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2019, Pharmacological ReportsCitation Excerpt :Dopamine and glutamate inputs can influence each other [52,53] and NAc MSNs express both DA and glutamate receptors [49,50]. Glutamate inputs from some brain areas, such as the prefrontal cortex (PFC), amygdala (AMG), and hippocampus [43–45] project on and activate MSNs of NAc, and blockade of glutamate receptors causes a reduction in the excitability of NAc MSNs [54,55], and affects excitatory postsynaptic potentials [55,56]. There is an anatomical relationship between orexin and dopamine neurons in the medial PFC, AMG, and NAc [57].
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2013, Journal of Pharmacological SciencesAMPA receptor plasticity in the nucleus accumbens after repeated exposure to cocaine
2010, Neuroscience and Biobehavioral ReviewsCitation Excerpt :This review will focus specifically on cocaine-induced alterations in glutamate transmission and plasticity involving α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors (AMPAR) in the NAc. Glutamate inputs acutely excite NAc MSN primarily by activating AMPAR (Pennartz et al., 1990; Hu and White, 1996) and results in many animal models of addiction indicate that AMPAR activation in the NAc is necessary for drug seeking. Thus, intra-NAc infusion of AMPAR antagonists blocks cue-induced cocaine seeking after withdrawal (Conrad et al., 20081), cocaine seeking under second-order schedules of reinforcement (Di Ciano and Everitt, 20012; Di Ciano and Everitt, 20041), cue-induced reinstatement (Bäckstrom and Hyytiä, 20071), and cocaine-primed reinstatement (Cornish and Kalivas, 20003; Famous et al., 20084).
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2009, European Journal of Medicinal ChemistryCitation Excerpt :During the recording, slices were maintained at 32–33 °C and were continuously superfused at a rate of 2 mL/min with a modified artificial cerebrospinal fluid (aCSF) consisting of (in mM) NaCl, 126; KCl, 3.0; MgCl2, 1.5; CaCl2, 2.4; NaH2PO4, 1.2; glucose, 11.0; NaHCO3, 26, and saturated with 95% O2 and 5% CO2. In order to isolate glutamate-driven synaptic potentials [51] the aCSF also contained the GABAA-receptor antagonist picrotoxin (100 μM) and the N-methyl-d-aspartate (NMDA)-type receptor antagonist APV (40 μM). Electrical stimulation was performed using a bipolar tungsten stimulating electrode placed near (<100 μm) the recording electrode, in the dorsal striatum.
Biological substrates of reward and aversion: A nucleus accumbens activity hypothesis
2009, NeuropharmacologyCitation Excerpt :These data provided early evidence that blockade of NMDA receptors in the NAc is sufficient for reward and, by extension, reward can be dopamine-independent. Blockade of NMDA receptors would be expected to produce an overall reduction in the excitability of NAc MSNs without affecting baseline excitatory input mediated by AMPA receptors (Uchimura et al., 1989; Pennartz et al., 1990). Importantly, rats also self-administered NMDA antagonists into deep layers of the PFC (Carlezon and Wise, 1996), which project directly to the NAc (see Kelley, 2004) and have been conceptualized as a part of an inhibitory (STOP!)