Behavioral and neurochemical effects induced by reserpine in mice

Abstract

These findings suggest that the pharmacological blockage of vesicular monoamine transporter (VMAT) by reserpine caused neurochemical and behavioral alterations in mice.

Agmatine attenuates reserpine-induced oral dyskinesia in mice: Role of oxidative stress, nitric oxide and glutamate NMDA receptors

“…The Newman-Keuls post-hoc analysis indicated a reduction on the VCM frequency in mice that received sub-effective doses of agmatine (10 mg/kg) in combination with amantadine (1 mg/kg), as compared to the reserpine-treated group. Similar to this data, MK801 at doses of 0.03-0.3 mg/kg produced an orofacial antidyskinetic effect [F (5,35) =10.07, P<0.0001] (Fig. 4C).…”

“…The administration of amantadine at doses of 40 and 60 mg/kg reduced the VCM frequency [F (5,36) =7.31, P<0.001], which did not occur at doses of 1-10 mg/kg (Fig. 4A).…”

“…In this context, a previous study observed that MK801, an NMDAR antagonist, reduced the VCM frequency in reserpine-treated mice [18]. Furthermore, a recent study [5] In this context, we hypothesized that agmatine may exhibit antidyskinetic effects on orofacial dyskinesia induced by reserpine. This endogenous polyamine is synthesized from L-arginine decarboxylation by arginine decarboxylase (ADC) and is degraded by agmatinase and diamine oxidase enzymes [19].…”

“…For instance, drug-induced dyskinesia can be observed in several psychotic and neurological disorders, such as schizophrenia and Parkinson's disease (PD), following the prolonged use of antipsychotics and levodopa (L-DOPA), respectively [1][2][3]. Dopaminergic and non-dopaminergic mechanisms are involved in drug-induced dyskinesia with the development of abnormal neuronal plasticity in the striatum and prefrontal cortex [4,5]. In this context, the reserpineinduced orofacial dyskinesia model in rodents has been extensively used in the investigation of behavioral alterations, neurochemical and molecular mechanisms of orofacial dyskinesia [5][6][7][8].…”

“…Dopaminergic and non-dopaminergic mechanisms are involved in drug-induced dyskinesia with the development of abnormal neuronal plasticity in the striatum and prefrontal cortex [4,5]. In this context, the reserpineinduced orofacial dyskinesia model in rodents has been extensively used in the investigation of behavioral alterations, neurochemical and molecular mechanisms of orofacial dyskinesia [5][6][7][8]. This model is characterized by an increase in vacuous chewing movements (VCM), facial twitching (FT), and tongue protrusion (TP) [9,10].…”