Effect of ethanolic extract of Coriandrum sativum L. on tacrine induced orofacial dyskinesia.

The effect of ethanolic extract of Coriandrum sativum L. seeds (100, 200 mg/kg) was studied on tacrine induced orofacial dyskinesia. Tacrine (2.5 mg/kg, i.p.) treated animals were observed for vacuous chewing movements (VCM), tongue protrusions (TP) and orofacial bursts (OB) for 1 h followed by observations for locomotor changes and cognitive dysfunction. Sub-chronic administration of Coriandrum sativum L. seed extract (E-CS) (100, 200 mg/kg, p.o., for 15 days significantly (P <0.05) decreased the tacrine induced VCM, TP and OB; and also significantly (P <0.05), increased locomotion and cognition compared to the tacrine treated group. Biochemical analysis revealed that tacrine administration significantly (P <0.05) decreased the levels of superoxide dismutase (SOD), Catalase (CAT), glutathione reductase (GSH) levels and also significantly (P <0.05) increased lipid peroxidation (LPO) as an index of oxidative stress, whereas sub-chronic administration of E-CS significantly (P <0.05) improved the antioxidant enzyme (i.e. SOD, CAT, and GSH) levels and also significantly (P <0.05) decreased lipid peroxidation (LPO). The results have demonstrated the protective role of ethanolic extract of Coriandrum sativum. L against tacrine induced orofacial dyskinesia.

An examination of synaptic proteins following chronic haloperidol in a rat model of tardive dyskinesia

Tardive dyskinesia (TD) is a late-onset side effect mainly affecting the orofacial region of patients treated chronically with classic antipsychotic drugs such as haloperidol (HAL). The causes of TD remain unknown. We hypothesized that faulty synaptic re-organization might be related to TD-like syndromes and used the vacuous chewing movements (VCM) model in rats to investigate the expression of four synaptic proteins, synaptophysin, syntaxin, spinophilin and PSD-95, in brains of HAL-treated rats. Male Sprague-Dawley rats were treated for 14 weeks with either haloperidol decanoate (21 mg/kg once every 3 weeks, I.M) or vehicle and VCMs were monitored on a weekly basis. As expected, VCMs developed reliably and were consistently more pronounced in some rats than in others. Using immunohistochemistry in anatomically preserved brain sections as well as Western Blot analyses of whole cells or synaptosomal fractions in striatal tissue, we found no significant effect of chronic HAL on levels of these proteins. Neither did we find significant differences in the levels of the four synaptic markers when comparing rats showing High vs. Low levels of VCMs. These results suggest that structural synaptic alterations (e.g. involving increased number of synapses) may not be the underlying mechanism of oral dyskinesias induced by chronic antipsychotic drug treatment. The possibility that functional neuroplastic changes occur remains to be investigated

Effect of MK-801 on the Prevention and Treatment of Tardive Dyskinesia

Tardive dyskinesia(TD) is a serious side effect of long-term treatment with neuroleptic medications. To investigate if glutamatergic hyperfunction is associated with TD, effect of MK-801 on the prevention and treatment of TD was studied using a rat model, i.e., vacuous chewing movements(VCM). When comparing VCM scores of Group I(haldol decanoate+MK-801) with that of Group II(hadol decanoate+phosphate buffer saline), late measured VCM scores of former were significantly lower than that of latter, meaning that MK-801 is effective in the prevention of VCM. Furthermore, when MK-801 is also effective in the treatment of VCM. From the above results, it is suggested that glutamatergic hyperfunction might be involved in the development of TD and MK801 could be effective in the prevention and treatment of it.