Problem set 5 (10 points) Questions on the paper by Tsien et al., due Tuesday 2/24/09 at the start of class: 1) (4 Points) Previous studies have demonstrate that disruption of NMDARs in the hippocampus leads to blockade of synaptic plasticity and memory malfunction. List two earlier in vivo (in the whole animal) experiments support this idea and also talk about the limitation of these experiments. • Experiment 1: Infusion of NMDAR antagonists (AP5) into hippocampus blocks LTP and causes deficit spatial memory. (1pt) Drawback: AP5 may diffuse to other brain regions and block NMDARs there. Thus the effect doesn’t necessary happen in hippocampus. (1pt) • Experiment 2: Genetically engineered mice lacking a gene encoding a component downstream of activated NMDARs, eg. α CaMKII, have impaired LTP and deficit spatial learning. (1pt) Drawback: Global gene KO; all the functions of the gene product are affected. It is possible that memory malfunction in mutants arises from lack of the gene product in other pathways
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