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strychnine/atrofia
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 39 tuloksia
Topical application of colchicine, vinblastine and vincristine prevents strychnine-enhanced transsynaptic degeneration in the medullary dorsal horn following transection of the inferior alveolar nerve in adult rats.
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The effect of topical application of axonal transport blockers to the transected peripheral nerve was assessed by quantitating the strychnine-enhanced transsynaptic degeneration following transection of the inferior alveolar nerve in adult rats. Systemic administration of strychnine (1 mg/kg/day)
Strychnine-enhanced transsynaptic degeneration of dorsal horn neurons in rats with an experimental painful peripheral neuropathy.
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A painful peripheral neuropathy was produced by loosely tying constrictive ligatures around the sciatic nerve of rats. Eight days after the nerve injury and after a series of injections a subconvulsive dose of strychnine, the animals were sacrificed and the spinal cord dorsal horn was examined for
Strychnine and L-allylglycine but not bicuculline and picrotoxin induce transsynaptic degeneration following transection of the inferior alveolar nerve in adult rats.
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The effects of the convulsants strychnine, bicuculline, picrotoxin and L-allylglycine on the transsynaptic destruction of medullary dorsal horn neurons were examined following transection of the inferior alveolar nerve in adult rats. Strychnine and L-allylglycine enhanced the transsynaptic effect of
Transsynaptic degeneration in the superficial dorsal horn after sciatic nerve injury: effects of a chronic constriction injury, transection, and strychnine.
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The lumbar and cervical spinal dorsal horns of adult rats with a chronic (8 days) constriction injury of the sciatic nerve on one side (and a sham operation on the other) were examined for signs of transsynaptic degeneration. The incidence of neurons with signs of degeneration (pyknosis and
Strychnine-enhanced neuronal degeneration in the brain stem following transection of the inferior alveolar nerve: selective labeling of brain stem neurons receiving synaptic input from injured inferior alveolar nerve in the rat.
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Subconvulsive dose of strychnine enhances the transneuronal effect of peripheral sensory nerve transection.
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The effect of transection of the inferior alveolar nerve on the trigeminal subnucleus caudalis neuron was examined under the influence of systemic strychnine in the rat. Chronic intoxication with a subconvulsive dose of strychnine induced electron dense degeneration of somata and dendrites at 30
Receptor alterations associated with spinal motoneuron degeneration in bovine Akabane disease.
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Akabane disease in cattle is characterized by congenital abnormalities including arthrogryposis, which is characterized by a depletion of spinal ventral horn motoneurons, a loss of axons, and depletion of myelin in the lateral and ventral tracts. These neuropathological changes produced major
Neuroprotective effects of the strychnine-insensitive glycine site NMDA antagonist (R)-HA-966 in an experimental model of Parkinson's disease.
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The neuroprotective effects of (R)-HA-966 and (S)-HA-966 (3-amino-1-hydroxy-2-pyrrolidinone) were examined in an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-induced animal model of Parkinson's disease. Systemic pretreatment of C57 black mice with the strychnine-insensitive glycine site
Manganese poisoning reduces strychnine-insensitive glycine binding sites in the globus pallidus of the mouse brain.
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Manganese (Mn) poisoning is characterized by central nervous system manifestations, including psychiatric disturbances and extrapyramidal disorders. This metal is thought to produce neuronal degeneration due to cytotoxic products originated by oxidative stress and through an indirect excitotoxic
Strychnine therapy in nonketotic hyperglycinemia.
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Nonketotic hyperglycinemia is an inborn error of metabolism resulting from a defect in the glycine cleavage enzyme system. It is characterized biochemically by elevated concentrations of glycine in blood, spinal fluid, and urine. Previous therapies which have been directed toward reducing the
A study of Semen Strychni-induced renal injury and herb-herb interaction of Radix Glycyrrhizae extract and/or Rhizoma Ligustici extract on the comparative toxicokinetics of strychnine and brucine in rats.
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Recently, the renal injury caused by Semen strychni and its major toxic constituents, strychnine and brucine, was reported in many clinical cases. Hence, this study was conducted to investigate the renal injury induced by Semen Strychni and the protective effects of Radix Glycyrrhizae and Rhizoma
The developmental neurotoxicity of fipronil: notochord degeneration and locomotor defects in zebrafish embryos and larvae.
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Fipronil is a phenylpyrazole insecticide designed to selectively inhibit insect gamma-aminobutyric acid (GABA) receptors. Although fipronil is often used in or near aquatic environments, few studies have assessed the effects of this neurotoxicant on aquatic vertebrates at sensitive life stages. We
Deterioration of spinal reflex in quails orally ingesting clioquinol.
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Ataxia occurred in quails on long-term oral ingestion of clioquinol (CQ). Crossed extensor reflexes and spinal reflex potentials in the normal and the treated quails were recorded. The incidence of these reflexes was reduced in quails given CQ. As long as the spinal reflexes were detected, there
[Effect of stimulation of the facial nucleus on discharge of respiratory neurons in the pre-Bözinger complex and its neurotransmitter mechanism in rats].
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The experiments were carried out on adult Sprague-Dawley rats. We investigated the discharge response of respiratory neurons (RNs) in the pre-Bözinger complex (PBC) to electrical stimulation of the facial nucleus in which the motor neurons were retrogradely degenerated and the antagonistic effects
Deafferentation weakens excitatory synapses in the developing central auditory system.
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Decreased excitatory synaptic activity during development often leads to pre- and postsynaptic atrophy, as assessed anatomically. The present study considers the effect of decreased excitatory transmission on the maturation of synaptic strength. Towards this end, cochlear nucleus neurons, which
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