Glutamate-Dopamine Balance in the Striatum: Pre- and Post-Synaptic Interactions

Abstract

The striatum receives a major dopaminergic input, the nigro-striatal pathway originating from the substantia nigra pars compacta (SNc) (Dahlström and Fuxe, 1964; Andén et al, 1966). It receives also a massive excitatory input originating from the cortex and the thalamus (Grofova, 1979; Parent, 1990). Glutamate (GLU) is the candidate neurotransmitter of both of these pathways (Mc Geer et al, 1977; Reubi and Cuenod, 1979; Fonnum et al., 1981; Lapper and Bolam, 1992), although the neurotransmitter of the thalamo-striatal pathway is still controversial (Nieoullon et al., 1985; Nieoullon, 1986; Kilpatrick and Phillipson, 1986). During the past years, various experimental studies have established that the striatum is the site of reciprocal interactions between dopaminergic and glutamatergic neurotransmissions leading to the hypothesis that imbalance of these interactions may be involved in the pathogenesis of Parkinson’s disease (Nieoullon et al., 1982) or schizophrenia (Kim et al, 1980; Carlsson and Carlsson, 1990; Grace, 1991). Our purpose here is to review these interactions and their functional implications.