Biomedica : revista del Instituto Nacional de Salud · 2007
[Decreased number neurons expressing GABA in the cerebral cortex of rabies-infected mice].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Rengifo Aura Caterine, Torres-Fernández Orlando
Аннотация
INTRODUCTION: GABAergic neurons synthesize and release gamma-aminobutyric acid, the predominant inhibitory neurotransmitter in the brain. Certain clinical signs of rabies and previous experimental studies have suggested that rabies viral infections affect the host GABAergic system.
OBJECTIVE: The effect of rabies virus infection on the expression of GABA was evaluated in neurons of the mouse cerebral cortex.
MATERIALS AND METHODS: Adult mice were inoculated by intramuscular injection with the standard strain of rabies (CVS virus). The animals were sacrificed in the terminal stage of the illness and perfused with 4% paraformaldehyde and 1% glutaraldehyde. Frontal sections were obtained in a Vibratome(R) and treated with appropriate immunohistochemical reactions for identifying the GABAergic neurons in the cerebral cortex. Counts and comparative quantitative analysis of the GABA+ neurons were compared in samples of infected and normal mice.
RESULTS: In the animals infected with rabies virus, the distribution pattern of cortical GABAergic neurons was not changed, but their number diminished significantly. The mean value of GABA+ cells number in 1 microm2 of cerebral cortex was 293+/-32 in normal samples and 209+/-13 in infected samples. Despite the loss in GABA+ cell number, the average size of GABA+ cells per unit increased from 104+/-8 microm2 in normal mice to 122+/-10 microm2 in infected mice because the cell loss consisted more frequently of smaller neurons. Nevertheless, the rank of GABA+ cell sizes in infected samples was similar to normal samples.
CONCLUSION: This evidence supported the hypothesis that GABA is involved in rabies pathology.
OBJECTIVE: The effect of rabies virus infection on the expression of GABA was evaluated in neurons of the mouse cerebral cortex.
MATERIALS AND METHODS: Adult mice were inoculated by intramuscular injection with the standard strain of rabies (CVS virus). The animals were sacrificed in the terminal stage of the illness and perfused with 4% paraformaldehyde and 1% glutaraldehyde. Frontal sections were obtained in a Vibratome(R) and treated with appropriate immunohistochemical reactions for identifying the GABAergic neurons in the cerebral cortex. Counts and comparative quantitative analysis of the GABA+ neurons were compared in samples of infected and normal mice.
RESULTS: In the animals infected with rabies virus, the distribution pattern of cortical GABAergic neurons was not changed, but their number diminished significantly. The mean value of GABA+ cells number in 1 microm2 of cerebral cortex was 293+/-32 in normal samples and 209+/-13 in infected samples. Despite the loss in GABA+ cell number, the average size of GABA+ cells per unit increased from 104+/-8 microm2 in normal mice to 122+/-10 microm2 in infected mice because the cell loss consisted more frequently of smaller neurons. Nevertheless, the rank of GABA+ cell sizes in infected samples was similar to normal samples.
CONCLUSION: This evidence supported the hypothesis that GABA is involved in rabies pathology.