Nicotine Administration Normalizes Behavioral and Neurophysiological Perturbations in the MAM Rodent Model of Schizophrenia

Abstract Background The present study utilized the methylazoxymethanol (MAM) neurodevelopmental rodent model of schizophrenia (SCZ) to evaluate the hypothesis that individuals with SCZ smoke in an attempt to “self-medicate” their symptoms through nicotine (NIC) intake. Methods To explore this questi...

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Bibliographic Details
Published in:The international journal of neuropsychopharmacology 2021-12, Vol.24 (12), p.979-987
Main Authors: Weeks, Jillian J, Grace, Anthony A, Sved, Alan F
Format: Article
Language:English
Subjects:
Animals
Care and treatment
Development and progression
Disease Models, Animal
Dopaminergic Neurons - drug effects
Health aspects
Hippocampus - drug effects
Male
Methylazoxymethanol Acetate - analogs & derivatives
Nicotine
Nicotine - administration & dosage
Prepulse Inhibition - drug effects
Rats
Rats, Sprague-Dawley
Regular s
Schizophrenia
Schizophrenia - drug therapy
Self Medication
Testing
Ventral Tegmental Area - drug effects
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Summary:Abstract Background The present study utilized the methylazoxymethanol (MAM) neurodevelopmental rodent model of schizophrenia (SCZ) to evaluate the hypothesis that individuals with SCZ smoke in an attempt to “self-medicate” their symptoms through nicotine (NIC) intake. Methods To explore this question, we examined the effects of acute and chronic administration of NIC in 2 established behavioral tests known to be disrupted in the MAM model: prepulse inhibition of startle and novel object recognition. Additionally, we assessed the effects of acute and chronic NIC on 2 indices of the pathophysiology of SCZ modeled by MAM, elevated dopamine neuron population activity in the ventral tegmental area and neuronal activity in the ventral hippocampus, using in vivo electrophysiological recordings. Results Our findings demonstrated that both acute and chronic administration of NIC significantly improved deficits in prepulse inhibition of startle and novel object recognition among MAM rats and normalized elevated ventral tegmental area and ventral hippocampal neuronal activity in these animals. Conclusion Together, these findings of NIC-induced improvement of deficits lend support for a “self-medication” hypothesis behind increased cigarette smoking in SCZ and illustrate the potential utility of nicotinic modulation in future pharmacotherapies for certain SCZ symptoms.
ISSN:1461-1457
1469-5111
DOI:10.1093/ijnp/pyab064