Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An in vitro mammalian model neuronal system to evaluate the intrinsic toxicity of soman and other neurotoxicants as well as the efficacy of potential countermeasures was investigated. The link between soman toxicity, glutamate hyperactivity and neuronal death in the central nervous system was investigated in primary dissociated cell cultures from rat hippocampus and cerebral neocortex. Exposure of cortical or hippocampal neurons to glutamate for 30 min produced neuronal death in almost 80% of the cells examined at 24 h. Hippocampal neurons exposed to soman for 15-120 min at 0.1 microM concentration caused almost complete inhibition (> or = 90%) of acetylcholinesterase but failed to show any evidence of effects on cell viability, indicating a lack of direct cytotoxicity by this agent. Acetylcholine (ACh, 0.1 mM), alone or in combination with soman, did not potentiate glutamate toxicity in hippocampal neurons. Memantine, a drug used for the therapy of Parkinson's disease, spasticity and other brain disorders, significantly protected hippocampal and cortical neurons in culture against glutamate and N-methyl-D-aspartate (NMDA) excitotoxicity. In rats a single dose of memantine (18 mg/kg) administered 1 h prior to a s.c. injection of a 0.9 LD50 dose of soman reduced the severity of convulsions and increased survival. Survival, however, was accompanied by neuronal loss in the frontal cortex, piriform cortex and hippocampus.
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PMID:Assessment of primary neuronal culture as a model for soman-induced neurotoxicity and effectiveness of memantine as a neuroprotective drug. 749 76

Spasticity is a disorder of hypertonus associated with neurological diseases, characterized by a decrease in stretch reflex threshold. Stretch reflex threshold of wrist flexors has been recorded in subjects affected by forearm spasticity due to acute neurological lesions, occurred from one to sixty-one months before. In all the subjects a decreased stretch reflex threshold was recorded and a negative correlation between stretch reflex threshold and time of the disease resulted. In five subjects affected by mild spasticity the velocity stretch reflex threshold was tested one-three months after stroke and then six months later. In three cases a further decrease in stretch reflex threshold was recorded. Sixteen subjects affected by heavy forearm spasticity (quantified by Ashworth scale), were treated with Botulinum toxin injections to reduce spasticity. Fourteen of 16 subjects were responsive to the antispastic therapy: a decrease of at least 1 point in the Ashworth scale was detected after the treatment. In all the responsive cases an increase of stretch reflex threshold was recorded. The results confirm that the stretch reflex threshold is decreased in spastic muscles; it decreases progressively in time after the acute lesion. In addition, these results demonstrate that the decreased stretch reflex threshold can be reversed with Botulinum toxin injections. It is known that Botulinum toxin reduce the presynaptic release of Acetylcholine of neuromuscular synapses, but there are experimental evidences that it acts even on spindle's fibres, decreasing the sensitivity of intrafusal muscle fibres. This effect explains how Botulinum toxin increases the stretch reflex threshold in spastic muscles.
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PMID:Change of stretch reflex threshold in spasticity: effect of botulinum toxin injections. 1526 Mar 80

Botulinum toxin is one of the most toxic natural substances; it acts by blocking the neuromuscular transmission by inhibiting Acetylcholine (Ach) releasing from the motor nerve into the neuromuscular junction. Although the toxin inhibits ACh release, other transmitters can also be inhibited. Botulinum toxin, specifically toxin type A (BONT-A) has been used since the 1970s to treat many different disorders, such as general spasticity resulting from stroke, multiple sclerosis or cerebral palsy, strabismus, hyperhidrosis or excessive sweating, pain, and it is effective in combating migraine and tension headaches. Since prostate gland is under the influence of autonomic innervation and associated neurotransmitters, the effects of BONT-A on the prostate have gained attention in the urological community and it has been studied in different species, including rats, dogs and humans. The aim of this paper is to review the mechanism of action of botulinum toxin and to discuss in particular the results of BONT-A treatment for benign prostatic hyperplasia (BPH), providing perspectives on potential therapy according to actual knowledge.
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PMID:Botulinum toxin A in prostate disease: a venom from bench to bed-side. 2240 79