Modulation of striatal adenosine A1 and A2 receptors induces rotational behaviour in response to dopaminergic stimulation in intact rats
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2021, European Journal of PharmacologyAdenosine A<inf>2A</inf> receptor as potential therapeutic target in neuropsychiatric disorders
2019, Pharmacological ResearchCitation Excerpt :Several preclinical studies support the involvement of adenosine in schizophrenia [191]. In general, A2AR agonists were shown to produce behavioral effects similar to those of dopamine antagonists (used against positive symptoms with antipsychotic–like effects) [192,194,195] and to counteract the motor stimulant effect induced by amphetamine or by D1/D2 receptor agonists [196,197]. On the basis of these and other studies, the A2AR agonist is considered an atypical antipsychotic-like drug that exerts its effects mainly by interacting with the A2A–D2 heteroreceptor complex, where it inhibits D2-mediated Gi/o signaling and increases the D2-mediated β-arrestin2 signaling [198–200].
Cannabinoid-induced depression of synaptic transmission is switched to stimulation when dopaminergic tone is increased in the globus pallidus of the rodent
2016, NeuropharmacologyCitation Excerpt :Pilot experiments showed that injection of ACEA (10 μg) alone into the GPe did not elicit significant effects on turning rate. Since prior studies show that induction of turning behavior by unilateral intracerebral injections of neural modulators may require a significant level of dopaminergic activation (Jiang et al., 1993; Popoli et al., 1994, 1996; Floran et al., 2002), we examined whether stimulating dopamine release in the brain by intraperitoneal administration of methamphetamine would reveal the effect of injecting the CB1R agonist. Systemic i.p. administration of methamphetamine (10 mg/kg) alone did not have a significant effect on turning behavior (7A and 7B red circles), however, when ACEA (10 μg i.c.) was next injected unilaterally into the ipsilateral GPe (Fig. 7A) turning was induced, at a maximum rate of about 7 turns per minute that decreased over time.
Adenosine receptor control of cognition in normal and disease
2014, International Review of NeurobiologyCitation Excerpt :Adenosine, via activation of inhibitory A1 and facilitatory A2A receptors, has the unique capability to integrate and fine-tune glutamatergic and dopaminergic outputs. For adenosine modulation of dopaminergic signaling, an adenosine deficit can enhance dopamine release because of the inhibitory effect of A1R on dopamine release (Golembiowska & Zylewska, 1998; Solinas et al., 2002) and potentiate amphetamine-induced locomotion (Popoli, Pezzola, & de Carolis, 1994). Antagonistic interactions between A2AR and D2R (Ferre et al., 1991; Ferre, Herrera-Marschitz, Grabowska-Anden, Ungerstedt, et al., 1991; Ferre et al., 2001; Sebastiao & Ribeiro, 2000) predict that increased basal D2R occupancy in schizophrenia patients (Abi-Dargham et al., 2000) could reduce A2AR's effect on D2R and thereby increases the affinity of the D2R for dopamine (Ferre, Herrera-Marschitz, Grabowska-Anden, Casas, et al., 1991; Ferre, Herrera-Marschitz, Grabowska-Anden, Ungerstedt, et al., 1991; Ferre, von Euler, Johansson, Fredholm, & Fuxe, 1991).
Adenosine hypothesis of schizophrenia - Opportunities for pharmacotherapy
2012, Neuropharmacology