Oral tremor induced by the muscarinic agonist pilocarpine is suppressed by the adenosine A2A antagonists MSX-3 and SCH58261, but not the adenosine A1 antagonist DPCPX

Collins, Lyndsey E.; Galtieri, Daniel; Brennum, Lise T.; Sager, Thomas N.; Hockemeyer, Jörg; Müller, Christian; Hinman, James R.; Chrobak, James J.; Salamone, John D.

doi:10.1016/j.pbb.2009.11.011

Cited by 36 publications

(31 citation statements)

References 97 publications

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“…First, we ascertained the anti-tremor effects of the A 2A R antagonist SCH58261, previously reported to attenuate pilocarpine-induced TJMs [17]. As expected, in WT mice SCH58261 produced a significant reduction of TJMs between 20 to 30 minutes after the administration of pilocarpine ( Fig.…”

Section: Page 6 Of 16mentioning

confidence: 64%

“…For instance, assessing the impact of The ability of A 2A R antagonists suppressing parkinsonian tremor is well-established [14,15,17], but the precise mechanism behind this effect is not fully understood. It has been shown that A 2A R blockage may help to inhibit the release of acetylcholine from striatal cholinergic interneurons, where the receptor is expressed in nerve terminals [22].…”

Section: Page 6 Of 16mentioning

confidence: 99%

“…Here, we focused on characterizing the influence of GPR37 expression on the development of PD symptomatology. Thus, we aimed to evaluate differences between wild-type (WT) and GPR37 knock-out (GPR37-/-) mice in the generation of parkinsonian-like tremulous jaw movements (TJMs), which is a drug [14] and [17]) and tropicamide (Alcón, El Masnou, Spain; 2.5 mg/kg, based on [18]) were administered i.p. 30 minutes before pilocarpine injection.…”

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Adenosine A2A receptor-mediated control of pilocarpine-induced tremulous jaw movements is Parkinson's disease-associated GPR37 receptor-dependent

Gandía

Morató

Štagljar

et al. 2015

Behavioural Brain Research

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Section: Page 6 Of 16mentioning

confidence: 64%

Section: Page 6 Of 16mentioning

confidence: 99%

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confidence: 99%

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Adenosine A2A receptor-mediated control of pilocarpine-induced tremulous jaw movements is Parkinson's disease-associated GPR37 receptor-dependent

Gandía

Morató

Štagljar

et al. 2015

Behavioural Brain Research

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“…8). Acute administration of several A 2A receptor antagonists significantly reversed jaw tremor induced by tacrine, pilocarpine, haloperidol, reserpine, and pimozide in rats, suggesting a beneficial use of these compounds as specific drugs against this parkinsonian symptom (Table 7.1; Betz et al 2009;Collins et al 2010Collins et al , 2012Collins-Praino et al 2011;Correa et al 2004;Pinna et al 2010;Salamone et al 2008;Simola et al 2004Simola et al , 2006Tronci et al 2007). Consistent with these findings, A 2A receptor antagonism or genetic deletion of the adenosine A 2A receptor significantly attenuated the TJMs induced by pilocarpine in mice (Table 7. 1;Salamone et al 2013).…”

Section: Effect Of a 2a Receptor Antagonist On Tremor Model Of Pdmentioning

confidence: 96%

Adenosine A2A Receptor Antagonists as Drugs for Symptomatic Control of Parkinson’s Disease in Preclinical Studies

Pinna

2015

Current Topics in Neurotoxicity

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Parkinson's disease (PD) is primarily a neurological basal ganglia (BG)-related disorder caused by progressive degeneration of the nigrostriatal dopaminergic neurons, which results in the cardinal motor symptoms of PD, including bradykinesia (slow movement and difficulty in initiation movement), resting tremor, muscle tone rigidity, postural instability, and sensorimotor integration deficits. The gold standard of PD therapy is characterized by the dopamine precursor L-DOPA however, after several years, this therapy leads to neuropsychiatric and motor complications, including fluctuations in motor response and dyskinesias, which develop in the majority of patients. Consequently, one of the main targets of research in PD is to identify alternative therapeutic approaches to ameliorate PD symptoms without inducing motor complications. Among the non-dopaminergic strategies for PD, one of the most promising is represented by adenosine A 2A receptor antagonists, due to the colocalization of these receptors and dopamine D 2 receptors in the striatopallidal neurons of the BG, which provides the anatomical basis for the existence of a functional antagonistic interaction between these receptors. Thus, extensive preclinical studies have been performed to prove the effectiveness of adenosine A 2A receptor blockade in counteracting the cardinal motor symptoms of PD.This chapter describes the effects of A 2A antagonists alone or in combination with L-DOPA against the cardinal motor symptoms of PD, using rodent and primate models of PD, and the main mechanisms responsible for these anti-parkinsonian effects. In addition, findings suggesting the potential utilization of A 2A antagonists, as adjunctive treatments to L-DOPA to reduce the L-DOPA induced wearing-off without modifying dyskinetic movements, have been reviewed. Keywords Parkinson's disease · Rodent models · Non-human primate models · Catalepsy · Rigidity · Tremor · 6-Hydroxydopamine lesion · MPTP lesion · A 2A receptor antagonists · Adenosine

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“…Depletions of striatal dopamine by the neurotoxic agent 6-OHDA (Jicha and Salamone, 1991; Finn et al, 1997b; Rodriguez-Diaz et al, 2001) or acute administration of reserpine (Baskin and Salamone, 1993; Steinpreis and Salamone, 1993; Salamone and Baskin, 1996; Salamone et al, 2008b) have been shown to induce TJM activity in rats. Several studies have demonstrated that TJMs are also induced by acute or sub-chronic administration of “typical” antipsychotic drugs that act as DA antagonists (Glassman and Glassman, 1980; Rupniak et al, 1985, 1986; Jicha and Salamone, 1991; Steinpreis and Salamone, 1993; Steinpreis et al, 1993; Egan et al, 1996; Trevitt et al, 1998; Wisniecki et al, 2003; Ishiwari et al, 2005; Betz et al, 2007, 2009; Collins et al, 2010a). In contrast, “atypical” antipsychotic drugs, such as clozapine, olanzapine, and quetiapine, which are less likely to induce motor side effects in humans, do not induce TJMs (Trevitt et al, 1998, 1999; Betz et al, 2005, 2009).…”

Section: The Tremulous Jaw Movement Model In Rodents: Development Andmentioning

confidence: 99%

Pharmacological and Physiological Characterization of the Tremulous Jaw Movement Model of Parkinsonian Tremor: Potential Insights into the Pathophysiology of Tremor

Collins-Praino¹,

Paul²,

Rychalsky³

et al. 2011

Front. Syst. Neurosci.

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Tremor is a cardinal symptom of parkinsonism, occurring early on in the disease course and affecting more than 70% of patients. Parkinsonian resting tremor occurs in a frequency range of 3–7 Hz and can be resistant to available pharmacotherapy. Despite its prevalence, and the significant decrease in quality of life associated with it, the pathophysiology of parkinsonian tremor is poorly understood. The tremulous jaw movement (TJM) model is an extensively validated rodent model of tremor. TJMs are induced by conditions that also lead to parkinsonism in humans (i.e., striatal DA depletion, DA antagonism, and cholinomimetic activity) and reversed by several antiparkinsonian drugs (i.e., DA precursors, DA agonists, anticholinergics, and adenosine A2A antagonists). TJMs occur in the same 3–7 Hz frequency range seen in parkinsonian resting tremor, a range distinct from that of dyskinesia (1–2 Hz), and postural tremor (8–14 Hz). Overall, these drug-induced TJMs share many characteristics with human parkinsonian tremor, but do not closely resemble tardive dyskinesia. The current review discusses recent advances in the validation of the TJM model, and illustrates how this model is being used to develop novel therapeutic strategies, both surgical and pharmacological, for the treatment of parkinsonian resting tremor.

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Oral tremor induced by the muscarinic agonist pilocarpine is suppressed by the adenosine A2A antagonists MSX-3 and SCH58261, but not the adenosine A1 antagonist DPCPX

Cited by 36 publications

References 97 publications

Adenosine A2A receptor-mediated control of pilocarpine-induced tremulous jaw movements is Parkinson's disease-associated GPR37 receptor-dependent

Adenosine A2A receptor-mediated control of pilocarpine-induced tremulous jaw movements is Parkinson's disease-associated GPR37 receptor-dependent

Adenosine A2A Receptor Antagonists as Drugs for Symptomatic Control of Parkinson’s Disease in Preclinical Studies

Pharmacological and Physiological Characterization of the Tremulous Jaw Movement Model of Parkinsonian Tremor: Potential Insights into the Pathophysiology of Tremor

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