Long-term enhancement of dopamine release by high frequency tetanic stimulation via aN-methyl-d-aspartate-receptor-mediated pathway in rat striatum

We studied the effects of high frequency tetanic stimulation of the striatum on the KCl (20 mM)-evoked dopamine release in rat striatal slices. The KCl-evoked dopamine release was potentiated by high frequency tetanic stimulation (10-20 Hz) of the striatum including the corticostriatal fibers, and this potentiation was observed until 3 h after high frequency tetanic stimulation. Potentiation of dopamine release after high frequency tetanic stimulation was induced not only by KCl but also by glutamate in Mg²⁺-free medium,N-methyl-d-aspartate in Mg²⁺-free medium, and bydl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid. 2-amino-5-phosphovalerate, 3-[(±)-2-carboxypiperazine-4-yl]-propyl-1-phosphonate or dibenzocycloheptaneimine,N-methyl-d-aspartate receptor inhibitors, abolished enhancement by tetanus, whereas, 6,7-dinitroquinoxaline-2,3-dione, an antagonist ofdl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid ionotropic receptors, orl-2-amino-4-phosphonobutyrate, an antagonist of glutamate metabotropic receptors, showed no effect. Moreover, pretreatment with glutamate orN-methyl-d-aspartate in the absence of Mg²⁺ also facilitated dopamine release evoked by KCl concentrations. When extracellular Ca²⁺ was removed from the medium during pretreatment, potentiation by glutamate disappeared. We conclude that activation ofN-methyl-d-aspartate receptors on dopaminergic nerve terminals in the striatum produces the long-term changes in efficacy of the response to KCl or glutamatergic agents. That is, plastical phenomena could exist at presynaptic levels between glutamatergic neurons and dopaminergic neurons in striatum.