Influence of Cortico-Striatal Glutamatergic Neurons on Dopaminergic Transmission in the Striatum

Several studies performed on rat striatal slices and in some cases on synaptosomes have indicated that dopamine (DA) and most neurotransmitters found in the striatum regulate presynapticaily the release of DA from nerve terminals of the nigro-striatal DA neurones (chesselet, 1984). These neurotransmitters include excitatory or inhibitory amino-acids, amines and several neuropeptides found either in afferent fibers, interneurones or in collaterals of efferent projections from the striatum. These regulations are either direct or indirect, ie mediated through receptors located on DA nerve terminals or on neurones in contact with these nerve terminals. This has been mainly shown by examining the persistance or disappearance of these presynaptic regulations in the presence of tetrodotoxin (TTX), a neurotoxine which interrupts nerve impulse flow. There is some evidence that some neurotransmitters may diffuse at some distance from their release sites before their inactivation. Nevertheless, the physiological significance of some presynaptic regulations of DA release has been often challenged by neuroanatomists since up to now few axo-axonic contacts have been observed between DA neurones and other neurones innervating the striatum (Bouyer et al., 1984). In vivo studies, in which identified pathways projecting to the striatum can be activated are of great value for determining the physiological relevance of these presynaptic regulations. Therefore, we will first summurize results of in vivo experiments made in halothane anesthetized cats implanted with push-pull cannulae which have allowed to demonstrate the role of the corticostriatal glutamatergic projection in the presynaptic control of DA release. We will also describe more recent experiments made either in vivo or in vitro in which attempts were made to identify the types of glutamatergic receptors involved in the presynaptic control of DA release and to distinguish direct and indirect effects mediated by local circuits.