First Author | Brown KL | Year | 2010 |
Journal | Front Behav Neurosci | Volume | 4 |
Pages | 166 | PubMed ID | 20976039 |
Mgi Jnum | J:180417 | Mgi Id | MGI:5306220 |
Doi | 10.3389/fnbeh.2010.00166 | Citation | Brown KL, et al. (2010) Trace eyeblink conditioning is impaired in alpha7 but not in beta2 nicotinic acetylcholine receptor knockout mice. Front Behav Neurosci 4:166 |
abstractText | Nicotinic acetylcholine receptors (nAChRs) are essentially involved in learning and memory. A neurobiologically and behaviorally well-characterized measure of learning and memory, eyeblink classical conditioning, is sensitive to disruptions in acetylcholine neurotransmission. The two most common forms of eyeblink classical conditioning - the delay and trace paradigms - differentially engage forebrain areas densely-populated with nAChRs. The present study used genetically modified mice to investigate the effects of selective nAChR subunit deletion on delay and trace eyeblink classical conditioning. alpha7 and beta2 nAChR subunit knockout (KO) mice and their wild-type littermates were trained for 10 daily sessions in a 500-ms delay or 500-ms trace eyeblink conditioning task, matched for the interstimulus interval between conditioned stimulus and unconditioned stimulus onset. Impairments in conditioned responding were found in alpha7 KO mice trained in trace - but not delay - eyeblink conditioning. Relative to littermate controls, beta2 KO mice were unimpaired in the trace task but displayed higher levels of conditioned responding in delay eyeblink conditioning. Elevated conditioned response levels in delay-conditioned beta2 KOs corresponded to elevated levels of alpha responding in this group. These findings suggest that alpha7 nAChRs play a role in normal acquisition of 500 ms trace eyeblink classical conditioning in mice. The prominent distribution of alpha7 nAChRs in the hippocampus and other forebrain regions may account for these genotype-specific acquisition effects in this hippocampus-dependent trace paradigm. |