Taurine is one of the most abundant free
amino acids in the mammalian central nervous system, where it is crucial to proper development. Moreover,
taurine acts as a
neuroprotectant in various diseases; in
epilepsy, for example, it has the capacity to reduce or abolish
seizures. In the present study,
taurine levels has been determine in mice treated with
Kainic Acid (KA) and results showed an increase of this
amino acid in hippocampus but not in whole brain after 3 and 7 days of KA treatment. This increase occurs when
gliosis was observed. Moreover,
taurine transporter (TAUT) was found in astrocytes 3 and 7 days after KA treatment, together with an increase in
cysteine sulfinic acid decarboxylase (csd)
mRNA, that codifies for the rate-limiting
enzyme of
taurine synthesis, in the hippocampus at the same times after KA treatment. Glial cultures enriched in astrocytes were developed to demonstrate that these cells are responsible for changes in
taurine levels after an injury to the brain. The cultures were treated with proinflammatory
cytokines to reproduce
gliosis. In this experimental model, an increase in the immunoreactivity of GFAP was observed, together with an increase in CSD and
taurine levels. Moreover, an alteration in the
taurine uptake-release kinetics was detected in glial cells treated with
cytokine. All data obtained indicate that astrocytes could play a key role in
taurine level changes induced by neuronal damage. More studies are, therefore, needed to clarify the role
taurine has in relation to neuronal death and repair.