AI Article Synopsis
- Taurine may act as an inhibitory transmitter in the substantia nigra (SN), but its release and uptake mechanisms are not well understood.
- A study using microdialysis in rats showed that taurine levels increase when cells are depolarized, influenced by glutamate (GLU), its receptors, and zinc.
- Administration of taurine raises levels of gamma-aminobutyric acid (GABA) and GLU, indicating its complex interaction with these neurotransmitters and the role of glial cells in regulating taurine levels in the SN.
Article Abstract
Taurine has been proposed as an inhibitory transmitter in the substantia nigra (SN), but the mechanisms involved in its release and uptake remain practically unexplored. We studied the extracellular pool of taurine in the rat's SN by using microdialysis methods, paying particular attention to the taurine-glutamate (GLU) interaction. Extracellular taurine increased after cell depolarization with high-K(+) in a Ca(2+)-dependent manner, being modified by the local perfusion of GLU, GLU receptor agonists, and zinc. Nigral administration of taurine increased the extracellular concentration of gamma-aminobutyric acid (GABA) and GLU, the transmitters of the two main inputs of the SN. The modification of the glial metabolism with fluocitrate and L-methionine sulfoximine also changed the extracellular concentration of taurine. The complex regulation of the extracellular pool of taurine, its interaction with GABA and GLU, and the involvement of glial cells in its regulation suggest a volume transmission role for taurine in the SN.
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| http://dx.doi.org/10.1002/jnr.20108 | DOI Listing |
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