Objective: The study was undertakento investigate the role of striatal neurotransmitters and neuroinflammatory cytokines in the neuroprotective effect of lycopene against haloperidol induced orofacial dyskinesia in Wistar rats.

Background: Tardive Dyskinesia is a severe side effect of chronic neuroleptic treatment consisting of abnormal involuntary movements, characterized by orofacial dyskinesia. Lycopene, a potent antioxidant and anti-inflammatory agent has been reported to provide neuroprotection in animal models of other movement disorders.

Methods: Rats were administered with haloperidol (1 mg/kg, i.p for 21 days) to induce orofacial dyskinesia. Lycopene (5 and 10 mg/kg, p.o) was given daily 1 hour before haloperidol treatment for 21 days. Behavioral observations (vacuous chewing movements, tongue protrusions, facial jerking, rotarod activity, grip strength, narrow beam walking) were made on 0th, 7th, 14th, 21st day after haloperidol treatment. On 22nd day, animals were sacrificed and striatum was used for estimation of biochemical parameters (malondialdehyde, nitrite and endogenous enzyme (GSH), proinflammatory cytokines [Tumor necrosis factor, Interleukin 1β, Interleukin 6] and neurotransmitters level (dopamine, serotonin, nor epinephrine, 5-Hydroxyindole acetic acid (5-HIAA), Homovanillic acid, 3,4- dihydroxyphenylacetic acid).

Results: Haloperidol treatment for 21 days significantly impaired muscle co-ordination, motor activity and grip strength with enhanced orofacial dyskinetic movements. In addition, haloperidol treatment significantly increases free radical generation (increases MDA and nitrite levels, decreasing GSH levels) and level of pro-inflammatory cytokines (Tumor necrosis factor, Interleukin 1β, Interleukin 6) whereas decrease the level of striatal neurotransmitters (dopamine, serotonin, nor epinephrine, 5-Hydroxyindole acetic acid (5-HIAA), Homovanillic acid, 3,4- dihydroxyphenylacetic acid). Lycopene (5 and 10 mg/ kg, p.o) treatment along with haloperidol significantly attenuated impairment in behavioral, biochemical, neurochemical and neuroinflammatory markers.

Conclusions: The present study highlight the neuroprotective effect of lycopene and is attributed to antioxidant property, modulation of of neuro-inflammatory cytokines and striatal neurotranmitters level.

References: Bishnoi, M., Chopra, K., Kulkarni, S.K., 2008. Activation of striatal inflammatory mediators and caspase-3 is central to haloperidol-induced orofacial dyskinesia. Eur. J. Pharmacol. 590, 241–245. Kumar, P., Kalonia, H., Kumar, A., 2009. Lycopene modulates nitric oxide pathways against 3-nitropropionic acid-induced neurotoxicity. Life Sci. 85, 711–718. Qu, M., Li, L., Chen, C., Li, M., Pei, L., Chu, F., Yang, J., Yu, Z., Wang, D., Zhou, Z., 2011. Protective effects of lycopene against amyloid β-induced neurotoxicity in cultured rat cortical neurons. Neurosci. Lett. 505, 286–290.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/lycopene-ameliorates-haloperidol-induced-orofacial-dyskinesia-in-rats-possible-neurotransmitters-and-neuroinflammation-modulation/