The release of the inhibitory
amino acid taurine is markedly enhanced under ischemic conditions in both adult and developing brain stem, together with a pronounced increase in the release of the
neuromodulator adenosine. We now studied the effects of
adenosine receptor agonists and antagonists on [(3)H]
taurine release in the brain stem in normoxia and
ischemia, using a superfusion system. Under standard conditions, the
adenosine A(1) receptor agonist
N(6)-cyclohexyladenosine (CHA) potentiated basal
taurine release in adult mice, which response was blocked by the antagonist
8-cyclopentyl-1,3-dipropylxanthine (
DPCPX). CHA and the A(2a) receptor agonist 2-p-(2-carboxyethyl)phenylamino-5'-N-ethylcarboxaminoadenosinehydrochloride (
CGS 21680) had no effect on the release in developing mice. In
ischemia, CHA depressed both basal and K(+)-stimulated
taurine release in developing mice in a receptor-mediated manner, blocked by
DPCPX. The A(2a) receptor agonist
CGS 21680 was also inhibitory.
Taurine and
adenosine may thus not cooperate in developing mice to prevent ischemic neuronal damage. On the other hand,
CGS 21680 enhanced
taurine release in the adult brain stem in
ischemia, both basal and K(+)-stimulated release being affected. These effects were abolished by the antagonist
3,7-dimethyl-1-propargylxanthine (
DMPX), indicating a receptor-mediated process. In this case elevated levels of
taurine could be beneficial, protecting against hyperexcitation and excitotoxicity.