Anxiolytic-like and anxiogenic-like effects of nicotine are regulated via diverse action at β2*nicotinic acetylcholine receptors.

ABSTRACT:

Background and purpose

Nicotine dose-dependently activates or preferentially desensitizes β2 subunit containing nicotinic ACh receptors (β2*nAChRs). Genetic and pharmacological manipulations assessed effects of stimulation versus inhibition of β2*nAChRs on nicotine-associated anxiety-like phenotype.

Experimental approach

Using a range of doses of nicotine in β2*nAChR subunit null mutant mice (β2KO; backcrossed to C57BL/6J) and their wild-type (WT) littermates, administration of the selective β2*nAChR agonist, 5I-A85380, and the selective β2*nAChR antagonist dihydro-β-erythroidine (DHβE), we determined the behavioural effects of stimulation and inhibition of β2*nAChRs in the light-dark and elevated plus maze (EPM) assays.

Key results

Low-dose i.p. nicotine (0.05 mg·kg(

SUBMITTER: Anderson SM 

PROVIDER: S-EPMC4439881 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature