Recent evidence indicates that, besides demyelination, axonal and neuronal degeneration also occurs in both multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model for MS. The mechanisms underlying neuronal dysfunction in MS and EAE remain elusive. To address this issue, we have analyzed the neurotransmitter release from cerebrocortical synaptosomes from EAE and control animals. The effect on evoked release of glutamate stimulated by KCl or ionomycin was monitored using an enzyme-linked fluorometric assay. The results showed a diminished ionomycin-triggered glutamate release from EAE synaptosomes compared with both that from control synaptosomes and the K+-evoked glutamate release from the same EAE synaptosomes. This inhibited synaptosomal activity was restored by increasing extracellular Ca+2 levels. The observed alteration in neurotransmitter release could be due to a possible variation of the synaptosome membranes isolated from animals with EAE, which as well could affect the normal operation of the cerebrocortical nerve terminals.
Recent evidence indicates that, besides demyelination, axonal and neuronal degeneration also occurs in both multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model for MS. The mechanisms underlying neuronal dysfunction in MS and EAE remain elusive. To address this issue, we have analyzed the neurotransmitter release from cerebrocortical synaptosomes from EAE and control animals. The effect on evoked release of glutamate stimulated by KCl or ionomycin was monitored using an enzyme-linked fluorometric assay. The results showed a diminished ionomycin-triggered glutamate release from EAE synaptosomes compared with both that from control synaptosomes and the K+-evoked glutamate release from the same EAE synaptosomes. This inhibited synaptosomal activity was restored by increasing extracellular Ca+2 levels. The observed alteration in neurotransmitter release could be due to a possible variation of the synaptosome membranes isolated from animals with EAE, which as well could affect the normal operation of the cerebrocortical nerve terminals.
