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Depressive Behavior and Alterations in Receptors for Dopamine and 5-Hydroxyiryptamine in the Brain of the Senescence Accelerated Mouse (SAM)-P10.
Author(s) -
Takahiro Onodera,
Ritsuko Watanabe,
Kyi Kyi Tha,
Yuka Hayashi,
Toshihiko Murayama,
Yasunobu Okuma,
Chizuko Ono,
Yoneshiro Oketani,
Masanori Hosokawa,
Yasuyuki Nomura
Publication year - 2000
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.83.312
Subject(s) - senescence , medicine , endocrinology , quinpirole , receptor , ketanserin , dopamine , behavioural despair test , dopamine receptor d2 , psychology , hippocampus , serotonin , 5 ht receptor , biology , antidepressant
The senescence accelerated mouse (SAM) is known as a murine model of aging. SAM consists of senescence accelerated-prone mouse (SAMP) and senescence accelerated-resistant mouse (SAMR). Previous studies reported that SAMP10 exhibits age-related learning impairments and behavioral depression in a tail suspension test after 7 months. We investigated the changes in emotional behavior in a forced swimming test and in receptors for dopamine and 5-hydroxytryptamine (5-HT) in SAMP10. SAMP10 at 8 months showed an increase of immobility in the test compared with SAMR1. Treatment with desipramine (25 mg/kg, i.p., 3 days) in SAMP10 caused a decrease in immobility. In the cortex from SAMP10, [3H]quinpirole binding to D2/D3 dopamine receptors increased significantly compared with control SAMR1. In the hippocampus from SAMP10, [3H]8-hydroxy DPAT binding to 5-HT1A receptor increased. In midbrains from SAMP10, bindings of [3H]quinpirole and [3H]8-hydroxy DPAT increased. [3H]SCH23390 binding to D1/D5 receptors and [3H]ketanserin binding to 5-HT2 receptor in brain regions examined in SAMP10 were similar to those in SAMR1. The present findings represent the first neurochemical evidence of an increase of D2/D3 and 5-HT1A receptors in SAMP10. SAMP10 may be a useful model of aging associated depressive behavior.

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