Microinjection of a glutamate antagonist into the nucleus accumbens reduces psychostimulant locomotion in rats
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Cited by (84)
Caffeine induces neurobehavioral effects through modulating neurotransmitters
2020, Saudi Pharmaceutical JournalCitation Excerpt :Moreover, caffeine treatments have also been reported to induce sleep disturbances, in part by downregulating GABAA receptors in the mouse hypothalamus (Ko et al., 2018). NMDAR antagonists and glutamate antagonists did not affect the hyperlocomotion activity induced by caffeine, suggesting that caffeine increased locomotion activity through acting on other neurotransmitters systems such as dopaminergic pathways (Pulvirenti et al., 1989, 1991). In addition to preclinical studies, clinical findings showed promising effects of caffeine against neurological diseases (Lucas et al., 2011; Kahathuduwa et al., 2019; Haskell et al., 2005; Borota et al., 2014).
Injection of Cocaine-Amphetamine Regulated Transcript (CART) peptide into the nucleus accumbens does not inhibit caffeine-induced locomotor activity: Implications for CART peptide mechanism
2016, Pharmacology Biochemistry and BehaviorCitation Excerpt :This observation further corroborates the evidence that caffeine does not increase DA levels in the NAc core by showing that it also does not consequentially increase extracellular GLUT in this region (Dalia et al., 1998; Solinas et al., 2002). The distinctions in extracellular GLUT activity in the NAc core between cocaine and caffeine is buttressed by pharmacological and behavioral evidence showing that intra-NAc core injection of a non-selective GLUT antagonist (Pulvirenti et al., 1989) and a selective GLUT NMDA receptor antagonist inhibited cocaine-induced LMA (Pulvirenti et al., 1994), but had no effect on caffeine-induced LMA (Pulvirenti et al., 1991). Intriguingly, these reports are similar to our results showing that intra-NAc core CART peptide attenuates cocaine-induced LMA but not caffeine mediated motor activity, suggesting that extracellular DA and/or downstream extracellular DA-GLUT mechanisms may be involved in CART peptide activity in the NAc.
Ceftriaxone attenuates locomotor activity induced by acute and repeated cocaine exposure in mice
2013, Neuroscience LettersCitation Excerpt :The possibility that CTX efficacy against acute cocaine is dependent on disruptions in dopamine signaling is supported by evidence that CTX attenuates the acute locomotor-stimulant effects of caffeine [37]. Caffeine and cocaine both require increased dopamine signaling to produce acute hyperlocomotion; however, only cocaine requires increased glutamate signaling for the said effect [10,12,26]. It should also be noted that a broad-spectrum glutamate transporter inhibitor (l-trans-pyrrolidine-2,4-dicarboxylic acid) increases extracellular glutamate as well as dopamine levels in the striatum [11], suggesting that glutamate transporters may regulate dopamine release from the striatal dopaminergic nerve terminals.
Ceftriaxone prevents the induction of cocaine sensitization and produces enduring attenuation of cue- and cocaine-primed reinstatement of cocaine-seeking
2011, Behavioural Brain ResearchCitation Excerpt :Acute cocaine injections increase striatal dopamine release [33] and DA receptor 1 (D1) antagonists decrease cocaine-induced locomotion [34]. Glutamate is also involved in the acute effects of cocaine on locomotion, as both AMPA [35] and NMDA antagonists [36] exert inhibitory effects on cocaine-induced locomotion. There is an extensive literature that demonstrates that glutamate and not dopamine transmission is involved in the induction of cocaine sensitization (for review see [26]).
Glutamate-mediated neuroplasticity in an animal model of self-injurious behaviour
2008, Behavioural Brain Research
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Visiting scientist from: 3rd Dept. of Neurology, University of Pavia, Italy.