Catiuscia Molz de Freitas

Gallic acid decreases vacuous chewing movements induced by reserpine in rats

Involuntary oral movements are present in several diseases and pharmacological conditions; however, their etiology and efficient treatments remain unclear. Gallic acid is a natural polyphenolic acid found in gall nuts, sumac, oak bark, tea leaves, grapes and wine, with potent antioxidant and antiapoptotic activity. Thus, the present study investigated the effects of gallic acid on vacuous chewing movements (VCMs) in an animal model induced by reserpine. Rats received either vehicle or reserpine (1mg/kg/day, s.c.) during three days, followed by treatment with water or different doses of gallic acid (4.5, 13.5 or 40.5mg/kg/day, p.o.) for three more days. As result, reserpine increased the number of VCMs in rats, and this effect was maintained for at least three days after its withdrawal. Gallic acid at two different doses (13.5 and 40.5mg/kg/day) has reduced VCMs in rats previously treated with reserpine. Furthermore, we investigated oxidative stress parameters (DCFH-DA oxidation, TBARS and thiol levels) and Na(+),K(+)-ATPase activity in striatum and cerebral cortex, however, no changes were observed. These findings show that gallic acid may have promissory use in the treatment of involuntary oral movements.

Anandamide attenuates haloperidol-induced vacuous chewing movements in rats

Antipsychotics may cause tardive dyskinesia in humans and orofacial dyskinesia in rodents. Although the dopaminergic system has been implicated in these movement disorders, which involve the basal ganglia, their underlying pathomechanisms remain unclear. CB1 cannabinoid receptors are highly expressed in the basal ganglia, and a potential role for endocannabinoids in the control of basal ganglia-related movement disorders has been proposed. Therefore, this study investigated whether CB1 receptors are involved in haloperidol-induced orofacial dyskinesia in rats. Adult male rats were treated for four weeks with haloperidol decanoate (38mg/kg, intramuscularly - i.m.). The effect of anandamide (6nmol, intracerebroventricularly - i.c.v.) and/or the CB1 receptor antagonist SR141716A (30μg, i.c.v.) on haloperidol-induced vacuous chewing movements (VCMs) was assessed 28days after the start of the haloperidol treatment. Anandamide reversed haloperidol-induced VCMs; SR141716A (30μg, i.c.v.) did not alter haloperidol-induced VCM per se but prevented the effect of anandamide on VCM in rats. These results suggest that CB1 receptors may prevent haloperidol-induced VCMs in rats, implicating CB1 receptor-mediated cannabinoid signaling in orofacial dyskinesia.

Gabapentin prevents behavioral changes on the amphetamine-induced animal model of schizophrenia

Fig. 1. Effect of gabapentin on behavioral changes induced by acute amphetamine administratio for 5min in an open field arena, analyses of workingmemory in Ymaze by (B) percentage of cor 15 min (animals tested in pairs) and (D) stereotyped behavior of mice observed in glass cage absence (0) or presence and amount (from 1 to 3) types of abnormal movements (head nodd way ANOVA followed by post hoc Tukeys test. Data are expressed as mean ± S.E.M. for 11–1 control group, p b 0.05 when compared with the amphetamine group.

Gabapentin reduces haloperidol-induced vacuous chewing movements in mice

ABSTRACT Tardive dyskinesia (TD) is a common adverse effect observed in patients with long‐term use of typical antipsychotic medications. A vacuous chewing movement (VCM) model induced by haloperidol has been used to study these abnormalities in experimental animals. The cause of TD and its treatment remain unknown, but several lines of evidence suggest that dopamine receptor supersensitivity and gamma‐aminobutyric acid (GABA) insufficiency play important roles in the development of TD. This study investigated the effects of treatment with the GABA‐mimetic drug gabapentin on the development of haloperidol‐induced VCMs. Male mice received vehicle, haloperidol (1.5 mg/kg), or gabapentin (GBP, 100 mg/kg) intraperitoneally during 28 consecutive days. Quantification of VCMs was performed before treatment (baseline) and on day 28, and an open‐field test was also conducted on the 28th day of treatment. The administration of gabapentin prevented the manifestation of haloperidol‐induced VCMs. Treatment with haloperidol alone reduced the locomotor activity in the open‐field test that was prevented by co‐treatment with gabapentin. We did not find any differences among the groups nor in the tyrosine hydroxylase (TH) or glutamic acid decarboxylase (GAD) immunoreactivity or monoamine levels in the striatum of mice. These results suggest that treatment with gabapentin, an analog of GABA, can attenuate the VCMs induced by acute haloperidol treatment in mice without alterations in monoamine levels, TH, or GAD67 immunoreactivity in the striatum. HighlightsGabapentin prevented haloperidol‐induced vacuous chewing movements.Gabapentin attenuates the reduction in locomotor activity caused by haloperidol.Any alteration was found in TH, GAD67 or monoamines levels in striatum of mice treated with haloperidol and/or gabapentin.