Abstract
Objective: The present study was designed to evaluate the neuroprotective effect of methanolic extract of Sargassum wightii on haloperidol-induced catalepsy and tardive dyskinesia in Wistar albino rats.
 Methods: In this study, thirty Wistar albino rats were randomly divided into six groups. Gr-I served as control. Haloperidol (1 mg/kg intraperitoneally) was administered to rats of Gr-II to Gr-V for twenty-one consecutive days to induce catalepsy and tardive dyskinesia. Animals of Gr-II to Gr-V were orally administered with vehicle, levodopa carbidopa combination (30 mg/kg), Sargassum extract 200 and 400 mg/kg respectively. All the drugs and vehicles were given orally one hour before haloperidol injection for twenty one consecutive days. The cataleptic scores were recorded using standard bar test. Tardive dyskinesia was assessed in terms of vacuous chewing movement (VCM) and tongue protrusion (TP) scores. After behavioural testing, all animals were sacrificed on twenty-second day and various biochemical parameters like MDA, SOD and GSH were estimated in brain tissue.
 Results: Chronic administration of haloperidol significantly increased cataleptic scores, VCM and TP scores. (p<0.001) Sargassum wightii extract (400 mg/kg) significantly inhibited haloperidol-induced catalepsy, VCM and TP (p<0.001) Haloperidol increased MDA and decreased SOD and GSH in brain tissue to a highly significant extent (p<0.001) Sargassum extract at 400 mg/kg also significantly reversed the haloperidol-induced alteration in brain oxidative stress markers.
 Conclusion: Sargassum wightii inhibits haloperidol-induced catalepsy and tardive dyskinesia. Thus it may be used as a unique therapeutic adjunct for the prevention of neuroleptic-induced extrapyramidal symptoms, however, it has to be explored more.
Highlights
Neuroleptics used in the treatment of schizophrenia and other psychiatric illness are very often associated with extrapyramidal side effects like catatonia and tardive dyskinesia [1, 2]
With L dopa-carbidopa 30 mg/kg, the reference standard drug treatment, there was a highly significant decrease in the Haloperidol induced vacuous chewing movement (VCM) and tongue protrusion (TP) throughout the study period. (p
Evidence in support of the “free radical hypothesis” proposes that the free radical byproducts of dopamine metabolism impart neurotoxic effects at basal ganglia and substantia nigra which explains one of the mechanisms involved in the process of neurodegeneration in neuroleptic-induced tardive dyskinesia and PD [29, 30]
Summary
Neuroleptics used in the treatment of schizophrenia and other psychiatric illness are very often associated with extrapyramidal side effects like catatonia and tardive dyskinesia [1, 2]. Haloperidol, a typical antipsychotic produces extrapyramidal syndrome (EPS) like Parkinsonism, due to a blockade of D2 receptors within the striatum and reduced dopaminergic transmission [3, 4]. It produces a behavioural state of catalepsy and movement disorders like akathisia, dystonia, and at last, chronic tardive dyskinesia [5]. Evidence from many experimental and clinical studies suggests that neuroleptics induce oxidative stress and cell death. Even lipid peroxidation byproducts in blood and cerebrospinal fluid are increased in patients with tardive dyskinesia [7, 8]
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