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Increased Neostriatal Tyrosine Hydroxylation During Stress: Role of Extracellular Dopamine and Excitatory Amino Acids
Author(s) -
Castro Sandra L.,
Sved Alan F.,
Zigmond Michael J.
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.66020824.x
Subject(s) - chemistry , endocrinology , medicine , tyrosine , extracellular , dopamine , cnqx , excitatory postsynaptic potential , amino acid , nmda receptor , ampa receptor , biochemistry , receptor , biology
We examined the regulation of neostriatal tyrosine hydroxylation during acute stress, testing the hypothesis that excitatory amino acids (EAAs) contribute to the stress‐evoked increase in dopamine (DA) synthesis. Dialysis probes implanted into neostriatum permitted delivery of drugs and sampling of extracellular fluid. Rats were exposed to 30 min of intermittent tail shock during infusion of an inhibitor of aromatic amino acid decarboxylase (AAAD), NSD‐1015 (100 µ M ), and DOPA was measured in the dialysate. Tail shock was applied beginning either 15 min after the onset of NSD‐1015 treatment (the initial rate of DOPA accumulation) or 75 min after the onset of treatment (when DOPA had approached steady state). Tail shock increased the steady‐state levels of extracellular DOPA in neostriatum (+40%). However, there was no change in the initial rate of DOPA accumulation unless animals also received the D 2 receptor antagonist eticlopride (50 n M ), in which case an increase was observed (+228%). The impact of tail shock on the steady‐state level of DOPA was attenuated by the D 2 agonist quinpirole (100 µ M ), or by 2‐amino‐5‐phosphonovalerate (APV) (100 µ M ) or 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX) (100 µ M ), EAA antagonists acting at NMDA or d , l ‐α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole‐4‐propionate (AMPA) receptors, respectively. These data suggest that acute stress normally has little effect on tyrosine hydroxylation in neostriatum due to the inhibitory influence of DA in the extracellular fluid. However, when that influence is absent (e.g., during extended inhibition of DOPA decarboxylation or blockade of DA receptors), stress increases tyrosine hydroxylation via EAAs acting on NMDA and AMPA receptors. Thus, EAAs released from corticostriatal projections may stimulate DA synthesis and thereby restore dopaminergic activity under conditions in which the availability of DA for release has been compromised.