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The effects of galangin in prepulse inhibition test and experimental schizophrenia models

Published online by Cambridge University Press:  20 October 2021

Bilgin Kaygisiz*
Affiliation:
Faculty of Medicine, Department of Medical Pharmacology, Eskisehir Osmangazi University, Eskisehir, Turkey
Sule Aydin
Affiliation:
Faculty of Medicine, Department of Medical Pharmacology, Eskisehir Osmangazi University, Eskisehir, Turkey
Engin Yildirim
Affiliation:
Faculty of Medicine, Department of Medical Pharmacology, Eskisehir Osmangazi University, Eskisehir, Turkey
Ahmet Musmul
Affiliation:
Faculty of Medicine, Department of Biostatistics, Eskisehir Osmangazi University, Eskisehir, Turkey
Kevser Erol
Affiliation:
Faculty of Medicine, Department of Medical Pharmacology, Eskisehir Osmangazi University, Eskisehir, Turkey
Fatma Sultan Kilic
Affiliation:
Faculty of Medicine, Department of Medical Pharmacology, Eskisehir Osmangazi University, Eskisehir, Turkey
*
Author for correspondence: Bilgin Kaygisiz, Email: bilginkay@yahoo.com

Abstract

Objective:

Acetylcholinesterase inhibitors are the focus of interest in the management of schizophrenia. We aimed to investigate the effects of acute galangin administration, a flavonoid compound with acetylcholinesterase inhibiting activity, on schizophrenia-associated cognitive deficits in rats and schizophrenia models in mice.

Methods:

Apomorphine-induced prepulse inhibition (PPI) disruption for cognitive functions, nicotinic, muscarinic, and serotonergic mechanism involvement, and brain acetylcholine levels were investigated in Wistar rats. Apomorphine-induced climbing, MK-801-induced hyperlocomotion, and catalepsy tests were used as schizophrenia models in Swiss albino mice. The effects of galangin were compared with acetylcholinesterase inhibitor donepezil, and typical and atypical antipsychotics haloperidol and olanzapine, respectively.

Results:

Galangin (50,100 mg/kg) enhanced apomorphine-induced PPI disruption similar to donepezil, haloperidol, and olanzapine (p < 0.05). This effect was not altered in the combination of galangin with the nicotinic receptor antagonist mecamylamine (1 mg/kg), the muscarinic receptor antagonist scopolamine (0.05 mg/kg), or the serotonin-1A receptor antagonist WAY-100635 (1 mg/kg) (p > 0.05). Galangin (50,100 mg/kg) alone increased brain acetylcholine concentrations (p < 0.05), but not in apomorphine-injected rats (p > 0.05). Galangin (50 mg/kg) decreased apomorphine-induced climbing and MK-801-induced hyperlocomotion similar to haloperidol and olanzapine (p < 0.05), but did not induce catalepsy, unlike them.

Conclusion:

We suggest that galangin may help enhance schizophrenia-associated cognitive deficits, and nicotinic, muscarinic cholinergic, and serotonin-1A receptors are not involved in this effect. Galangin also exerted an antipsychotic-like effect without inducing catalepsy and may be considered as an advantageous antipsychotic agent.

Type
Original Article
Copyright
© The Author(s), 2021. Published by Cambridge University Press on behalf of Scandinavian College of Neuropsychopharmacology

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