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Altered Baseline and Nicotine-Mediated Behavioral and Cholinergic Profiles in ChAT-Cre Mouse Lines
Edison Chen1, Valeria Lallai1, Yasmine Sherafat1
1Department of Neurobiology and Behavior, University of California Irvine, Irvine, California 92697.
Summary
Transgenic ChAT-Cre mouse lines show altered behaviors, impacting nicotine self-administration and locomotor activity. Researchers must consider these genetic modifications when interpreting study results.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Transgenic rodent models are crucial for studying neural circuit function.
- Genetic modifications, including cre recombinase expression, can introduce unintended effects.
- Choline acetyltransferase (ChAT)-Cre mouse lines are widely used but require thorough characterization.
Purpose of the Study:
- To extensively characterize ChAT(BAC)-Cre and ChAT(IRES)-Cre mouse lines for behavioral and molecular differences.
- To assess the impact of genetic modifications on locomotor activity, anxiety, and nicotine-related behaviors.
- To provide guidance on interpreting data from ChAT-Cre rodent studies.
Main Methods:
- Behavioral assessments including locomotor activity, anxiety tests, drug-induced cataplexy, and operant conditioning.
- Intravenous nicotine self-administration paradigms.
- Molecular analysis of vesicular acetylcholine transporter and ChAT expression in the hippocampus.
Main Results:
- ChAT(BAC)-Cre mice showed deficits in nicotine self-administration, linked to increased hippocampal ChAT expression.
- ChAT(IRES)-Cre transgenic mice exhibited altered locomotor activity and nicotine response, with increased cre and decreased ChAT expression.
- ChAT(IRES)-Cre hemizygous mice displayed phenotypes closer to wild-type controls.
Conclusions:
- Both ChAT(BAC)-Cre and ChAT(IRES)-Cre lines present distinct behavioral and molecular alterations.
- The interpretation of research using these lines must account for line- and genotype-specific effects.
- Findings highlight the necessity of careful validation of transgenic models to understand cholinergic signaling.
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