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At least 631 records · Page 35Linked to original sources
PubMed1982

Distribution of primary sensory nerve terminals in the cat urinary bladder wall.

Distribution of the primary sensory nerve terminals has been investigated in the cat urinary bladder wall in the normal state and after extirpation of certain spinal ganglia. In the normal state the adventitia of the bladder base contained simple sensory corpuscles, Pacinian corpuscles and free nerve endings. In the bladder wall the afferent nerve endings appeared to be free nerve endings without terminal modification. After extirpation of spinal ganglia, some of the nerve fibres degenerated and were located mostly in the trigone and the ventral neck regions of the bladder. After 7 days neither Pacinian nor simple sensory nerve corpuscles could be observed in the wall.

Animals↗
PubMed2006

The histopathogenesis of paralytic rabies in six-week-old C57BL/6J mice following inoculation of the CVS-11 strain into the right triceps surae muscle.

A fatal encephalomyelitis was developed after intracerebral and hind limb inoculation of in 6-week-old C57BL/6J mice by the inoculation of fixed rabies virus (CVS-11 strain), intracerebrally and into hind. After the intracerebral inoculation, virus antigens were detected in the cerebral cortex and hippocampus at 2 days postinoculation (PI), and later spread centrifugally to thalamus, brain stem, cerebellum, spinal cord and spinal ganglia. At 4 days PI, severe apoptosis and DNA fragmentation were observed in the hippocampus and cerebral cortex. All mice infected intracerebrally were dead without limb paralysis at from 10 to 11 days PI. In contrast, mice infected with virus intramuscularly were persistently observed virus antigens in the myocytes at the site of inoculation from 2 days PI. At 4 days PI, the antigens were demonstrated in the spinal dorsal root ganglia, spinal cord and muscle spindles without their detection in the cerebrum and hippocampus. There were no apoptosis in the spinal cord and dorsal root ganglia, however hind limb paralysis was found in all infected mice. Hind limb paralysis was progressed to quadriparalysis, and mice were dead from 11 to 13 days PI. From 4 days PI, necrosis of neuron was observed in the the spinal and dorsal ganglia with infiltration of lymphocyte. This study suggested that the necrosis of spinal neurons was more important to cause the paralysis of hind limb rather than the severe cerebral infection and apoptosis in C57BL/6J mice infected with CVS-11 strain. The virus primarily replicated in the muscles was ascended the spinal cord via afferent fibers and retrogradely invaded the cerebrum, and with subsequent spread to muscle spindles.

Animals↗
PubMed1988

Origin of lingual proprioceptive afferents in Japanese monkey, M. fuscata fuscata. Studied by HRP-labeling technique.

The peripheral course of the axon of the lingual proprioceptive neurons in 5 Japanese monkeys was studied by injecting HRP into the distal part of the hypoglossal nerve through the proximal stump. The present authors confirmed that the HRP-labeled cell bodies appeared ipsilaterally in the C2, C3 and C4 spinal ganglia. The afferents to the C2, C3 and C4 ganglia pass through the ansa hypoglossi and direct neuronal anastomosis existing between the first cervical nerve and the hypoglossal nerve. It was confirmed that in the Japanese monkey, having abundant muscle spindles in the tongue, the lingual proprioceptive neuron soma exist in the C2, C3 and C4 spinal ganglia, their peripheral axons passing through the ansa hypoglossi and the direct neuronal anastomosis.

Animals↗
PubMed2002

Activation of p38 MAP kinase in the rat dorsal root ganglia and spinal cord following peripheral inflammation and nerve injury.

The intrathecal administration of p38 MAP kinase (p38) inhibitor has been shown to reduce hyperalgesia. In the present study, we investigated the activation of p38 in the rat dorsal root ganglion (DRG) and spinal cord following peripheral tissue inflammation and nerve injury immunohistochemically. Peripheral inflammation and chronic constriction injury (CCI) of the sciatic nerve induced a significant increase in the percentage of phosphorylated (P-) p38-immunoreactive (IR) neurons, primarily small sized ones in bilateral DRGs. In contrast, following axotomy, a significant decrease in the percentage of IR neurons was observed in ipsilateral DRGs. In addition, a marked increase was observed in the number of P-p38-IR microglia in the ipsilateral laminae I-IV and IX of the spinal cord following peripheral inflammation, CCI or axotomy. These findings suggest that p38 may play an important role in hyperalgesia and the activation of the spinal microglia.

Animals↗
PubMedDate not supplied

[Morphological and histochemical changes in the spinal cord after epidural administration of prosidol in dogs].

Morphological, histochemical, and histoenzymatic changes in the nervous tissue of the spine and spinal ganglia after epidural injection of narcotic analgetic prosidol were studied in acute experiment on 12 mongrel dogs. No negative effect of prosidol on neuronal structure and nervous tissue microcirculatory bed were observed in experimental vs. control animals. The type of changes and their direction in various compartments of the nervous system (spine and spinal ganglia) were similar in control and experimental animals.

Acid Phosphatase↗
PubMed1997

Increased brain-derived neurotrophic factor immunoreactivity in rat dorsal root ganglia and spinal cord following peripheral inflammation.

Our recent study showed that peripheral inflammation induced an increased expression of brain-derived neurotrophic factor (BDNF) mRNA which was mediated by nerve growth factor (NGF) in the dorsal root ganglion (DRG). In the present study, we evaluated the change of BDNF immunoreactivity in the DRG and spinal cord following peripheral inflammation by means of immunohistochemistry. Significant increases in the percentage of BDNF-immunoreactive (IR) neuron profiles in the L5 DRG and marked elevation in the expression of BDNF-IR terminals in the spinal dorsal horn were observed following peripheral tissue inflammation produced by an intraplantar injection of Freund's adjuvant into the rat paws. These findings suggest that peripheral tissue inflammation induces an increased BDNF synthesis in the DRG and an elevated anterograde transport of BDNF to the spinal dorsal horn. The functional role of this increased BDNF was discussed briefly.

Animals↗
PubMed1999

The perikaryal surface of spinal ganglion neurons: differences between domains in contact with satellite cells and in contact with the extracellular matrix.

The perikaryal surface of spinal ganglion neurons undergoes dynamic changes throughout life. In particular, numerous slender projections develop and retract continuously from this surface. We showed previously that the outgrowth of these projections, while an intrinsic property of spinal ganglion neurons, is also influenced by the surrounding microenvironment. Since the latter consists of satellite cells and the extracellular matrix, we sought to determine the relative contributions of each of these components to the outgrowth of perikaryal projections. To this end, we took advantage of a little known characteristic of the satellite cell sheaths: in the rabbit, these sheaths can exhibit gaps that leave the nerve cell body surface directly exposed to the extracellular matrix. We compared the surface domains covered by satellite cells with those in direct contact with the extracellular matrix. We found that the perikaryal projections are abundant in the former domains but are absent in the latter. We also found that the perineuronal extracellular matrix of rabbit spinal ganglia contains laminin and fibronectin, two glycoproteins that have been reported to promote the growth of axonal processes from sensory ganglion neurons. Laminin and fibronectin were also present at the level of the gaps in the satellite cell sheath. These results: (1) provide additional evidence that environmental factors influence the outgrowth of perikaryal projections from spinal ganglion neurons; (2) suggest that satellite cells permit the outgrowth of these projections; (3) suggest that in the spinal ganglia of adult rabbits the perineuronal extracellular matrix is not in itself able to promote the outgrowth of these projections. This study provides a further example of the influence that supporting neuroglial cells have on sensory ganglion neurons.

Animals↗
PubMed1987

Effect of ischaemia on protein synthesis in vitro.

Changes in the incorporation of 14C-amino acids into proteins in vitro were followed under conditions of ischemia induced by abdominal aorta ligature and subsequent recirculation in dogs. Cell saps isolated from L-S spinal cord, spinal ganglia, the sciatic nerve and medulla oblongata were added to the incorporation mixture composed of ribosomes and an enzymatic system from intact brains. Cytosols isolated from ischemic animals affected the rate of in vitro protein synthesis moderately, while repeated ischemia caused a profound decrease in the incorporation of amino acids into proteins. Cytosols from L-S spinal cord and especially from spinal ganglia after three days of recirculation substantially enhanced incorporation thus indicating a massive response of these tissues to ischemic injury. Cell saps from the medulla oblongata increased amino acid incorporation into proteins in vitro in all experimental groups.

Animals↗
PubMed1990

Abnormal glycosphingolipid metabolism in the nervous system of galactosialidosis.

In an autopsy case of galactosialidosis, GM3, GM2, GM1, and GD1a were accumulated in sympathetic and spinal ganglia and grey matter of the spinal cord. Especially, the accumulations of GM3 and GM2 amounted to 41- and 86-fold increases in sympathetic ganglia, respectively, as compared to normal controls. In addition LacCer, GA2 and GA1 were accumulated in sympathetic and spinal ganglia. The accumulations of GM3 and GD1a are considered to be the result of defective lysosomal sialidase activity and the accumulation of GM1, LacCer and GA1 is also considered to be due to decreased beta-galactosidase activity in this disorder. To better understand the possible mechanism of GM2 accumulation, we determined the activity of GM2 synthesizing enzyme (GM3:UDP-GalNAc transferase), as well as hexosaminidase activity, in sympathetic ganglia, but they did not change. Abnormal ganglioside and neutral glycosphingolipid metabolism, as well as sialyloligosaccharide and sialylglycoprotein metabolism, may be involved in the pathogenesis of this disorder.

Biomechanical Phenomena↗
PubMed1995

Phosphorylation and transport of neurofilament proteins in the rat spinal ganglion.

Neurofilament proteins (NFs) in rat spinal ganglia were labeled with [32P]orthophosphate injected into ganglia and analyzed by two-dimensional autoradiography and immunoblotting. Three polypeptides of NF were labeled irrespective of the extent of phosphorylation. Most of the labeled NFs were transported from cell bodies to proximal axons within 24 h. A major fraction of low phosphorylated NF-H changed to high phosphorylated form in intraganglionic nerve fibers and peripheral nerves adjacent to spinal ganglia. A small fraction of low phosphorylated NF-H appeared earlier than the high phosphorylated form in adjacent peripheral nerves, suggesting that newly synthesized NF-H in cell bodies migrate a long distance before they are extensively phosphorylated and assembled into the cytoskeleton in proximal axons.

Animals↗
PubMed1996

Neuroinvasive properties of herpes simplex virus type 1 glycoprotein variants are controlled by the immune response.

Neuroinvasiveness is a property central to the pathogenesis of herpes simplex virus (HSV) and most isolates demonstrate this property. Exceptions are HSV strains KOS and ANG, for which we have previously shown that the non-neuroinvasive phenotype is referable to single amino acid changes in glycoprotein D for ANG or glycoprotein B for KOS. Because glycoproteins B and D are immunologically significant, the possibility that the phenotype has an immunologic basis was examined. Nonimmunosuppressed mice could not be killed with any dose of these non-neuroinvasive viruses after footpad inoculation, but in cyclophosphamide-suppressed animals, the ratios of plaque-forming units to LD50 decreased by at least four orders of magnitude to levels comparable with that of ANG-path, a neuroinvasive derivative of ANG. KOS and ANG induced a more rapid circulating neutralizing Ab response than did ANG-path, and mice were protected when these agents were co-infected with the neuroinvasive strain. The noninvasive viruses engendered an enhanced mononuclear cell infiltrate in infected spinal ganglia which consisted of increased numbers of CD4+ and CD8+ T cells and an increased production and secretion of IgG. HSV-specific Ab-secreting cells were also observed. In addition, passive transfer of anti-HSV mouse serum protected immunosuppressed mice from lethal HSV challenge. Selective in vivo depletion of T lymphocytes increased the detectable levels of both KOS and ANG viruses in the spinal ganglia at 6 days postinfection, but it did not alter the ratios of plaque-forming units to LD50 or affect the HSV-induced increase in ganglionic IgG. Taken together, these data indicate that in these systems there is an immunologic basis for the control of HSV-1 neuroinvasiveness and that humoral, rather than cell-mediated immunity, is playing the major role.

Adjuvants, Immunologic↗
PubMedDate not supplied

[Drug stimulation of the peripheral nerve regeneration].

A comparative study of the effects of xymedone, riboxin, and piracetam upon the regeneration of myelinated axons and the number of surviving sensory neurons in spinal ganglia L4-L5 was studied on the model of sciatic nerve transection in rats. The three drugs decrease the number of neurons entering the posttraumatic apoptosis. Riboxin and xymedone stimulate the regeneration of myelinated axons, the latter drug being more effective and producing a 21.3 and 14.7% increase in the number of regenerated myelinated axons and a 29.3 and 37.7% increase in the relative number of sensory neurons (the transected/contralateral side ratio) in spinal ganglia L4-L5 relative to control by the 60th and 90th day upon transection, respectively.

Animals↗
PubMed1981

Antagonism by gamma-aminobutyric acid of the stimulant effect of angiotensin II on cardiac sympathetic ganglia in spinal dogs.

The effects of angiotensin II and neuro-aminoacids administered through the right subclavian artery (i.a.) to the cardiac sympathetic ganglia were investigated in spinal dogs. Angiotensin II (1--8 micrograms) elicited a dose-dependent positive chronotropic effect which was reduced after i.a. injection of saralasin (100 micrograms). The effect of angiotensin II was not reduced after combined treatment with either hexamethonium (10 mg/kg) plus atropine (0.1 mg/kg) or hemicholinium-3 (5 mg/kg) plus preganglionic stimulation. The dose-dependent response to angiotensin II of heart rate was inhibited by GABA (50, 500 micrograms), GABOB (500 micrograms) and muscimol (50, 100 micrograms). The inhibition of the response to angiotensin II by a small dose of GABA (50 micrograms), but not by a high one (500 micrograms), was antagonized by i.a. injection of picrotoxin (2 mg). The positive chronotropism induced by bethanechol (25, 50 micrograms) and a small dose of acetylcholine (25 micrograms) were significantly inhibited by a high dose (500 micrograms) but not by a low dose (50 micrograms) of GABA. These results confirm that angiotensin II stimulates cardiac chronotropism by acting on the angiotensin II receptor located at the cardiac ganglia and show that this stimulant effect is antagonized by GABA.

Angiotensin II↗
PubMed1999

Expression of mRNAs encoding full-length and truncated TrkB receptors in rat dorsal root ganglia and spinal cord following peripheral inflammation.

Peripheral inflammation induces an increased brain-derived neurotrophic factor (BDNF) synthesis in the dorsal root ganglion (DRG) and an elevated anterograde transport of BDNF to axon terminals in the spinal dorsal horn. To characterize whether expression of trkB is modulated in response to BDNF elevation in these areas, we evaluated changes in expression of full-length and truncated trkB (trkB.FL and trkB.T) mRNAs after injection of complete Freund's adjuvant into the hind paw of the rat. Reverse transcription-polymerase chain reaction analysis revealed that BDNF and trkB.T mRNAs levels in the DRG increased, while no change of expression of trkB.FL mRNA was observed. There was no detectable change in both trkB.FL and trkB.T mRNAs levels in the spinal cord. Considering that trkB.T mRNA is expressed mainly in the perineuronal satellite cells, these results suggest a possible paracrine role of BDNF within the DRG in addition to an important role related with nociception following peripheral inflammation.

Animals↗
PubMed1989

Cytochemistry of the trigeminal and dorsal root ganglia and spinal cord of the rat.

1. The primary sensory neurones have been classified into large light (LLC), type A, small dark (SDC), type B and type C cells on the basis of size, ultrastuctural and immunocytochemical characteristics. 2. Subclassifications have been described according to the configuration and spatial organization of cytoplasmic organelles. 3. Furthermore, the LLC are immunoreactive with a monoclonal antibody, RT97, directed against a neurofilament protein and the SDC are positive with anti-arginine vasopressin (AVP). 4. The majority of the neurochemical substances including substance P (SP), somatostatin (SOM), fluoride resistant acid phosphatase (FRAP), 5-hydroxytryptamine (5-HT) and glutamate were localized to the small and intermediate diameter neurones measuring 9-40 microns. 5. The cytochemistry of the dorsal horn was similar to the dorsal root ganglia (DRG). 6. There is good evidence that substance P (SP) and somatostatin (SOM) are transmitters for a proportion of nociceptive neurones but the neurotransmitters utilized by the rest of the subtypes are unknown. 7. 5-hydroxytryptamine (5-HT) and glutamate may be putative transmitters of the primary sensory neurones as they are localized in 28-30% of the SDC. 8. The wider distribution and extensive coexistence of the neuropeptides is incompatible with neurotransmitter function, but some may be neuromodulators whereas others such as arginine vasopressin (AVP) are useful markers for identifying type B neurones.

Animals↗
PubMed1990

[Cosinor analysis of the circadian dynamics of transcription in populations of neurocytes from a number of sections of the rat nervous system].

Diurnal fluctuations of endogenous RNA polymerases activity were studied in the cell nucleus of the cerebral stem and spinal nervous system populations (neurocytes of the hypothalamic suprachiasmatic nuclei, superior cervical ganglia, spinal ganglia L5, motoneurones of the spinal cord and Purkinje cells) were revealed. The acrophases of the visual cortex neurones were observed just before light reception.

Animals↗
PubMed2002

Expression of orphanin FQ/nociceptin and its receptor in rat peripheral ganglia and spinal cord.

Expression of the neuropeptide orphanin FQ/nociceptin (OFQ/N) and its receptor, the opioid receptor-like receptor (ORL1), have been found to have a wide distribution in the central nervous system, and in brain areas involved in sensory perception in particular. The effects of OFQ/N on, e.g., sensory transmission are very complex, and a modulatory effect on pain perception has been suggested. We therefore wanted to investigate the distribution of OFQ/N and ORL1 in the spinal cord and DRG, and also in SCG and some other peripheral tissues. The methods used were in situ hybridization, immunohistochemistry and ligand binding. We found that OFQ/N and ORL1 mRNA are expressed in DRG; primarily in small and large neurons, respectively. In spinal cord, mRNA for OFQ/N and ORL1 is expressed in neurons in laminae I, II and X, and in ventral horn neurons. Further, immunoreactivity for OFQ/N is observed in fibers and neurons in the superficial laminae of the dorsal horn and around the central canal, and also in neurons in the ventral horn of the spinal cord. Receptor ligand binding to the spinal cord grey matter is demonstrated, primarily concentrated to the dorsal horn and around the central canal, and also to medium and large size DRG neurons. These findings on the morphological distribution pattern of OFQ/N and ORL1 at the cellular level may support the notion that OFQ/N is involved in modulating pain transmission. Further, expression of OFQ/N and ORL1 mRNA was also found in SCG, whereas expression was undetectable in skin.

Animals↗