Animal models having deficiency in leatning and memory

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Our project is to make animal models having deficency in learning and memory, especially in relation with Alzheimer's desease. In Alzheimer's patients it is generally known that there is degenration in Meynert nucleus which contains chelinergic neurons innervationg the frontal and parietal cortices. Standing on these considetations we carried experimaents and following resuls were obtained.I) Injection of prBMC (proplybenzilylcholine mustard), irrversible antagonist of muscatinic acetylcholine receptor, into rat brain frontal and parietal cortices caused dificit in passive avoidance learning. But its injection into the occipital cortex did not cause significant deficit. Furthermore we examine the effect of prBCM on three phases of the memory, acquisition, retention and recalling phase. By out results, acquisition and recalling phases were impaired by prBCM byt retention phase was not significantly influenced by the injection.II) In shuttle active aboicdance leatning we also observed a deficient by injection of PrBCM iinto fronatl and parieral cortices of the rat. These results indicate that impairment in cholinergin synapses caused deficits in leatning and memory process.III) In search for endfogenous substances which cause degeneration of cholinergic neurons, we found taht injection of quinolinic acid, a metablit tryptophan, into basal nucleus to Meynert caused degenetation of cholinergic neuron in rat brain cortex by estimation of CAT (choline acetyl transterase) activity. Behavioral study on learning- and memory on these quinolinatetrasted rats progressed in our laboratory new. In the other hand we found that quainolinic acid have high affinity on gultamate receprots by binding experiments with^3H-gultamate of^3H-CPP (3-(2-carboxypiperazin-4yl)-propyl-phosphoric acid). This quinolinic acid-trated rats maybe one type of deficit model animal on learning and memory.