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3 Role of neurones and astrocytes in monoamine homeostasis
Author(s) -
Hösli E.,
Hösli L.
Publication year - 1996
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(96)80198-5
Subject(s) - citation , monoamine neurotransmitter , library science , neuroscience , psychology , computer science , biology , genetics , receptor , serotonin
Inflammatory disorders including multiple sclerosis and traumatic disorders such as spinal cord injury are characterized by demyelination which impairs axonal conduction. Several aspects of our gtial cell research program may be relevant to restoration of conduction in demyeliited axons: A) The intemodal axon membrane, under the myelin contains a low Na+ channel density. Restoration of conduction after demyelination requires a higher-than-normal Na+ channel density in the axon membrane. It has been speculated that astmcytes may syntbesize Na+ channels which are transferred to axons. Recent results will be reviewed showing thal: i) astrocytes express rat brain Na+ channel ml7NA.s; ii) these mRNAs are effectively translated. producing channel protein; iii) functional Na+ channels are deployed in astrocytes in vilro and in situ; iv) some astrocytic Na+ channels have a neuronal physiological signature B) Transplanted glial cells can form anatomically compact myelin within demyelinated axons, but tbe physiological properties of the remyelinated axons have not been examined. Our recent results show that, as a result of remyeliition by exogenous, transplanted glial cells, conduction velocities. refractory period, and high-frequency following capability return to nearly normal levels. Glii cell transplantation may thus represent a reasonable strategy in the search for therapies Ural will restore function to patients with detnyelinating disorders. L. Hertz Dept. Pharmacol., Univ. Saskatchewan, Canada