MinireviewPresynaptic dopaminergic modulation of cortical input to the striatum
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Lipid-based nanodelivery approaches for dopamine-replacement therapies in Parkinson's disease: From preclinical to translational studies
2020, BiomaterialsCitation Excerpt :In PD pathogenesis, despite the impaired function of nigrostriatal DAergic neurons and the loss of DA transmitters, an imbalance in GLUT and GABAergic transmitters has also been documented [48,62]. More precisely, in the putamen, GLUT/N-methyl-d-aspartate (NMDA) presynaptically inhibits DA2 on DAergic neurons, thereby substantially increasing DA deficits (Fig. 2) [63,64]. However, NMDA antagonists substantially reverse the dyskinetic effects, while the metabotropic GLUT receptor m5GluR has also been documented to exert a strong inhibitory effect on DAergic neurons in the putamen [65,66].
Reappraising striatal D1- and D2-neurons in reward and aversion
2016, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Importantly, D2Rs are also found presynaptically, where they can modulate neurotransmitter release (Benoit-Marand et al., 2001). In the striatum, D2Rs are present on corticostriatal inputs and function to decrease glutamate release by presynaptic mechanisms (Kornhuber and Kornhuber, 1986; Maura et al., 1988; Yamamoto and Davy, 1992). Additionally, these Gi/o −coupled inhibitory receptors also play a major part in shaping dopamine transmission (Benoit-Marand et al., 2001).
Treatment with 1,2,3,4,-tetrahydroisoquinoline affects glutamate release in the striatum but not the binding of [<sup>3</sup>H]MK-801 to NMDA receptors in the dopaminergic structures of the rat brain
2009, Pharmacological ReportsCitation Excerpt :Further illustrating the effects of TIQ on the release of neurotransmitters in the mammalian brain, our earlier study demonstrated that a single dose of this compound administered systemically at 100 mg/kg enhanced DA and serotonin (5-HT) release in the rat striatum [28]. Biochemical, behavioral and electrophysiological studies have suggested that DA released from the dopaminergic nigrostriatal terminals exerts inhibitory effects on the activity of the glutamatergic pathways from the cortex and thalamus [14,20,61]. Hence, it was reasonable to assume that TIQ acting indirectly via DA, which activates presynaptic dopamine D2 receptors localized on the terminals of glutamatergic cortico- and thalamostriatal pathways, could decrease glutamate release in the rat striatum.
Ketamine induces hyperactivity in rats and hypersensitivity to nicotine in rat striatal slices
2008, Pharmacology Biochemistry and BehaviorNMDA receptor blockade augmented nicotine-evoked dopamine release from rat prefrontal cortex slices
2008, Neuroscience LettersPrenatal protein deprivation in rats induces changes in prepulse inhibition and NMDA receptor binding
2004, Brain ResearchCitation Excerpt :Second, changes in glutamate receptor binding have been observed post-mortem in the brains of patients with schizophrenia. However, the observed changes differ in nature from our results, with increases in receptor binding occurring in cortex [26,45,61,85], decreases in receptor number and gene expression occurring in the hippocampus [31,42,47] and increases in receptor number occurring in striatum [50]. These reported receptor changes are hypothesized to occur as compensatory responses to decreased NMDA-mediated glutamate release [45,85].