title: Presynaptic dopaminergic control of high affinity glutamate uptake in the striatum.
abstract: The high affinity glutamate uptake (HAGU) was measured in homogenates obtained from striata of control rats and animals submitted to electrical stimulation of the frontal cortical areas. Results show that the stimulation of the corticostriatal neurons induces an activation of the uptake of glutamate (Glu) in the striatum resulting from an increase in the affinity of the transport site for Glu. In other experiments we have obtained evidence that, when stimulated, presumed dopaminergic receptors can inhibit HAGU. The dopaminergic antagonist haloperidol was shown not to influence that basal Glu uptake but this neuroleptic highly potentiates the excitatory effects of cortical stimulations. The nigrostriatal dopaminergic pathway may exert a modulatory action on the corticostriatal glutamatergic neurons as it counteracts increasing glutamatergic activity.
mesh_terms: D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology; D003342:Corpus Striatum / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D006220:Haloperidol / Q000494:pharmacology; D007700:Kinetics; D009433:Neural Inhibition / Q000187:drug effects; D051381:Rats; D011954:Receptors, Dopamine / Q000502:physiology*; D013378:Substantia Nigra / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects
chemical_list: D005971:Glutamates; D011954:Receptors, Dopamine; D018698:Glutamic Acid; D006220:Haloperidol; D004298:Dopamine