Animal Model of Multiple Sclerosis:

    To help in research of multiple sclerosis (MS) researchers utilize an animal model, experimental allergic encephalitis (EAE). EAE is an acute autoimmune demyelination disease, that matches the symptomatology of MS.  Guinea pigs with EAE are reported to have a reduction of serotonin within the central nervous system (CNS), when compared to control subjects. The reduction of serotonin within the CNS leads to an effect on CNS serotonin transmissions in EAE, either at the level of serotonin receptor itself, or at the level of serotonin transmitting neurons (Scott, Cashman, and Spitler, 1982-83). The symptoms of EAE are due to the inhibition of serotonin transmission.
    In animals with EAE, administration of L-5-hydroxytrytophan, a precursor to serotonin, reversed the effects of impaired serotonergic transmission. Suggesting that there might be a blockade of serotonin receptors (Scott, Cashman, and Spitler, 1982-83), which can be overcome by the addition of a drug that increases the CNS serotonin levels. The addition of a precursor of serotonin has such an effect, and then the addition of antidepressant type drugs may  affect the symptoms of EAE in a positive way.
    When an antidepressant is administered the ultimate goal of the drug is to raise the levels of serotonin in the synapse. The drug can act as a serotonin reuptake blocker increasing the levels of serotonin in the synapse or will increase the serotonergic transmissions. As postulated earlier if the levels of serotonin can be raised then there would be a positive effect on the symptoms of MS and EAE. This suggests that further studies of the EAE model should be completed measuring the effects of antidepressant drugs such as serotonin selective reuptake inhibitors (SSRI's).  Data shows that drugs that increase serotonin in the CNS such as imipramine hydrochloride, tryptophan and carbidopa, prolonged the survival in animals with EAE, whereas reserpine, a drug that diminishes the amount of serotonin in the CNS provided evidence of impairment of serotonergic transmissions.
 
 
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