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Results for “GANGLIA, SPINAL”

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At least 163 records · Page 9Linked to original sources
PubMed1993

Herpes simplex virus type-2 infection by a footpad route results in neuronal death in mouse spinal ganglia.

We have examined the effects of herpes simplex virus type 2 (HSV-2) infection on neuron numbers in mouse dorsal root ganglia (DRG) following unilateral hind footpad inoculation. One month following HSV-2 strain MS inoculation, tissue sections of decalcified spine containing the paired 4th and 5th lumbar DRGs were stained with cresyl violet. Neuronal numbers, somal areas and ganglion volumes were determined for ganglia ipsilateral and contralateral to both HSV-2 and medium inoculations. One month following HSV-2 infection, 47-88% of neurons disappeared in the ipsilateral ganglia. The somal areas of the remaining neurons in these ganglia fell within the range of the uninfected population. Ganglionic shrinkage did not occur as a result of HSV-2 infection; neurons were replaced by large numbers of inflammatory cells. Neuron numbers in the contralateral control ganglia of the HSV-2 inoculated mice appeared slightly decreased. Mice inoculated with medium contained similar numbers of neurons in ipsilateral and contralateral ganglia. These results show that, in addition to other previously described host alterations, infection with HSV-2 strain MS results in neuronal death in the affected host ganglia. This is the first in vivo quantitative documentation of neuronal death induced by herpes simplex virus infection.

Animals↗
PubMed1991

Electrophoretic analysis of neuronal genomic DNA from hypertrophic spinal ganglia during lizard tail regeneration.

Cytoplasmic and nuclear hypertrophy in neurons from the last 3 pairs of sensory ganglia left in situ cranially to the plane of amputation occurs during lizard tail regeneration. Cytophotometry after Feulgen staining demonstrated the presence of some neurons, from hypertrophic ganglia, whose quantity of DNA exceeded the diploid level (hyperdiploid neurons). In the present work agarose gel electrophoresis of total genomic DNA extracted from hypertrophic ganglia showed one or two bands migrating below the high molecular weight DNA, pointing to a selective amplification of discrete DNA segments.

Amputation, Surgical↗
PubMed1992

Nicotine- and capsaicin-, but not potassium-evoked CGP-release from cultured guinea-pig spinal ganglia is inhibited by Ruthenium red.

In the present study we have investigated the effects of nicotine, capsaicin, potassium, glutamate and aspartate on release of calcitonin gene-related peptide (CGRP)-like immunoreactivity (-LI) from guinea-pig dorsal root ganglion (DRG) cultures. In addition the possible influence of Ruthenium red (RR), neuropeptide Y (NPY) and noradrenaline (NA) on the CGRP-LI outflow has been evaluated. Nicotine, capsaicin and potassium, but not glutamate or aspartate, evoked a Ca(2+)-dependent increase in the culture medium, suggesting release of CGRP-LI. RR inhibited the effect of both capsaicin and nicotine but did not influence potassium-induced CGRP-LI release. Furthermore, the nicotine- but not capsaicin-evoked CGRP-LI release was inhibited by NPY. It is concluded that DRG cultures represent an experimental model where regulation of CGRP-LI release can be studied. The ability of RR to inhibit not only capsaicin but also nicotine effects indicate that the proposed selectivity of RR may depend on the agent used to evoke peptide release and/or concentrations used.

Animals↗
PubMed2004

Gamma-aminobutiric acid immunostaining in trigeminal, nodose and spinal ganglia of the cat.

Gamma-aminobutyric acid (GABA) is a principal inhibitory neurotransmitter in the vertebrate nervous system. It is found mainly in local circuit neurons, but it has also been described in sensory organs and dorsal root ganglia (DRG). The present study describes the presence of GABA in primary afferent neurons of feline sensory ganglia: trigeminal ganglia (TrG), nodose ganglia (NG), and DRG. Quantitative analysis revealed that approximately 20% of the cells in the TrG, NG and DRG are GABAergic. GABA-expressing neurons varied in size. GABA-containing neuronal fibres were also observed in the neuropil. Some of these were in close apposition to both GABA-positive and GABA-negative ganglionic neuronal perikarya. The localization of GABA in small primary afferent neurons, which are considered to be nociceptors, suggests that the amino acid may function as a pain transmitter or modulator, whereas processing of other sensory modalities, such as somatosensory and proprioceptive, may also be affected by GABA.

Animals↗
PubMed2006

Robust increase of cutaneous sensitivity, cytokine production and sympathetic sprouting in rats with localized inflammatory irritation of the spinal ganglia.

We investigated the role and mechanisms of inflammatory responses within the dorsal root ganglion (DRG) in the development of chemogenic pathological pain. DRG inflammation was induced by a single deposit of the immune activator zymosan in incomplete Freund's adjuvant in the epidural space near the L5 DRG via a small hole drilled through the transverse process. After a single zymosan injection, rats developed bilateral mechanical hyperalgesia and allodynia which began by day 1 after surgery, peaked at days 3-7, and lasted up to 28 days. The number of macrophages in ipsilateral and contralateral DRGs increased significantly, lasting over 14 days. Robust glial activation was observed in inflamed ganglia. Cytokine profile analysis using a multiplexing protein array system showed that, in normal DRG, all but interleukin (IL)-5, IL-10 and granulocyte-macrophage colony stimulating factor (GM-CSF) were detectable with concentrations of up to 180 pg/mg protein. Local inflammatory irritation selectively increased IL-1beta, IL-6, IL-18, monocyte chemoattractant protein-1 (MCP-1), and growth-related oncogene (GRO/KC) up to 17-fold, and decreased IL-2 and IL-12 (p70) up to threefold. Inflaming the DRG also remarkably increased the incidence of spontaneous activity of A- and C-fibers recorded in the dorsal root. Many of the spontaneously active A-fibers exhibited a short-bursting discharge pattern. Changes in cytokines and spontaneous activity correlated with the time course of pain behaviors, especially light stroke-evoked tactile allodynia. Finally, local inflammation induced extensive sprouting of sympathetic fibers, extending from vascular processes within the inflamed DRG. These results demonstrate the feasibility of inducing chronic localized inflammatory responses in the DRG in the absence of traumatic nerve damage, and highlight the possible contribution of several inflammatory cytokines/chemokines to the generation of spontaneous activity and development and persistence of chemogenic pathologic pain.

Action Potentials↗