[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).