High intake of unsaturated, unhydrogenated fats may be protective against Alzheimer disease, whereas intake of saturated or trans-unsaturated (hydrogenated) fats may increase risk.
Transgenic mice in which the tetracycline transactivator (tTA) is driven by the forebrain-specific calcium-calmodulindependent kinase IIa promoter (CaMKIIa-tTA mice) are used to study the molecular genetics of many behaviors. These mice can be crossed with other transgenic mice carrying a transgene of interest coupled to the tetracycline-responsive promoter element to produce mice with forebrain-specific expression of the transgene under investigation. The value of using CaMKIIa-tTA mice to study behavior, however, is dependent on the CaMKIIatTA mice themselves lacking a behavioral phenotype with respect to the behaviors being studied. Here we present data that suggest CaMKIIa-tTA mice have a behavioral phenotype distinct from that of their wildtype (WT) littermates. Most strikingly, we find that CaMKIIa-tTA mice, both those with a C57BL/6NTac genetic background (B6-tTA) and those with a 129S6B6F1/Tac hybrid genetic background (F1-tTA), exhibit decreased locomotor activity compared with WT littermates that could be misinterpreted as altered anxiety-like behavior. Despite this impairment, neither B6-tTA nor F1-tTA mice perform differently than their WT littermates in two commonly used learning and memory paradigms -Pavlovian fear conditioning and Morris water maze. Additionally, we find data regarding motor coordination and balance to be mixed: B6-tTA mice, but not F1-tTA mice, exhibit impaired performance on the accelerating rotarod and both perform as well as their WT littermates on the balance beam.
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