일시적 국소 뇌허혈을 일으킨 수컷 쥐의 뇌에서는 프로락틴이 새로운 세포 생성을 촉진하지 못할 가능성이 있다: 예비 연구
Prolaction May not Stimulate Generation of New Cells after Transient Focal Cerebral Ischemia in Adult Male Rat Brain: a Preliminary Study
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Background: Production of neuronal progenitors is usually stimulated in the forebrain subventricular zone of mice after the intracerebroventricular infusion of prolactin. As a preliminary study, we infused prolactin to the male rat brain to test the hypothesis that prolactin promotes new cell proliferation in the brain and functional recovery after focal ischemia. Methods: Male rats were subjected to intraluminal middle cerebral artery occlusion. Prolactin was administered to the surface of the brain for 5 or 14 days starting 24 or 48 hours after stroke onset at doses of 6.4 µg per day. We administered the same volume of saline to the other ischemic rats used as a control group. Some rats were killed 6 or 17 days after stroke for analysis of infarct volume and newly generated cells within the subventricular zone and the striatum. The other rats were tested for neurological recovery 24 days after stroke. Results: There was no significant difference of infarct volume among the experiment groups. Treatment with prolactin did not increase the numbers of bromodeoxyuridine-immunoreactive cells in the subventricular zone and the striatum. Treatment with prolactin did not enhance neurological recovery in all tests performed. Conclusions: In this preliminary study, prolactin did not enhance new cell generation in the male rat brain nor reduce the neurological deficits after ischemic stroke.
Abstract
Background: Production of neuronal progenitors is usually stimulated in the forebrain subventricular zone of mice after the intracerebroventricular infusion of prolactin. As a preliminary study, we infused prolactin to the male rat brain to test the hypothesis that prolactin promotes new cell proliferation in the brain and functional recovery after focal ischemia. Methods: Male rats were subjected to intraluminal middle cerebral artery occlusion. Prolactin was administered to the surface of the brain for 5 or 14 days starting 24 or 48 hours after stroke onset at doses of 6.4 µg per day. We administered the same volume of saline to the other ischemic rats used as a control group. Some rats were killed 6 or 17 days after stroke for analysis of infarct volume and newly generated cells within the subventricular zone and the striatum. The other rats were tested for neurological recovery 24 days after stroke. Results: There was no significant difference of infarct volume among the experiment groups. Treatment with prolactin did not increase the numbers of bromodeoxyuridine-immunoreactive cells in the subventricular zone and the striatum. Treatment with prolactin did not enhance neurological recovery in all tests performed. Conclusions: In this preliminary study, prolactin did not enhance new cell generation in the male rat brain nor reduce the neurological deficits after ischemic stroke.
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