Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Doses of the 5-hydroxytryptamine precursor, 5-hydroxytryptophan, which markedly increased lumbar monosynaptic response (MSR) amplitude in control rats failed to do so in rats paralyzed with experimental allergic encephalomyelitis (EAE). However, lumbar MSR amplitude could be increased in EAE rats just as in control rats by tetanically stimulating the dorsal root. Post-tetanic potentiation of MSR amplitude occurred in the EAE paralyzed rats both prior to and following 5-hydroxytryptophan injection. It was concluded that, as has been reported for the peripheral system in EAE guinea pigs, central nervous system 5-hydroxytryptamine neurotransmission is impaired, at least in the lumbar spinal cord, in EAE rats with hindlimb paralysis.
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PMID:Failure of 5-hydroxytryptophan to increase lumbar MSR amplitude in rats paralyzed with experimental allergic encephalomyelitis. 31 56

Serotonin (5-HT) and the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA) were collected by in vivo dialysis in the lumbar spinal cord of control rats and rats with hindlimb paralysis induced by experimental allergic encephalomyelitis (EAE). Both 5-HT and 5-HIAA were significantly decreased in baseline samples from EAE rats compared to controls. This decrease in extracellular 5-HT and 5-HIAA in the EAE rats was accompanied by marked morphological changes in spinal cord axons and axon terminal plexuses that were stained for 5-HT-like immunoreactivity. The 5-HT precursor, 5-hydroxytryptophan (5-HTP)-increased 5-HT and 5-HIAA levels in dialysate samples from both control and EAE animals. However, the 5-HTP-induced increase in extracellular 5-HT was significantly greater in the EAE rats than in the controls, despite a lower baseline 5-HT level in the EAE animals. In contrast to 5-HT, both baseline and post-5-HTP levels of 5-HIAA were significantly higher in control animals than in EAE animals. The decreased extracellular 5-HT and 5-HIAA in baseline samples from the EAE rats compared to controls is probably a consequence of the damage to descending 5-HT axons and axon terminals that occurs during the disease. The larger increase in extracellular 5-HT in EAE animals after precursor injection may reflect both decreased 5-HT reuptake from the extracellular space by damaged 5-HT terminals and disruption of the blood-brain barrier that allows entry into the central nervous system of 5-HT that was synthesized from 5-HTP in the periphery.
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PMID:Effects of 5-hydroxytryptophan on extracellular serotonin in the spinal cord of rats with experimental allergic encephalomyelitis. 172 45

Pixuna, a strain of intermediate virulence of venezuelan equine encephalomyelitis virus, was inoculated intracranially to 24-day-old mice. Signs of encephalitis were present in 60% of the animals between 6 and 9 days with a maximum at 7 days postinoculation. The rest of the infected mice did not show clinical signs of encephalitis. In order to study the functional state of serotonergic systems a series of tests susceptible to modifications by serotonin activity were carried out. Locomotor activity was measured in an open field test. Virus-inoculated animals presented a variety of changes in their locomotor behavior at various days postinoculation with respect to the sham-inoculated group, however, they were not significant. Central serotonergic function was examined by the production of the serotonergic syndrome with the receptor agonist, 5-methoxy-N,N-dimethyltryptamine and the precursor, 5-hydroxytryptophan, both administered 4 days after the inoculation. The dose of the agonists was established by a prior drug-response analysis. Intensity of the syndrome was significantly higher in infected mice than in the sham-inoculated group only in 5-methoxy-N,N-dimethyltryptamine-treated animals. The behaviour in the swim test was also measured. Duration of immobility was much shorter in infected than in control mice. The decrease in central serotonin turnover previously reported might be responsible for the modification in locomotor behaviour and for the supersensitivity of serotonin receptors observed in infected mice.
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PMID:Behavioural effects produced in mice infected with venezuelan equine encephalomyelitis virus. 317 41