Toward mediated learning in mice: Differential effects of PLCβ1 gene knock-out on different modalities of associative learning in mice
- Toward mediated learning in mice: Differential effects of PLCβ1 gene knock-out on different modalities of associative learning in mice
- 김혜진; 도지혜; 고혜영
- schizophrenia; mediated learning; plcbeta1
- Issue Date
- In animal model studies, deficits in learning and memory are generally accepted as behavioral endophenotypes relevant to the negative/cognitive symptoms of schizophrenia. These include deficits in working memory (Y-maze, T-maze tasks), spatial learning (Morris water maze task), and associative learning. Earlier studies have shown that the mice lacking phospholipase Cβ1 (PLCβ1-/-), one of the genetic models for schizophrenia, have deficits in spatial learning, working memory, and fear conditioning, as well as other phenotypes relevant to positive symptoms. In the present study, we seek to verify the associative learning abilities of PLCβ1-/- mice in the modalities of associative learning other than fear conditioning (auditory CS + foot shock US): olfactory associative learning and conditioned taste aversion. PLCβ1-/- mice showed normal olfactory associative learning in an odor discrimination paradigm. PLCβ1-/- mice also performed well in a conditioned food aversion learning task which used sucrose pellets and LiCl-induced illness. PLCβ1 is expressed mainly in forebrain areas: cerebral cortex, hippocampus, amygdala, lateral septum and olfactory bulb, and thus is involved in diverse critical functions. Both fear conditioning and conditioned taste aversion learning are known to involve amygdale functions. Therefore, the amygdala component of the circuit controlling conditioned taste aversion does not seem to involve PLCβ1 function. We are currently trying to develop a new behavioral testing system that requires normal olfactory associative learning and conditioned taste aversion learning abilities.
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