[Functional analysis of pain pathway in posterior horn cells using spinal cord slice and in-vivo patch clamp method].
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Animals↗
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Acute central cervical cord injury presenting with only upper extremity involvement.
Twenty-four patients with acute central cervical cord injury with motor and sensory impairment involving only the upper extremities are described; none had any abnormality in the lower extremities. They were all treated conservatively with one exception in whom an anterior decompression was performed. Seventeen had complete recovery of motor function; the remaining 7 had some weakness of the palmar interosseous muscles. The time to recovery was from 2 weeks to 4 months. Sensory recovery took from 4 to 6 months after injury. This type of injury is caused by damage to the anterior and posterior horn cells in the cervical cord.
Accidental Falls↗
Decrease in Cu/Zn- and Mn-superoxide dismutase activities in brain and spinal cord of patients with amyotrophic lateral sclerosis.
Amyotrophic lateral sclerosis (ALS) is a degenerative disorder of motor neurons in the central nervous system (CNS). Mutation of the Cu/Zn-superoxide dismutase (SOD) gene on chromosome 21 has been found in some families with autosomal dominant familial ALS (FALS). We sought to determine whether there may be differences in the distribution and activity of SOD in the CNS of patients with sporadic ALS, and of control patients without neurological disorders. The frontal cortex, cerebellum, and spinal cord were obtained at autopsy on 5 patients with ALS and from 10 controls. Immunohistochemically, in the controls, the cytosols of the large pyramidal neurons of the cerebral cortex, anterior and posterior horn cells, and neurons of the nucleus thoracicus of spinal cord were stained homogeneously with anti-human Cu/Zn-SOD antibody, and in a granular manner with anti-human Mn-SOD antibody. Pia mater and epithelial cells of choroid plexus also stained well. Conversely, in the CNS of the ALS patients, most neurons were stained faintly, or not at all with both anti-Cu/Zn- and Mn-SOD antibodies, whereas the pia mater and the epithelial cells of choroid plexus stained intensely. There was no difference in total SOD activity in the entire CNS between ALS patients and controls, as determined by enzyme assay. Results suggest that, in cases of sporadic ALS, the activities of Cu/Zn- and Mn-SOD are decreased and superoxide produced within the neurons accumulates because of an insufficient elimination, leading to the development or acceleration of cell damage, ultimately producing neuronal degeneration and necrosis.
Adolescent↗
Painful legs and moving toes syndrome associated with herpes zoster myelitis.
A 75-year-old woman developed painful legs and moving toes syndrome (PLMT) 16 months after the onset of herpes zoster (HZ) myelitis. Although the scattered extensive lesions due to HZ myelitis were observed to be eccentric near the posterior horn on MRI, these changes had disappeared upon the development of PLMT. Combined median and tibial nerve somatosensory evoked potentials demonstrated abnormal findings only in the tibial nerve stimuli, suggesting that a severe alteration occurred in the somatosensory fibers coming selectively from the lower legs. These findings suggest plasticity in the ascending somatosensory pathway including the posterior horn cells, probably involving the interneuron networks, for the lower legs may underlie the development of PLMT associated with HZ myelitis.
Aged↗
Epidural morphine in treatment of pain.
Epidural injections of a 2 mg morphine were given to 10 patients with severe acute or chronic pain. All cases had considerable amelioration of pain, which commenced within 2-3 min, reached a peak in 10-15 min, and was effective for 6-24 h. It is suggested that the morphine reached the subarachnoid space and produced its effect by direct action on the specific opiate receptors in the substantia gelatinosa of the posterior-horn cells of the spinal cord.
Acute Disease↗
Distribution of trigeminothalamic and spinothalamic lamina I terminations in the cat.
The distribution in the thalamus of terminal projections from lamina I neurons of the trigeminal, cervical, and lumbosacral dorsal horn was investigated with the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L) in the cat. Iontophoretic injections were guided by single- and multi-unit physiological recordings. The injections in particular cases were essentially restricted to lamina I, whereas in others they spread across laminae I-III or laminae I-V. The trigemino- and spinothalamic (TSTT) terminations were identified immunohistochemically. In all cases, regardless of the level of the injections, terminal fibers were consistently distributed in three main locations: the submedial nucleus; the ventral aspect of the basal ventral medial nucleus and ventral posterior nuclei; and, the dorsomedial aspect of the ventral posterior medial nucleus. The terminal fields in the submedial nucleus and the ventral aspect of the ventral posterior group were topographically organized. Terminations along the ventral aspect of the ventral posterior group extended posterolaterally into the caudal part of the posterior nucleus and anteromedially into the ventromedial part of the ventral lateral nucleus. In several cases with trigeminal lamina I injections, a terminal labeling patch was observed within the core of the ventral posterior medial nucleus. In cases with spinal lamina I injections, terminations were also consistently found in the lateral habenula, the parafascicular nucleus, and the nucleus reuniens. Isolated terminal fibers were occasionally seen in the zona incerta, the dorsomedial hypothalamus, and other locations. These anatomical observations extend prior studies of TSTT projections and identify lamina I projection targets that are important for nociceptive, thermoreceptive, and homeostatic processing in the cat. The findings are consistent with evidence from physiological (single-unit and antidromic mapping) and behavioral studies. The novel identification of spinal lamina I input to the lateral habenula could be significant for homeostatic behaviors.
Animals↗
Chromatolysis in alcoholic encephalopathies. Pellagra-like changes in 22 cases.
In 22 patients with alcoholic encephalopathies, chromatolysis similar to that reported in endemic pellagra was found on postmortem examination. No gross macroscopic changes were seen in affected areas and only neurons were involved. The changes consisted of central chromatolysis, seen predominantly in the brainstem, especially in the pontine nuclei, where they were constant, and in the cerebellar dentate nuclei. Nuclei of cranial nerves (mainly the third, sixth, seventh and eighty), the reticular nuclei, arcuate nuclei and posterior horn cells, were also markedly affected. Changes were sometimes seen in the cerebral cortex, the interpeduncular nuclei, the central mesencephalic grey matter, the colliculi, the tenth and twelfth cranial nerve and perihypoglossal nuclei, the gracile and cuneate nuclei and anterior horn cells. This distribution was different from that reported in endemic and 'endogenous' pellagra or in isoniazid-induced pellagra encephalopathy. Central chromatolysis was the only pertinent finding of the CNS examination in 9 cases. In 8 cases, chromatolysis was associated with Marchiafava-Bignami encephalopathy, in 4 cases with Wernicke-Korsakoff encephalopathy, and in 1 other case with both. Mild degeneration of spinal cord tracts was seen in 3 cases. The chromatolysis of alcoholic pellagra did not appear to be a retrograde change related to axonal degeneration. Systemic examination showed liver changes in 15/16 cases. Treatment of these cases had not included niacin. No differences were found between cases given thiamine and pyridoxine and those which had not. Microscopic examination of the pons is essential in alcoholic encephalopathies.
Alcoholism↗
Structural scoliosis model in dogs with experimentally induced syringomyelia.
STUDY DESIGN: Animal scoliosis model associated with syringomyelia. OBJECTIVE: To investigate the pathogenesis of scoliosis produced in dogs with kaolin-induced syringomyelia. SUMMARY OF BACKGROUND DATA: Kaolin injected into the cisterna magna produces basilar arachnoiditis, leading to hydrocephalus and syringomyelia. There have been no reports on scoliosis associated with kaolin-induced syringomyelia. METHODS: Kaolin was injected percutaneously into the cisterna magna of 11 beagles 6-8 weeks after birth. Roentgenograms, computed tomography, and magnetic resonance imaging were obtained. The spinal cord and the paraspinal muscles were examined histologically. Structural changes of the vertebral column were analyzed with calcein and tetracycline labeling. RESULTS: Hydrocephalus occurred in nine dogs. A communicating syringomyelia appeared in five dogs. Mild scoliosis developed in two dogs, and severe cervical scoliosis in one dog. In the syringomyelia cases, acute or subacute inflammatory changes were found in the spinal cord. Damage of the anterior and posterior horn cells was more marked in the scoliotic animals than in the nonscoliotic animals. In three of the syringomyelia cases, including two scoliosis cases, the paraspinal muscles revealed neurogenic changes. The deformed vertebrae appeared to diminish rather than to increase the deformity in severe scoliosis. CONCLUSION: The exact mechanism of the development of scoliosis could not be identified, although an etiologic relation with malfunction of the central nervous system was noted. This model may be useful to study scoliosis experimentally.
Animals↗
Widespread thalamic terminations of fibers arising in the superficial medullary dorsal horn of monkeys and their relation to calbindin immunoreactivity.
The relay of pain fibers from the spinal and medullary dorsal horn in the thalamus has become a controversial issue. This study analyzed the relationship of fibers arising in lamina I to nuclei in and around the caudal pole of the ventral posterior nuclear complex and especially to a zone of calbindin-dense immunoreactivity (VMpo) identified by some authors as the sole thalamic relay for these fibers. We show that the densest zone of calbindin immunoreactivity is part of a more extensive, calbindin-immunoreactive region that lies well within the medial tip of the ventral posterior medial nucleus (VPM), as delineated by other staining methods, and prove that the use of different anti-calbindin antibodies cannot account for differences in interpretations of the organization of the posterior thalamic region. By combining immunocytochemical staining with anterograde tracing from injections involving lamina I, we demonstrate widespread fiber terminations that are not restricted to the calbindin-rich medial tip of VPM and show that the lamina I arising fibers are not themselves calbindin immunoreactive. This study disproves the existence of VMpo as an independent thalamic pain nucleus or as a specific relay in the ascending pain system.
Afferent Pathways↗
Intramuscular injection of hypertonic saline: in vitro and in vivo muscle tissue toxicity and spinal neurone c-fos expression.
Intramuscular injection of hypertonic saline (4-6% NaCl) is widely used to induce muscle pain in volunteers. The quality of the pain is comparable to clinical muscle pain with localised and referred pain. The objective was to evaluate the muscle toxicity of hypertonic saline by characterisation of 1) cytotoxicity in vitro, 2) local muscle toxicity in rabbits and 3) number of spinal dorsal horn neurones expressing c-fos after intramuscular injection in pigs as an indicator of nociception. Rat myocyte cultures and erythrocyte suspensions were treated with hypertonic NaCl solutions. The creatine kinase activity remaining in the myocytes and haemolysis were measured. Groups of six rabbits were given an intramuscular injection of 0.5 ml of 0.9, 3 or 6% NaCl. Three days later, creatine kinase activity was determined in injection site muscle tissue and normal contralateral muscle. The amount of injection site muscle tissue totally depleted of creatine kinase was calculated. Groups of two pigs were given an intramuscular injection of 3.0 ml of 6% NaCl. The spinal cord was sampled 1, 2 or 3 hr later and processed for stereological quantification of the number of dorsal horn neurones expressing c-fos. Saline was not toxic in vitro at 0.9-6%, but toxic to erythrocytes at 7% or higher and rat myocytes at 15% or higher. No muscle toxicity was seen in rabbits. The number of dorsal horn neurones expressing c-fos was not above basal level. In conclusion, 6% saline caused no in vitro or in vivo toxicity in sensitive models. Consequently, the pain caused by intramuscular injection of hypertonic saline is most likely not related to tissue damage. Consistently, intramuscular injection of 6% NaCl did not activate dorsal horn neurones in pigs to express c-fos beyond basal level.
Animals↗
In vivo control of NMDA receptor transcript level in motoneurons by viral transduction of a short antisense gene.
Glutamate receptors play critical roles in normal and pathological processes. We developed an antisense gene delivery strategy to modulate the NMDA type of glutamate receptor. Using transient transfection in vitro and viral mediated gene transfer in vitro and in vivo, the effect of expression of an antisense gene fragment (60 bp) of the NR1 subunit was tested. Immunoblot analysis showed an antisense-concentration-dependent reduction in the NR1 subunit upon transient co-transfection of a plasmid expressing a sense NR1 gene and a plasmid expressing the antisense fragment into COS-7 cells. After recombination into an adenoviral vector, this antisense fragment reduced the amount of endogenous NR1 protein in PC12 cells. Finally, direct intraparenchymal injection of the viral vector into rat spinal cord resulted in diminished NR1 in motor neurons. Our results demonstrate the efficacy of this approach, which combines antisense with viral gene delivery to control the expression of specific genes in vivo. This approach may also be useful in reducing excitatory neurotransmission in vivo, with implications for the treatment of spinal disorders such as amyotrophic lateral sclerosis or chronic pain.
Adenoviridae↗
Specific expression of spinal Fos after PAR-2 stimulation in mast cell-depleted rats.
Protease-activated receptor-2 (PAR-2) in the sensory neurons may be involved in nociceptive processing. We attempted to detect and characterize specific expression of spinal Fos, a marker of nociception, in mast cell-depleted rats. Intraplantar (i.pl.) administration of not only the PAR-2 agonist SLIGRL-NH2, but also the control peptide LSIGRL-NH2, induced Fos expression in naive rats, whereas only the former specifically produced Fos expression in mast cell-depleted rats. This Fos expression was blocked by intrathecal DAMGO, a mu-opioid agonist, and, in part, by i.pl. calphostin C, a protein kinase C (PKC) inhibitor. Thus, specific expression of spinal Fos following peripheral PAR-2 activation is detectable in mast cell-depleted rats, suggesting activation of spinal nociceptive neurons, which is partially mediated by activation of PKC.
Animals↗
Position and size of the axon hillock in various groups of neurons.
The origin of the axon was studied in Golgi-Kopsch impregnated specimens prepared from the spinal cord and brain of adult rats. Five types of neurons were sampled: large ventral horn neurons, neurons in the intermediate zone and ventral horn of the spinal cord, antenna-type neurons in the spinal dorsal horn, neurons in the thalamus, and neurons in the hypothalamus. The axon originated from the perikaryon in 76% of the large ventral horn neurons and in 64% of the neurons in the thalamus. In contrast, the axon emerged from one of the dendrites in 75% of the neurons in the intermediate zone and the ventral horn of the spinal cord and in 68% of the neurons in the hypothalamus. In the case of the antenna-type neurons in the spinal dorsal horn, the axon often originated from one of the dendrites, but never from a dorsally oriented dendrite. The mean distance of the axon hillock of dendritic origin was the longest in the neurons in the intermediate zone and the ventral horn of the spinal cord. The size of the axon hillock was proportional to the size of the perikaryon. The impregnated portion of the axon was longest in the large ventral horn neurons.
Animals↗
Modulation of presynaptic activity by phosphorylation in cultured rat spinal dorsal horn neurons.
UNLABELLED: Phosphorylation, in particular by protein kinase C (PKC), modulates spinal sensory transmission and nociceptive behaviors. Whereas PKC's postsynaptic actions are well established, its presynaptic effects in spinal sensory neurons are mostly inferred from postsynaptic recordings. Here we first show that the amphipathic styryl dye FM 1-43 can be used to image presynaptic activity in cultured spinal dorsal horn cultures and then test whether PKC modulates presynaptic activity in cultured spinal dorsal horn neurons. Pretreatment with the broad-spectrum kinase inhibitor staurosporine (2 micromol/L) inhibited dye release. Bisindolylmaleimide I, a PKC inhibitor, potentiated dye release at low doses (200 nmol/L and 1 micromol/L), while inhibiting it at a higher dose (5 micromol/L). Activating PKC with phorbol dibutyrate (0.5 micromol/L) induced an increase in exocytosis, which is partially blocked by bisindolylmaleimide I. These results indicate that styryl dyes can be used to observe presynaptic regulation of spinal dorsal horn neurons, and that PKC acts presynaptically to modulate spinal sensory transmission. PERSPECTIVE: With dye imaging technique, we demonstrate here that PKC presynaptically regulates sensory transmission in spinal dorsal horn neurons. In combination with conventional whole-cell patch-clamp recording technique, the present study provides a new methodology for studying spinal sensory transmission and modulation and facilitates our understanding of pain mechanism.
Animals↗
Chronic morphine treatment increases the expression of the neural cell adhesion molecule in the dorsal horn of the mouse spinal cord.
It is well known that prolonged exposure to morphine results in tolerance to morphine-induced antinociception. In the present study, we found that mice that were tolerant to morphine-induced antinociception exhibited an increase in immunoreactivity for the neural cell adhesion molecule in the dorsal horn of the spinal cord, which was highly overlapped with immunoreactivity for the increased metabotropic glutamate receptor 5 induced by morphine. These findings support the idea that repeated stimulation of mu-opioid receptors increases the expression of neural cell adhesion molecule and metabotropic glutamate receptor 5. This phenomenon leads to the enhanced excitatory synaptic transmission in the dorsal horn of the spinal cord, and in turn suppresses the morphine-induced antinociception.
Animals↗
[The morphological validation of the pathogenetic prerequisites for analgesic operations in the area of the foramina of the posterior roots].
Since 1983, a hundred and forty-five analgesic operations on the entry areas of the posterior roots were made in patients with deafferentational pain syndrome. Intraoperative findings made the authors reassess the pathogenetic mechanisms responsible for the pain syndrome and induce them to perform a thorough morphological studies of the changes occurring in the diseased posterior roots of the spinal cord and other regions of the nerve system. The morphological study was made on 20 rats that had developed chronic pain syndrome due to abruption of the brachial plexus from the spine. Experimental findings showed marked destructive changes at the site of injury, posterior, lateral, and anterior horns of the spinal cord, in the cerebellum, neurosecretory nuclei of the hypothalamus, thalamus, and cortex of the brain. These changes are regarded as transneuronal responses involving the cerebral cortex, which are accompanied by irritation and overirritation, which may be considered to be abnormal responses to a massive flux of afferent impulses emitting from the focus of the diseased spine. Changes were detected at the level of a traumatic lesion, but they were absent in other regions of the nervous system: status spongiosus in the posterior and lateral columns of the spine at the level of diseased posterior horns and glial cell proliferation in the diseased posterior horns. The proliferation contributes to the formation of hyperactive neurons that cause the pain syndrome. It may be suggested that spongious changes occurring around the spinal injury focus promote continuous glial proliferation and significantly impaired intertissue metabolism, thus maintaining abnormal activities in the focus of a lesion.
Animals↗
Effect of midthoracic spinal cord constriction on catalytic nitric oxide synthase activity in the white matter columns of rabbit.
The distribution and changes of catalytic nitric oxid synthase (cNOS) activity in the dorsal, lateral and ventral white matter columns at midthoracic level of the rabbit's spinal cord were studied in a model of surgically-induced spinal cord constriction performed at Th7 segment level and compared with the occurrence of nicotinamide adenine dinucleotide phosphate diaphorase expressing and neuronal nitric oxide synthase immunoreactive axons in the white matter of the control thoracic segments. Segmental and white-column dependent differences of cNOS activity were found in the dorsal (141.5 +/- 4.2 dpm/microm protein), lateral (87.3 +/- 11.5 dpm/microm protein) and ventral (117.1 +/- 7.6 dpm/microm protein) white matter columns in the Th5-Th6 segments and in the dorsal (103.3 +/- 15.5 dpm/microm protein), lateral (54.9 +/- 4.9 dpm/microm protein), and ventral (86.1 +/- 6.8 dpm/microm protein) white matter columns in the Th8-Th9 segments. A surgically-induced constriction of Th7 segment caused a disproportionate response of cNOS activity in the rostrally (Th5-Th6) and caudally (Th8-Th9) located segments in both lateral and ventral white matter columns. While a statistically significant decrease of cNOS activity was detected above the constriction site in the ventral columns, a considerable, statistically significant increase of cNOS activity was noted in the white lateral columns below the site of constriction. It is reasoned that the changes of cNOS activity may have adverse effects on nitric oxide (NO) production in the white matter close to the site of constriction injury, thus broadening the scope of the secondary mechanisms that play a role in neuronal trauma.
Animals↗
Regional changes of cyclic 3',5'-guanosine monophosphate in the spinal cord of the rabbit following brief repeated ischemic insults.
The regional distribution of cyclic 3',5'-guanosine monophosphate was studied in the lumbosacral segments of the spinal cord of the rabbit under physiological conditions and following brief repeated sublethal ischemic insults. While the basal cGMP level in the gray matter was about 0.120 nmol cGMP/mg wet. wt., the level of cGMP in non-compartmentalized white matter was about half of this value. The highest level of cGMP in the compartmentalized gray matter was found in the dorsal horns, about 0.180 nmol cGMP/mg wet. wt., whereas the level of cGMP was greatly reduced in the ventral horns, reaching one half of the previous value. Multiple sublethal ischemic insults, repeated at 1-h intervals, caused a statistically significant decrease of cGMP in all gray matter regions. While the post-ischemic and post-reperfusion level of cGMP in the dorsal horns remained relatively high in comparison with the intermediate zone and ventral horns, the changes of cGMP level detected in the white matter columns differed considerably and resulted in a statistically significant cGMP increase in the dorsal and ventral columns and, vice versa, a statistically significant decrease of cGMP was found in the lateral columns.
Animals↗