TY - JOUR
T1 - Age-related changes in learning and memory and cholinergic neuronal function in senescence accelerated mice (SAM)
AU - Nitta, Atsumi
AU - Naruhashi, Kazumasa
AU - Umemura, Masayuki
AU - Hasegawa, Takaaki
AU - Furukawa, Shoei
AU - Sekiguchi, Fujio
AU - Ishibashi, Kotaro
AU - Nabeshima, Toshitaka
N1 - Funding Information:
This studyw as supportedin part by grantsf rom the Ministry of Health and Welfare of Japan for GerontologicaSlc ienceR esearch( 91A-2406)a, n SRF Grant for BiomedicaRl esearcha, nd a grant from the UeharaM emorialF oundation.
PY - 1995/12/14
Y1 - 1995/12/14
N2 - The senescence-accelerated mouse (SAM) has been established as a murine model of accelerated aging. We investigated learning ability and memory in various tasks in a SAM strain, SAMPITA, and in a control strain of SAMR1TA at the ages of 20, 30 and 40 weeks. We also measured choline acetyltransferase (ChAT) and cholinesterase (ChE) activity in the brains of these mice at the same ages. In a Y-maze task, in which short-term memory can be examined, there was no difference in learning ability between SAMP1TA and SAMR1TA at any age. Ability in latent learning and passive-avoidance tasks was less in SAMP1TA at 30 weeks of age than in age-matched SAMR1TA. The level of ChAT activity in the striatum of SAMP1TA was lower, than that of SAMR1TA at the ages of 20 and 30 weeks. At the ages of 40 and 50 weeks, ChE activity in the striatum of SAMP1TA was lower than that of SAMR1TA. These results suggest that SAMP1TA has a deficit, with cholinergic neuronal dysfunction, in learning ability and memory, as shown by impairment of performance in latent learning and long-term memory, but not in short-term memory.
AB - The senescence-accelerated mouse (SAM) has been established as a murine model of accelerated aging. We investigated learning ability and memory in various tasks in a SAM strain, SAMPITA, and in a control strain of SAMR1TA at the ages of 20, 30 and 40 weeks. We also measured choline acetyltransferase (ChAT) and cholinesterase (ChE) activity in the brains of these mice at the same ages. In a Y-maze task, in which short-term memory can be examined, there was no difference in learning ability between SAMP1TA and SAMR1TA at any age. Ability in latent learning and passive-avoidance tasks was less in SAMP1TA at 30 weeks of age than in age-matched SAMR1TA. The level of ChAT activity in the striatum of SAMP1TA was lower, than that of SAMR1TA at the ages of 20 and 30 weeks. At the ages of 40 and 50 weeks, ChE activity in the striatum of SAMP1TA was lower than that of SAMR1TA. These results suggest that SAMP1TA has a deficit, with cholinergic neuronal dysfunction, in learning ability and memory, as shown by impairment of performance in latent learning and long-term memory, but not in short-term memory.
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U2 - 10.1016/0166-4328(96)00040-X
DO - 10.1016/0166-4328(96)00040-X
M3 - Article
C2 - 8788856
AN - SCOPUS:0029656211
SN - 0166-4328
VL - 72
SP - 49
EP - 55
JO - Behavioural Brain Research
JF - Behavioural Brain Research
IS - 1-2
ER -