Combined treatment with pantothenic acid derivatives and memantine alleviates scopolamine-induced amnesia in rats: The involvement of the thiol redox state and coenzyme A


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Аннотация

Free-radical-mediated processes are involved in a variety of physiological events, while oxidative stress and related redox deregulation are implicated in various pathological events. Tripeptide glutathione plays an important role in the antioxidant defense of the brain, particularly in the maintenance of the optimal redox state in neurons and glial cells. We studied the combined effects of pantothenic acid derivatives, pantothenol and calcium pantothenate, and memantine, which is a glutamate receptor antagonist that is widely used for the treatment of dementia, on amnesia induced by scopolamine in rats. Scopolamine induced amnesia in rats; however, unexpectedly, this effect was even more expressed in the memantine-pretreated animals. Memory impairments were less manifested in the rats that were pretreated with memantine in combination with panthenol or calcium pantothenate. The detrimental scopolamine effect on memory was accompanied by significant depletions of glutathione and coenzyme A in the brain. While memantine recovered the glutathione status to some extent, it nevertheless further aggravated the scopolamine influence on coenzyme A levels. An alleviation of scopolamine-induced memory impairments that was observed after combined pretreatment with memantine and panthenol or calcium pantothenate was accompanied by a normalization of coenzyme A levels, while the effects on glutathione redox did not correlate with the behavioral data.

Авторлар туралы

M. Stepanichev

Institute of Higher Nervous Activity and Neurophysiology

Email: nata_gul@pisem.net
Ресей, Moscow

D. Markov

Institute of Higher Nervous Activity and Neurophysiology

Email: nata_gul@pisem.net
Ресей, Moscow

S. Freiman

Institute of Higher Nervous Activity and Neurophysiology

Email: nata_gul@pisem.net
Ресей, Moscow

O. Frolova

Institute of Higher Nervous Activity and Neurophysiology

Email: nata_gul@pisem.net
Ресей, Moscow

S. Omelyanchik

Institute of Biochemistry of Biologically Active Compounds

Email: nata_gul@pisem.net
Белоруссия, Grodno

T. Borodina

Institute of Biochemistry of Biologically Active Compounds

Email: nata_gul@pisem.net
Белоруссия, Grodno

M. Novikova

Institute of Higher Nervous Activity and Neurophysiology

Email: nata_gul@pisem.net
Ресей, Moscow

N. Kanunnikova

Grodno State Medical University

Email: nata_gul@pisem.net
Белоруссия, Grodno

M. Onufriev

Institute of Higher Nervous Activity and Neurophysiology

Email: nata_gul@pisem.net
Ресей, Moscow

A. Moiseenok

Institute of Biochemistry of Biologically Active Compounds

Email: nata_gul@pisem.net
Белоруссия, Grodno

N. Gulyaeva

Institute of Higher Nervous Activity and Neurophysiology

Хат алмасуға жауапты Автор.
Email: nata_gul@pisem.net
Ресей, Moscow

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