[Experimental techniques for developing new drugs acting on dementia (1)--Senescence-accelerated mouse: neurochemical approaches and the findings].
The senescence-accelerated mouse (SAM) was established by Takeda et al (1991) as a model of accelerated aging. A P/8 strain of SAM spontaneously shows learning and memory disturbances with increasing age. Several neurochemical markers were examined in the brain of mice of P/8 strain and were compared with those in the R/1 strain as a control. Here, the author describes neurochemical methods and our findings obtained by the methods regarding measurement of: 1) the glutamate content, 2) release of glutamate and acetylcholine (ACh) from brain slices, 3) ligand bindings to neurotransmitter receptors (NMDA, muscarinic ACh), protein kinase C and glial cells and 4) mRNA expression and metabolism of amyloid precursor protein (APP).
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Department of Pharmacology, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
D000109:Acetylcholine / Q000378:metabolism; D000375:Aging / Q000378:metabolism* / Q000523:psychology; D000818:Animals; D001559:Benzhydryl Compounds / Q000494:pharmacology; D001923:Brain Chemistry; D004195:Disease Models, Animal; D005971:Glutamates / Q000378:metabolism; D008568:Memory; D051379:Mice; D008815:Mice, Inbred Strains; D011493:Protein Kinase C / Q000378:metabolism; D011976:Receptors, Muscarinic / Q000378:metabolism
D001559:Benzhydryl Compounds; D005971:Glutamates; D011976:Receptors, Muscarinic; D011493:Protein Kinase C; D000109:Acetylcholine; C031906:bifemelane