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WOODRUFF-PAK
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Tytuł oryginału:
Nefiracetam ameliorates associative learning impairment in the scopolamine-injected older rabbit.
Autorzy:
Pak
Jonathan T.,
Green
John T.,
Heifets
Boris,
Pak
Michelle H.,
Woodruff-Pak
Diana S.
Źródło:
Med. Sci. Monitor 2002: 8 (4) s.BR105-BR112, il., bibliogr. 27 poz.
Sygnatura GBL:
313,278
Hasła klasyfikacyjne GBL:
psychiatria i psychologia
farmacja
Typ dokumentu:
praca doświadczalna
tytuł obcojęzyczny
Wskaźnik treści:
zwierzęta
króliki
płeć żeńska
Streszczenie angielskie:
The cognition-enhancing drug, nefiracetam, is in Phase III clinical trials to treate memory impairment in Alzheimer's disease (AD). Nefiracetam ameliorates acquisition of delay eyeblink classical conditioning in older rabbits, a form of associative learning with striking behavioral and neurobiological similarities in rabbits and humans. In both species, delay eyeblink conditioning engages the septo-hippocampal cholinergic system and is disrupted when the cholinergic system is antagonized. Delay eyeblink classical conditioning is impaired in normal aging and severely disrupted in AD. To test further the efficacy of nefiracetam in an animal model that mimics some of the neurobiological and behavioral effects present in AD, we tested 56 older rabbits assigned to 7 treatment groups in the 750 ms delay eyeblink conditioning procedure. Older rabbits were injected with 1.5 mg/kg scopolamine to simulate disrutpion of the cholinergic system in AD. Three doses of nefiracetam (5, 10, or 15 mg/kg) were also injected in older rabbits receiving 1.5 mg/kg scopolamine. Control groups were treated with 1.5 mg/kg scopolamine + vehicle, wehicle alone, or explicitly unpaired presentations of conditioning stimuli and vehicle or 1.5 mg/kg scopolamine + 15 mg/kg nefiracetam. Rabbits injected with 1.5 mg/kg scopolamine alone were impaired, but a dose of 15 mg/kg nefiracetam reversed significantly the behavioral impairment. Nefiracetam had ameliorating effects on a task impaired in AD in an animal model of AD: older rabbits with cholinergic system antagonism.
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