作者: D.G. Herrera , H.A. Robertson
DOI: 10.1016/0306-4522(90)90081-E
关键词: Biology 、 Internal medicine 、 Antagonist 、 Lesion 、 NMDA receptor 、 Brain damage 、 Glutamate receptor 、 c-Fos 、 Atropine 、 Endocrinology 、 Nifedipine
摘要: Abstract The proto-oncogene c-fos is rapidly and transiently induced in the CNS by a variety of stimuli. Brain injury, disruption pia-arachnoid limited area, one situations that leads to dramatic increase immunoreactivity. This lesioned hemisphere. Injections atropine (25 mg/kg, i.p.), naltrexone (5 nifedipine f N -(6-aminohexyl-5-chloro-1-naphthalenesulfonamide (20 prior did not affect activation as assessed immunohistochemistry adult Sprague-Dawley rats perfused 2 h after lesion. non-competitive -methyl- d -aspartate antagonists ketamine (100 i.p.) MK-801 {(+)-5-methyl-10, 11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate} (1 3 markedly reduced activation. Phencyclicline (10 produced slight reduction damage-induced fos study suggests this particular model receptor mediated supports idea might play role plasticity and/or neurotoxic changes following brain damage.