Alterations in acetylcholine, NMDA, benzodiazepine receptors and protein kinase C in the brain of the senescence-accelerated mouse: an animal model useful for studies on cognitive enhancers

Effects of ZSET1446/ST101 on Cognitive Deficits and Amyloid ^|^beta; Deposition in the Senescence Accelerated Prone Mouse Brain

“…receptors) are decreased in the hippocampus of SAMP8 at the ages of 9 and 12 months, respectively (22,23). Additionally, choline acetyltransferase (ChAT) activity is decreased in the hippocampus of SAMP8 at the age of 12 months (24), and the Pearson correlation test shows that cognitive function is positively correlated with the level of ChAT in the cerebral cortex, hippocampus, and forebrain of SAMP8 (25).…”

Age-related changes in the brains of senescence-accelerated mice (SAM): Association with glial and endothelial reactions

“…This morphological analysis was followed by a series of studies focusing on alterations of the cell membrane or on the numbers of neurotransmitter receptors (binding sites) (Flood et al, 1992(Flood et al, , 1993Kitamura et al, 1989Kitamura et al, , 1992Nomura et al, 1996Nomura et al, , 1997Zhao and Nomura, 1990;Zhao et al, 1992). Age-related changes were found in receptors for N-methyl-D-aspartate (NMDA), acetylcholine (M 1 ), serotonin, dopamine, opioids, and ␥-aminobutyric acid (GABA), as well as in ␣-adrenoreceptors.…”

“…Expression of nerve growth factor (NGF) was lower at early stages, but equivalent levels of brain-derived neurotrophic factor (BDNF) mRNA during postnatal development were seen in both strains. Nomura et al (1997) studied the change in [ 3 H] phorbol 12,13-dibutyrate binding to protein kinase C (PKC), and found that both cytosolic and membrane-associated forms of PKC were significantly decreased in aged SAMP8 brain. Such a decrease may alter intracellular signal transduction and underlie the abnormal behavior.…”

Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research

“…In the hippocampus of SAMP8 at 12 months, binding of [ 3 H]pirenzepine, a M 1 muscarinic receptor antagonist, was significantly lower than that in SAMR1. However, in the cerebral cortex, binding was higher in SAMP8 than in SAMR1 at 12 months (Nomura et al, 1997). In addition, SAMP8 mice show decreased release of acetylcholine (Qiu et al, 2010).…”