Abstract:
RATIONALE:Prepulse inhibition (PPI) refers to the reduction of the startle response magnitude when a startling stimulus is closely preceded by a weak stimulus. PPI is commonly used to measure sensorimotor gating. In rats, the PPI reduction induced by the dopamine agonist apomorphine can be reversed by systemic administration of nicotine. A high concentration of nicotinic receptors is found in the lateral habenula (LHb), an epithalamic structure with efferent projections to brain regions involved in the modulation of PPI, which has been shown to regulate the activity of midbrain dopamine neurons. OBJECTIVES:The prospective role of nicotinic receptors in the LHb in the regulation of PPI was assessed in this study, using different pharmacological models of sensorimotor gating deficits. METHODS:Interactions between systemic amphetamine and haloperidol and intra-LHb infusions of mecamylamine (10 μg/side) or nicotine (30 μg/side) on PPI were analyzed in Experiments 1 and 2. Intra-LHb infusions of different nicotine doses (25, and 50 μg/side) and their interactions with systemic administration of amphetamine or dizocilpine on PPI were examined in Experiments 3 and 4. RESULTS:Infusions of nicotine into the LHb dose-dependently attenuated amphetamine-induced PPI deficits but had no effect on PPI disruptions caused by dizocilpine. Intra-LHb mecamylamine infusions did not affect PPI nor interact with dopaminergic manipulations. CONCLUSIONS:These results are congruent with previous reports of systemic nicotine effects on PPI, suggesting a role of the LHb in the attenuation of sensorimotor gating deficits caused by the hyperactivity of dopamine systems.
journal_name
Psychopharmacology (Berl)journal_title
Psychopharmacologyauthors
Larrauri JA,Burke DA,Hall BJ,Levin EDdoi
10.1007/s00213-015-3940-zsubject
Has Abstractpub_date
2015-08-01 00:00:00pages
3009-17issue
16eissn
0033-3158issn
1432-2072journal_volume
232pub_type
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