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PubMed1985

[An autopsy case of hereditary ataxia (hereditary spastic ataxia)].

An autopsy case of hereditary spastic ataxia is reported. There are four family members with similar symptomatology through three generations. A 36-year-old man developed atactic gait at the age of 22 years, with following dysarthria, scanning speech, pyramidal signs, dysmetria, dysdiadochokinesia, nystagmus and mild sensory disturbance. The clinical course was steadily progressive and terminated about 14 years after the onset. The gross examination showed smallness of the brain stem and spinal cord with marked symmetrical atrophy of the anterior and lateral columns, especially at thoracic level. Histologically, pronounced degeneration was found in the anterior and posterior spino-cerebellar tracts, spino-thalamic tracts, and spinal ganglia. The olivary nuclei, pons and cerebellum were spared. The dentate nuclei showed considerable loss of neurons with degeneration, however there were no clinical signs related to this pathology. This case is considered to fall in the group of hereditary spastic ataxia according to Greenfield's classification, however, there was no report on degeneration of the dentate nucleus in this disease for the present. Hereditary spastic ataxia is very rare disease and only four cases have well been documented in our country to the best of our knowledge. The presence of nystagmus and superficial sensory disturbance, and sparing of the posterior column of the spinal cord seems to be common clinico-pathology in Japanese cases, differing from those of foreign cases. The fact that reactive astrogliosis was immunohistochemistry demonstrated in the degenerative regions of the spinal cord and where is no discrepancy between degenerative and reparative processes as reported before is stressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

A familial peripheral neuropathy and glomerulopathy in Gelbvieh calves.

Nine Gelbvieh calves originating in four herds and clinically presenting with rear limb ataxia/paresis had histopathologically confirmed peripheral neuropathy and a proliferative glomerulopathy. Degenerative lesions were severe in peripheral nerves, dorsal and ventral spinal nerve roots, and less marked in dorsal fasciculi of the spinal cord. Cell bodies of spinal ganglia were minimally diseased; ventral horn neurons occasionally had central chromatolysis and nuclear displacement. Glomerular lesions ranged from mild mesangial hypercellularity to glomerulosclerosis. Pedigree analysis of affected animals from one herd indicated a strong familial relationship and probable hereditary basis for the syndrome.

Animals↗
PubMed1986

Differences in horseradish peroxidase labeling of sensory, motor and sympathetic neurons following chronic axotomy of the rat sural nerve.

In an attempt to clarify the ultimate fate of permanently axotomized adult primary neurons, horseradish peroxidase (HRP) was used as a cell marker to label the motor, sensory and postganglionic sympathetic neurons of rat sural nerves which had been sectioned at the ankle and prevented from regenerating for periods of up to 80 weeks. Axotomy did not affect sympathetic neurons, but resulted 4 weeks later in a sudden reduction in the number of labeled sensory and motor cells which persisted to the end of the study. The missing neuronal population amounted to 44.4% and 45.9% respectively of the normal sensory and motor contingent and included most of the large afferent and efferent neurons. However, examination of sural nerves at the thigh, 30 mm proximal to the neuroma, revealed marked axonal atrophy but no change in the number of myelinated and unmyelinated fibers up to 52 weeks after axotomy. Such prolonged survival of the peripheral processes is indirect evidence that axotomized neurons can endure long-term detachment from their end organs and suggests that the lack of HRP labeling in certain sensory and motor neurons does not imply their degeneration, but expresses one of many retrograde dysfunctions triggered by axotomy.

Animals↗
PubMed2006

Immunohistochemical localization of cannabinoid type 1 and vanilloid transient receptor potential vanilloid type 1 receptors in the mouse brain.

Cannabinoid type 1 receptors and transient receptor potential vanilloid type 1 channels have been proposed to act as metabotropic and ionotropic receptors, respectively, for two classes of endogenous polyunsaturated fatty acid amides, the acylethanolamides and the acyldopamides. Furthermore, we and others have shown that functional crosstalk occurs between these two receptors when they are expressed in the same cell. Although demonstrated in sensory neurons of the dorsal root ganglia, spinal cord and myenteric neurons, co-expression of cannabinoid type 1 and transient receptor potential vanilloid type 1 has not yet been studied in the brain. In the present study, we addressed this issue by using commercially available specific antibodies whose specificity was confirmed by data obtained with brains from cannabinoid type 1(-/-) and transient receptor potential vanilloid type 1(-/-) mice. Double cannabinoid type 1/transient receptor potential vanilloid type 1 immunofluorescence and single cannabinoid type 1 or transient receptor potential vanilloid type 1 avidin-biotin complex immunohistochemistry techniques were performed and both methods used point to the same results. Cannabinoid type 1/transient receptor potential vanilloid type 1 expression was observed in the hippocampus, basal ganglia, thalamus, hypothalamus, cerebral peduncle, pontine nuclei, periaqueductal gray matter, cerebellar cortex and dentate cerebellar nucleus. In particular, in the hippocampus, cannabinoid type 1/transient receptor potential vanilloid type 1 expression was detected on cell bodies of many pyramidal neurons throughout the CA1-CA3 subfields and in the molecular layer of dentate gyrus. In the cerebellar cortex, expression of cannabinoid type 1/transient receptor potential vanilloid type 1 receptors was found surrounding soma and axons of the vast majority of Purkinje cell bodies, whose cytoplasm was found unstained for both receptors. Cannabinoid type 1 and transient receptor potential vanilloid type 1 immunoreactivity was also detected in: a) the globus pallidus and substantia nigra, in which some intensely transient receptor potential vanilloid type 1 immunopositive cell bodies were found in dense and fine cannabinoid type 1/transient receptor potential vanilloid type 1 positive and cannabinoid type 1 positive nerve fiber meshworks, respectively; b) the cytoplasm of thalamic and hypothalamic neurons; and c) some neurons of the ventral periaqueductal gray. These data support the hypothesis of a functional relationship between the two receptor types in the CNS.

Animals↗
PubMed1998

Kinesin accumulation in chick spinal axonal swellings with beta,beta'-iminodipropionitrile (IDPN) intoxication.

Kinesin is a major molecular motor responsible for anterograde axonal transport. Chicks were injected with beta,beta'-iminodipropionitrile (IDPN) to induce axonal swellings in spinal motor neurons and spinal sensory ganglion neurons. Cylindrical swollen axons were found in the anterior horn and anterior funiculus of the spinal cord, anterior root, and spinal ganglia. All of the axonal swellings were heavily stained with two anti-kinesin monoclonal antibodies. The swellings were mildly stained with an anti-cytoplasmic dynein and anti-tubulin antibodies, and weakly stained with an anti-tau antibody. These suggest the isolated disturbance of kinesin transport with neurofilament accumulation in IDPN intoxication.

Animals↗
PubMed1981

[Preparation of the spinal neurons and their bushy receptors for morphophysiological study].

A preparation of the sensory neuron of the spinal ganglion with dendritic processes for simultaneous morphological and physiological investigations is described. It consists of a frog urinary bladder with bushy interoceptors in its wall, two vesicle neurons, two abdominal branches of the X spinal nerves and two IX spinal ganglia with ventral and dorsal roots branching off from them. The total length from the receptors to the ganglion neurons is 20-30 mm. In the ganglia a zone of the neuronal bodies localization is found, their processes form receptors; the zone includes as many as 9 neurons, 50-80 mkm in size. A vital fine structure of the ganglion cells and their satellites is traced. There are three types of cells in the ganglion--large, middle and small. Electrophysiological control has demonstrated that the preparation is viable for several hours.

Animals↗
PubMed1999

Antihyperalgesic effects of infection with a preproenkephalin-encoding herpes virus.

To test the utility of gene therapeutic approaches for the treatment of pain, a recombinant herpes simplex virus, type 1, has been engineered to contain the cDNA for an opioid peptide precursor, human preproenkephalin, under control of the human cytomegalovirus promoter. This virus and a similar recombinant containing the Escherichia coli lacZ gene were applied to the abraded skin of the dorsal hindpaw of mice. After infection, the presence of beta-galactosidase in neuronal cell bodies of the relevant spinal ganglia (lacZ-containing virus) and of human proenkephalin (preproenkephalin-encoding virus) in the central terminals of these neurons indicated appropriate gene delivery and expression. Baseline foot withdrawal responses to noxious radiant heat mediated by Adelta and C fibers were similar in animals infected with proenkephalin-encoding and beta-galactosidase-encoding viruses. Sensitization of the foot withdrawal response after application of capsaicin (C fibers) or dimethyl sulfoxide (Adelta fibers) observed in control animals was reduced or eliminated in animals infected with the proenkephalin-encoding virus for at least 7 weeks postinfection. Hence, preproenkephalin cDNA delivery selectively blocked hyperalgesia without disrupting baseline sensory neurotransmission. This blockade of sensitization was reversed by administration of the opioid antagonist naloxone, apparently acting in the spinal cord. The results demonstrate that the function of sensory neurons can be selectively altered by viral delivery of a transgene. Because hyperalgesic mechanisms may be important in establishing and maintaining neuropathic and other chronic pain states, this approach may be useful for treatment of chronic pain and hyperalgesia in humans.

Animals↗
PubMed1993

Pituitary adenylate cyclase activating peptide produces a marked and long-lasting depression of a C-fibre-evoked flexion reflex.

Pituitary adenylate cyclase activating peptide (PACAP) is a novel vasoactive intestinal peptide-like peptide. It has a neuronal localization and occurs in two forms, PACAP-38 and the C-terminally truncated PACAP-27. In a recent report we described a dense accumulation of PACAP-27-immunoreactive nerve fibres in the superficial layer of the dorsal horn in the spinal cord and a few PACAP-27-immunoreactive nerve cell bodies in the spinal ganglia in the rat. Double-immunostaining showed that immunoreactive PACAP-27 occurred in a subpopulation of the calcitonin gene related peptide/substance P-containing cell bodies and fibres. In this study, PACAP-27 (0.47-0.63 pmol) given intrathecally produced a significant and long-lasting suppression of C-fibre-evoked flexion reflex produced by the electrical stimulation of the plantar nerve and recorded as a reflex discharge in the peroneal nerve. With a higher dose, 1.25 pmol, the magnitude of the response was not increased further but the effect became longer-lasting. PACAP-38 and vasoactive intestinal peptide were tested in doses up to 5 pmol and produced a significant and, in the case of PACAP-38, long-lasting suppression of the spinal flexion reflex. PACAP-27 seemed to be much more potent than PACAP-38 and vasoactive intestinal peptide. Intrathecal PACAP-27 was without effect on the monosynaptic stretch reflex (evoked by electrical stimulation of the gastrocnemius nerve and recorded as a reflex discharge in the sciatic nerve), suggesting that its effect on the flexion reflex is specific.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Altering the expression kinetics of VP5 results in altered virulence and pathogenesis of herpes simplex virus type 1 in mice.

While many herpes simplex virus (HSV) structural proteins are expressed with strict-late kinetics, the HSV virion protein 5 (VP5) is expressed as a "leaky-late" protein, such that appreciable amounts of VP5 are made prior to DNA replication. Our goal has been to determine if leaky-late expression of VP5 is a requirement for a normal HSV infection. It had been shown previously that recombinant viruses in which the VP5 promoter was replaced with promoters of other kinetic classes (including a strict late promoter) exhibited no alterations in replication kinetics or virus yields in vitro. In contrast, here we report that alterations in pathogenesis were observed when these recombinants were analyzed by experimental infection of mice. Following intracranial inoculation, a recombinant expressing VP5 from a strict-late promoter (U(L)38) exhibited an increased 50% lethal dose and a 10-fold decrease in virus yields in the central nervous system, while a recombinant expressing VP5 from an early (dUTPase) or another leaky-late (VP16) promoter exhibited wild-type neurovirulence. Moreover, following infection of the footpad, changing the expression kinetics of VP5 from leaky-late to strict-late resulted in 100-fold-less virus in the spinal ganglia during the acute infection than produced by either the parent virus or the rescued virus. These data indicate that the precise timing of appearance of the major capsid protein plays a role in the pathogenesis of HSV infections and that changing the expression kinetics has different effects in different cell types and tissues.

Animals↗
PubMed2001

Embryonic hydromyelia: cystic dilatation of the lumbosacral neural tube in human embryos.

In a large collection of human embryos (the Kyoto Collection of Human Embryos, Kyoto University), we encountered five cases with abnormal dilatation of the neural tube at the lumbosacral level. In these examples, the central canal was enlarged, and the roof plate of the neural tube was extremely thin and expanded. The mesenchymal tissue was scarce or lacking between the roof plate and the surface ectoderm. This type of anomaly was assumed to be formed after neural tube closure and may be an early form of spina bifida. In two of the cases, some abnormal cells were found ectopically between the thin roof plate and the surface ectoderm. Morphologically, these cells resembled those forming spinal ganglia and could be of the neural crest origin. Since neural crest cells are pluripotent and can differentiate into a variety of tissues, such ectopic cells might undergo abnormal differentiation into teratomatous tumors and/or lipomas, which are frequently associated with spina bifida. We also discuss the definition of spina bifida and the classification of neural tube defects from the embryological and pathogenic viewpoints and propose a new classification of neural tube defects.

Dilatation, Pathologic↗
PubMed1989

Experimental exencephaly and myeloschisis in rats.

To elucidate the early sequential morphogenetic progress of exencephaly and myeloschisis, rat embryos whose mothers had been treated with hypervitaminosis A were studied at 1-day interval from gestation day 10.5 to 15.5. In exposed animals sequential change was found in both exencephaly and myeloschisis as the embryos grew up. The 10.5-day old exencephalic embryos had still widely open cephalic neural tubes. Exencephalic embryos older than 13.5 days of gestation showed strikingly severe eversion and overgrowth of the cephalic neuroepithelium, thus failed in forming normal primitive brain. The convex dorsal surface of the exencephaly was covered with ependyma, which was connected directly with surrounding surface eqithelium at the periphery. The earliest morphologically recognized myeloschisis was in the 13.5-day old embryos. In myeloschisis, divergence at the roof plate and eversion of the spinal neural tube, disorganized overgrowth of the neuroepithelium, malformed and misplaced spinal ganglia and nerve roots, and absence of the neural arch and dermal covering were characteristic. It is suggested that exencephaly results from failure of the cephalic neural tube closure which is followed by eversion and overgrowth of the neuroepithelium. And failure in closure of the posterior neuropore and disturbance in the development of the tail bud probably play major role in the morphogenesis of myeloschisis.

Animals↗
PubMed1980

Light, fluorescence, and electron microscopic features of neuronal intranuclear hyaline inclusions associated with multisystem atrophy.

Light, fluorescence, and electron microscopic features of intranuclear hyaline inclusions of neurons associated with multisystem atrophy in a 21-year-old woman are described. The neuronal inclusions resemble Marinesco bodies on light microscopy but differ from the latter in their distribution, autofluorescence, and ultrastructure. They are widespread in almost all central, peripheral, and autonomic neurons and are generally larger than Marinesco bodies. The inclusions emit yellow-green autofluorescence with ultraviolet light between 470 and 530 nm of the spectrum and are ultrastructurally composed of haphazardly arranged, uniform, fine, straight filaments (8-9 nm in diameter). The neuronal inclusions have neither the ultrastructural feature of known viral inclusions nor are associated with virus particles. Their chemical nature and pathogenesis remain to be elucidated.

Adult↗
PubMed1993

Vital dye labelling of Xenopus laevis trunk neural crest reveals multipotency and novel pathways of migration.

Although the Xenopus embryo has served as an important model system for both molecular and cellular studies of vertebrate development, comparatively little is known about its neural crest. Here, we take advantage of the ease of manipulation and relative transparency of Xenopus laevis embryos to follow neural crest cell migration and differentiation in living embryos. We use two techniques to study the lineage and migratory patterns of frog neural crest cells: (1) injections of DiI or lysinated rhodamine dextran (LRD) into small populations of neural crest cells to follow movement and (2) injections of LRD into single cells to follow cell lineage. By using non-invasive approaches that allow observations in living embryos and control of the time and position of labelling, we have been able to expand upon the results of previous grafting experiments. Migration and differentiation of the labelled cells were observed over time in individual living embryos, and later in sections to determine precise position and morphology. Derivatives populated by the neural crest are the fins, pigment stripes, spinal ganglia, adrenal medulla, pronephric duct, enteric nuclei and the posterior portion of the dorsal aorta. In the rostral to mid-trunk levels, most neural crest cells migrate along two paths: a dorsal pathway into the fin, followed by presumptive fin cells, and a ventral pathway along the neural tube and notochord, followed by presumptive pigment, sensory ganglion, sympathetic ganglion and adrenal medullary cells. In the caudal trunk, two additional paths were noted. One group of cells moves circumferentially within the fin, in an arc from dorsal to ventral; another progresses ventrally to the anus and subsequently populates the ventral fin. By labelling individual precursor cells, we find that neural tube and neural crest cells often share a common precursor. The majority of clones contain labelled progeny cells in the dorsal fin. The remainder have progeny in multiple derivatives including spinal ganglion cells, pigment cells, enteric cells, fin cells and/or neural tube cells in all combinations, suggesting that many premigratory Xenopus neural crest precursors are multipotent.

Affinity Labels↗
PubMed1989

The role of herpes simplex virus type 1 thymidine kinase in pathogenesis.

A genetically engineered herpes simplex virus type 1 (HSV-1)thymidine kinase (TK) deletion mutant has been constructed and used to investigate the role of this gene in pathogenesis. Inoculation of mice with the HSV TK deletion mutant resulted in the establishment of latent ganglionic infection as demonstrated by superinfection of explanted ganglia with wild-type (wt) virus but not by routine explant culture suggesting that the virus-encoded TK is not essential for the establishment of latent infection but may be necessary for either reactivation or virus replication following reactivation. In addition, Southern blot hybridization has been used to demonstrate in vivo complementation of this mutant by wt virus in both peripheral and central nervous system tissues of mice during acute infection and to show that such complementation can result in the establishment and reactivation of latent TK- infection.

Acute Disease↗
PubMed1983

Peptidergic and muscarinic excitation at amphibian sympathetic synapses.

A single-electrode voltage clamp was used to study the slow muscarinic and late slow peptidergic excitatory post-synaptic currents (e.p.s.c.s) in B cells of the paravertebral sympathetic ganglia of the bull-frog. Conductance decreases were measured during peptidergic e.p.s.c.s in nearly all cells at clamped potentials near the resting level. In about half of the cells the size of the peptidergic e.p.s.c.s increased with hyperpolarization and in some of these cells conductance increases were found at hyperpolarized levels. In the remaining cells conductance decreases occurred at all levels of membrane potential tested, and in a few of these the polarity of the e.p.s.c.s reversed at hyperpolarized potentials. A similar diversity was observed among muscarinic e.p.s.c.s. At least two simple ionic mechanisms are required to explain the heterogeneous voltage dependencies observed: a conductance decrease primarily to K+ that dominates at depolarized potentials and a conductance increase to other ions that is more prominent at hyperpolarized potentials. The proportion of these two mechanisms appears to differ among B cells. The two slow e.p.s.c.s recorded in the same neurone had the same voltage dependence and were accompanied by the same conductance changes in each of eight cells despite differences between cells. The muscarinic e.p.s.c. was reduced during the peptidergic e.p.s.c. in each of twenty-five neurones tested over a range of membrane potentials. Externally-applied luteinizing hormone releasing hormone (LHRH) produced currents with the same voltage dependence and conductance changes as the nerve-evoked peptidergic e.p.s.c. in each of fifteen cells tested. Bethanechol, a muscarinic agonist, and LHRH produced currents with the same voltage dependence and conductance changes in each of the twelve cells studied. In several cells a saturating response to a prolonged application of LHRH completely occluded the response to bethanechol, and vice versa. Slow currents were recorded from dissociated cell bodies in response to bethanechol and LHRH; these responses exhibited the same diversity of voltage dependence and conductance changes as was observed in intact ganglia. Activation of muscarinic and peptidergic receptors may control shared ionic mechanisms in single ganglion cells.

Animals↗
PubMed1986

Peripheral nerve autografts to the rat spinal cord: study on the origin and course of regenerating fibres.

Autologous sciatic nerve grafts were implanted to the lower thoracic spinal cord (SC) of adult rats. The grafts were longitudinally placed on both sides of the SC midline over the dura mater and their cut ends were inserted into the dorsal white matter of the SC. Eight to 60 weeks later the grafts were exposed. In a first experimental group (A) either horseradish peroxidase (HRP) or lectin conjugated horseradish peroxidase (WGA-HRP) was injected into the grafts in order to investigate the origin and the course of regenerated fibres entering the grafts. In a second experimental group (B) the SC was acutely transected between the upper and lower graft insertions and either HRP or WGA-HRP was injected into the caudal stump of the SC in order to investigate the ability of regenerating axons once entered the grafts to re-enter the SC. In group A retrogradely labelled cells were found in the SC scattered in proximity of both the caudal and rostral graft insertions and in the ventral horns as far as 30 mm rostrally to the grafts. Labelled cells were also located in the spinal ganglia, at the level of the grafts and up to 6 segments caudal to them. In group B retrogradely labelled cells were present in the SC rostrally to the transection, both in proximity of the upper graft insertions and in the ventral horns as far as 30 mm rostrally to the grafts. These findings demonstrate that PN grafts implanted to the SC of adults rats can be innervated by regenerated axons arising from both intraspinal neurons and dorsal root ganglion cells (group A); furthermore axons from intraspinal neurons entered and elongated in the grafts can re-enter the SC (group B).

Animals↗
PubMed1992

Restricted expression of N- and R-cadherin on neurites of the developing chicken CNS.

The expression of two cadherins, N- and R-cadherin, was mapped in the CNS of chicken embryos of 6-11 d incubation, focusing on the sensory and motor fiber systems. In the spinal cord, the laterally located fibers of the dorsal funiculus express N-cadherin while the medially located fibers do not. These two fiber systems have a different course within the CNS but associate to form the spinal dorsal roots. In the hindbrain, N-cadherin is expressed by the descending trigeminal (general somatic sensory) tract, which is contiguous with the N-cadherin-positive zone of the dorsal funiculus of the spinal cord. R-cadherin is not expressed by sensory fibers, but is expressed by the visceral motor system of the vagus and glossopharyngeal nerves, which are N-cadherin negative. The motor neurites expressing R-cadherin have a different course within the brain than the sensory neurites expressing N-cadherin, although they form the common sensory/motor roots of the vagus nerve at the surface of the brain. The possibility that N-cadherin provides a guidance cue for sensory axon migration within the CNS by a homophilic adhesion mechanism was investigated in vitro. Explants from sensory spinal ganglia expressing N-cadherin were placed on N-cadherin-transfected neuroblastoma cells, and axon outgrowth was visualized. Results showed that the sensory axons defasciculate and closely follow the cell-cell boundaries between transfected cells where high levels of N-cadherin are expressed. These results show that the two cadherins, like members of the immunoglobulin superfamily of molecules, are expressed in a topographically restricted fashion during chick brain development. They furthermore suggest that N-cadherin expression by neurites may play a role in guiding these neurites along CNS paths that express the same molecule.

Animals↗