survival and/or differentiation upon a factor contained in the neural tube, which is different from NGF.

Animals↗
PubMed1978

Beta-adrenoceptors modulate noradrenaline release from axonal sprouts in cultured rat superior cervical ganglia.

Superior cervical ganglia of rats grown in organ culture were used to study the effect of beta-receptor stimulants and antagonists on 3H-noradrenaline release in response to stimulation by KC1 (75 mM). (--)-Isoprenaline 1X 10(-9)--1 X 10(-7) M) increased 20--25% the release of 3H-noradrenaline from cultured ganglia exposed to KC1. Isoprenaline did not modify either the spontaneous (non-calcium dependent) release of 3H-noradrenaline from cultured ganglia, or the KC1-stimulated release from fresh ganglia. The effect of (--)-isoprenaline was blocked by (--)-propranolol 5 X 10(-9) -- 1 X 10(-8) M and by butoxamine 10(-6) M, but not by (+)-propranolol (1 -- 5 X 10(-8) M), practolol (1 X 10(-8) -- 1 X 10(-6) M), or sotalol (1 X 10(-7) -- 1 X 10(-6) M). Isoprenaline induced augmentation of 3H-noradrenaline release and its antagonism by (--)-propranolol still occurred in the presence of DMI. It is suggested that presynaptic beta-receptors in sympathetic nerve terminals may be involved in a positive feedback of noradrenaline release.

Adrenergic beta-Antagonists↗
PubMed1993

Ganglion-blocking activity of dequalinium in frog and rat sympathetic ganglia in vitro.

The effect of dequalinium on ganglionic transmission and responses to exogenous acetylcholine receptor agonists were studied in frog and rat sympathetic ganglia. In frog ganglia, dequalinium reduced ganglionic transmission (measured using gross extracellular recording) with an EC50 of 2 microM. At 1 microM, dequalinium produced non-surmountable antagonism of the ganglion depolarization evoked by nicotinic receptor activation. Dequalinium reduced the amplitude of evoked and spontaneous excitatory postsynaptic potentials recorded intracellularly from frog neurones, but had no effect on the action potential elicited by injection of a depolarizing current pulse. Hyperpolarizing and depolarizing responses to muscarine recorded extracellularly from frog ganglia were antagonized by 3 microM dequalinium. In rat ganglia, synaptic transmission and depolarization by an exogenous nicotinic agonist were only slightly inhibited by dequalinium at a concentration of 100 microM. At 30 microM, dequalinium produced a 17% reduction in the depolarization of this tissue by muscarine (1 microM). These results add to the evidence of the diversity of nicotinic and muscarinic acetylcholine receptors, and indicate that dequalinium may be a valuable tool for the study of these receptors. However its usefulness as a probe for calcium-activated potassium channels may be limited by its actions at acetylcholine receptors.

Action Potentials↗
PubMed1983

Stimulation of spermatogonial DNA synthesis in slug gonad by a factor released from cerebral ganglia under the influence of long days.

Incorporation of [3H]thymidine into gonadal DNA was shown to increase 1 week after implantation into an immature slug (Limax maximus) of a "brain" (circumesophageal ring of ganglia) from a male-phase donor. Light microscope autoradiography revealed that in stimulated gonads labeling was localized primarily in the nuclei of spermatagonia. Implant-stimulated spermatogonial DNA synthesis was found to depend upon implantation of supraesophageal (cerebral) ganglia. Neither subesophageal ganglia implants nor immature supraesophageal implants had an effect. Thymidine incorporation could also be stimulated by exposure of slugs to long-day lightcycles (LD 16:8) for 3 to 4 weeks. Similar duration of long-day treatment was also adequate to trigger male-phase development even after animals were returned to short days (LD 8:16). The results are consistent with the view that 3 to 4 weeks of long-day lightcycles are required to promote irreversibly the release from slug cerebral ganglia of a male-phase gonadotropic factor which directly or indirectly promotes spermatogonial proliferation.

Animals↗
PubMed1993

Stress-induced reactivation of latent herpes simplex virus infection in rat lumbar dorsal root ganglia.

Clinical reports suggest that stress precipitates recurrent cutaneous Herpes simplex virus (HSV) infection, presumably by reactivating latent infection in sensory ganglia with subsequent centrifugal axonal spread to the skin. As an initial test of this hypothesis, rats with latent HSV, type-1, (HSV-1) infection in lumbar dorsal root ganglia (DRG) were exposed to a well-characterized acute stressor that produced gastric ulcers (U) and elevated plasma corticosterone (CS) concentrations. Stress-induced reactivation of latent HSV infection was suggested by the earlier appearance of cytopathic effect (CPE) in human foreskin fibroblast monolayers co-cultivated with ganglia from stressed rats than from nonstressed ones (4.5 +/- 0.2 and 6.4 +/- 0.4 [mean +/- SEM] days respectively; p < 0.001). No CPE was detected in monolayers co-cultivated with ganglia from non-infected rats. These initial results suggest that acute stress reactivates latent HSV-1 ganglionic infection.

Animals↗
PubMed1978

Quantitative studies of dorsal root ganglia and neuropathologic observations on spinal cords in familial dysautonomia.

Intrauterine development and postnatal maintenance of dorsal root ganglion neurons are abnormal in familial dysautonomia, an autosomal recessive disorder associated with autonomic, motor and sensory deficits. Normally, dorsal root ganglion weight increases with age. This does not occur in the cervical plexus ganglia of dysautonomic patients. Neurons in dorsal root ganglia are found to be markedly diminished in the youngest patients and slow degeneration causes further depletion with age. Quantitative studies on C8 dorsal root ganglia show the normal neuron content to be between 42,500 and 53,600. In 3 patients with familial dysautonomia the range was 4,090-8,590 with the smallest number being in the oldest patient. Lateral root entry zones and Lissauer's tracts are severely depleted of axons. In older patients loss of dorsal column myelinated axons becomes evident and is first seen in lumbar fasciculus gracilis, cervical fasciculus cuneatus and interfascicular fasciculus. Temperature sensation is markedly impaired from infancy in familial dysautonomia. Loss of pain sensation is prominent and worsens with age. Vibration sense diminishes in adolescence and coordination of limb movements becomes poor in older patients. Neuron depletion in dorsal root ganglia and the progressive pattern of cord changes correlate well with these clinical observations.

Adolescent↗
PubMed1994

Somatomotor and cardiorespiratory responses to basal ganglia stimulation in cats.

The electrical stimulation of the neural elements within the basal ganglia circuitry caused characteristic somatomotor activities and changes in arterial blood pressure (BP), heart rate (HR), and respiratory rate (RR) in conscious, unrestrained cats. A highly constant pattern of responses was elicited by stimulating repeatedly at the same locus, but significant differences occurred among responses obtained from identified parts of the basal ganglia. Stimulation in the putamen evoked tachypnoe, but no remarkable change in BP and HR. Stimulation in the caudate nucleus produced either tachypnoe or respiratory arrest accompanied by a slight change in BP and HR. Stimulation within the medial dorsal nucleus of the thalamus and the substantia nigra caused increase in BP, HR, and RR of different magnitude. The increase in BP failed to appear under the effect of alpha-adrenergic blockade. The effects of procaine, injected through the arterial cannula, did not interfere with the electrically elicited responses. All the cardiorespiratory responses to basal ganglia stimulation diminished or did not appear in deeply anaesthetised animals. We conclude that besides its involvement in motor processing, the basal ganglia circuitry exerts an influence on the central cardiorespiratory mechanisms.

Animals↗
PubMed1994

Identification of insulin-like peptides in cerebral ganglia neurosecretory cells of the mussel Mytilus edulis.

The immunostaining patterns of cerebral ganglia sections from the mussel Mytilus edulis with monoclonal antibodies raised against cerebral ganglia (CG) extracts were compared to those obtained with various polyclonal anti-insulin-like antibodies. One of the monoclonal antibodies (MAB 46) revealed clusters of positive cells in localization comparable to those revealed by the polyclonal antibodies. The nature of the antigen recognized by MAB 46 and the polyclonal antibodies was compared by gel filtration-HPLC of a cerebral ganglia extract. Similar peaks were revealed by the monoclonal and polyclonal antibodies. MAB 46 significantly inhibited the cerebral ganglia induced stimulation of amino-acid incorporation by mantle edge cell suspensions, suggesting that the antigen recognized by MAB 46 is involved in the control of growth.

Animals↗
PubMed1994

Immunocytochemical localization of neuropeptide F-immunoreactivity in the circumoesophageal ganglia of the gastropod mollusc, Helix aspersa using electron microscopy.

Neuropeptide F (NPF)-immunoreactivity has been localized by electron microscopy in the central nervous system of the gastropod mollusc, Helix aspersa using a region-specific antiserum in conjunction with post-embedding immunogold labelling. The specific antiserum employed, designated NPF3, was raised to a synthetic N-terminal fragment of H. aspersa NPF. Gold-labelling revealed that NPF-immunoreactivity was found almost exclusively over the contents of dense-cored secretory vesicles within nerve axons in both cerebral and subesophageal ganglia. Double-labelling of NPF and FMRFamide demonstrated no apparent co-localization in the paired cerebral ganglia. Instead, immunoreactivities of the two neuropeptides were found to have distinct locations within the ganglia. These findings suggest that NPF may be an important neuroregulator in H. aspersa and that in the cerebral ganglia it may be anatomically-distinct from FMRFamide and related peptides.

Amino Acid Sequence↗
PubMed1992

Prevalence and distribution of latent simian varicella virus DNA in monkey ganglia.

We used polymerase chain reaction to analyze the prevalence and distribution of latent simian varicella virus (SVV) in ganglionic and nonganglionic tissues from nine African green monkeys experimentally infected with SVV. Primers specific for three different regions of the SVV genome were used for amplification. SVV DNA sequences were detected in trigeminal ganglia from seven of nine monkeys and in thoracic ganglia from seven of nine monkeys. Analysis of DNA from nonneuronal tissues of three monkeys and from adrenal glands of nine monkeys revealed the presence of SVV-specific sequences in the adrenal gland of one monkey. The results indicate that, like human varicella, SVV becomes latent primarily in ganglia at multiple levels of the neuraxis, and more than one region of the SVV genome is present in latently infected ganglia. SVV latency in primates may be a useful model for varicella latency in humans.

Animals↗
PubMed1982

The ultrastructural organization of sympathetic ganglia of the cat.

The organization and relations between nerve, glial, chromaffin and other structural components of sympathetic ganglia of the cat were studied electron microscopically. Cholinergic, adrenergic and, probably, peptidergic terminals of axons making different contacts with the surrounding ganglionic cells and processes are shown with electron histochemical methods. Ultrastructural features of some dendrites are revealed which characterize them as sensory terminals of sympathetic ganglia. Besides the known axo-dendritic, axo-somatic and axo-axonal synapses, the ganglia show axo-glial synapses, and also dendro-dendritic and dendro-somatic contacts. It is established that preliminary destruction of ganglionic connections with the central nervous system is fatal only to a proportion of these interneuronal contacts while the rest of them persist. Synaptic complexes are found showing contacts of several axons and dendrites and representing a morphological substrate for convergence and divergence. No synapses are found whose presynaptic pole would be formed by a chromaffin cell. The functional role of these cells in the ganglia is discussed.

Animals↗
PubMed1987

Demonstration of preganglionic fibers in the inferior mesenteric ganglion, pelvic ganglia and related nerves of the guinea pig by anterogradely transported wheat germ agglutinin-horseradish peroxidase conjugate.

Preganglionic sympathetic neurons in the guinea pig were labeled by injections of wheat germ agglutinin-horseradish peroxidase conjugate (WGA-HRP) into the L2 and L3 spinal cord segments. After anterograde transport of the tracer the following areas were examined for the presence of HRP-labeled fibers: the inferior mesenteric ganglion (IMG), the pelvic ganglia, the hypogastric and colonic nerves. In the ganglia labeling appeared predominantly as clusters of varicose-like profiles suggestive of being axon terminals. Particularly in the pelvic ganglia, these profiles appeared to surround the contours of some of the ganglion cell bodies. Numerous HRP-positive fibers were present in the hypogastric nerves, but only occasional fibers were observed in the colonic nerves. The pattern of labeling differed markedly from that described previously after anterograde transport of WGA-HRP in sensory fibers of the IMG, hypogastric and colonic nerves. Furthermore, the results from this and the previous study show that anterograde tracing with WGA-HRP can be a useful means for analyzing the structural organization of various fiber inputs to autonomic ganglia.

Animals↗
PubMed1988

Long-term hypoxia increases the turnover of dopamine but not norepinephrine in rat sympathetic ganglia.

The content and turnover of dopamine, 3,4-dihydroxyphenylacetic acid and norepinephrine have been investigated in the superior cervical, coeliac and mesenteric ganglia of rats exposed to moderate normobaric hypoxia (10% O2 in N2) lasting for 2-28 days. the turnover was estimated by the decrease in amine contents after inhibition of catecholamine biosynthesis with alpha-methyl-p-tyrosine. In all 3 sympathetic ganglia, long-term hypoxia elicited a sustained increase in the content and turnover of dopamine. In contrast, the content and turnover of norepinephrine remained unchanged, except for a moderate increase in the coeliac ganglion after 14 and 28 days of hypoxia. These results suggest that the dopamine and norepinephrine pools in ganglia have a different functional significance and that rat sympathetic ganglia contain a pool of dopamine specifically sensitive to long-term hypoxia.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Morphological and chemical identification of neurons that project from the colon to the inferior mesenteric ganglia in the guinea-pig.

Labelled nerve cells were located in the distal colon of the guinea-pig 4-5 days after the retrograde tracing agent, Fast blue, was injected into the inferior mesenteric ganglia. Labelled neurons were only found in the myenteric plexus. Their frequency increased from oral to anal and was greater towards the mesenteric border, compared with the anti-mesenteric aspect, of the colon. Many retrogradely labelled neurons were immunoreactive for vasoactive intestinal peptide or calbindin. In the inferior mesenteric ganglia, vasoactive intestinal peptide and calbindin immunoreactive nerve fibres surrounded the same clumps of nerve cell bodies. Almost all calbindin and vasoactive intestinal peptide immunoreactive terminals degenerated after the nerves running from the large intestine to the inferior mesenteric ganglia were cut. It is concluded that the great majority of calbindin and vasoactive intestinal peptide immunoreactive terminals in the inferior mesenteric ganglia arise from nerve cell bodies in the myenteric plexus of the large intestine.

Amidines↗
PubMed1995

The physiological and anatomical demonstration of functionally selective parasympathetic ganglia located in discrete fat pads on the feline myocardium.

Experiments utilizing surgical parasympathectomy of discrete fat pad ganglia on the surface of the heart have suggested that there are two anatomically segregated and physiologically independent parasympathetic intracardiac ganglia which are capable of selective control of sino-atrial (SA) rate and atrio-ventricular (AV) conduction. Some pharmacological data, however, are inconsistent with these conclusions. We have examined the cardiodynamic effects of discrete injections of a ganglionic blocking drug into two fat pads on the surface of the cat heart. These fat pads were shown to contain ganglion cells histologically. It was observed that vagal effects upon cardiac rate are selectively mediated by neurons located in ganglia overlying the right pulmonary veins at the junction of the right atrium and superior vena cava. On the other hand, vagal effects upon AV conduction were selectively mediated by neurons located in a fat pad at the junction of the inferior vena cava and the inferior left atrium. These pharmacological data support the concept that specific intracardiac ganglia are capable of selective control of SA rate and AV conduction.

Adipose Tissue↗