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Dopaminergic receptor antagonists attenuate memory consolidation and long‐term potentiation in guinea pig hippocampus in vivo
Author(s) -
Lee Kiera-Nicole,
Chirwa Sanika
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb513
Subject(s) - sulpiride , long term potentiation , dopaminergic , memory consolidation , pharmacology , antagonist , dopamine receptor , dopamine , saline , guinea pig , sch 23390 , dopamine antagonist , medicine , chemistry , endocrinology , hippocampus , neuroscience , biology , receptor
We examined the effects of dopamine D1 and D2 receptor antagonists on memory consolidation and long‐term potentiation (LTP, a cellular correlate for memory). Thus we conducted behavior tests in male guinea pigs (150–200 g) using customized Phenotyper home cages and Ethovision XT software from Noldus. Treatment with 0.25 mg/kg SCH23390 (D1R antagonist, n=6) or 1 mg/kg sulpiride (D2R antagonist, n=5) did not alter locomotor activity relative to pre‐drug or saline controls (n=4). We also found that injections of SCH23390 (n=6) or sulpiride (n=5) soon after familiarization to two similar objects, in the novel object recognition test, blocked subsequent discrimination for novel objects when tested after 5‐hours. By contrast guinea pigs treated with saline (n=8) showed robust discrimination for novel objects indicating memory consolidation. In addition, if drugs were given within 1 min after tetanic stimulation (100 Hz, 1 sec; 3 trains), this decreased the success rate for expression of LTP, in vivo, in SCH23390 (2 of 6) and sulpiride (2 of 6) treated guinea pigs; success rates were higher in saline controls (5 of 8). When LTP was expressed, its maintenance was attenuated in guinea pigs treated with SCH23390 and sulpiride but not saline. Our data suggest memory consolidation and LTP share common processes which partly require early dopaminergic signaling for stabilization.(Supported by NIH grants DA021471 and NS061201)