通过脑室内给予TrkB受体抗体选择性抑制点燃发展。
Selective inhibition of kindling development by intraventricular administration of TrkB receptor body.
作者信息
Binder D K, Routbort M J, Ryan T E, Yancopoulos G D, McNamara J O
机构信息
Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
出版信息
J Neurosci. 1999 Feb 15;19(4):1424-36. doi: 10.1523/JNEUROSCI.19-04-01424.1999.
Abstract
Recent work has shown that neurotrophin gene expression is increased after seizures evoked in the kindling model of epilepsy, but whether neurotrophins regulate kindling development is as yet unclear. In this study, we attempted to block selectively the activation of distinct neurotrophin receptors throughout kindling development in the rat via chronic intracerebroventricular administration of trk receptor bodies. The efficacy and selectivity of the trk receptor bodies were established by inhibition of neurotrophin-induced trk receptor phosphorylation in pheochromocytoma (PC12) cells and primary cultures of cortical neurons. The intracerebroventricular infusion of trkB receptor body (trkB-Fc) inhibited development of kindling in comparison with that seen with saline or human IgG controls, trkA-Fc, or trkC-Fc. These results imply that activation of trkB receptors contributes to the development of kindling, a form of activity-dependent behavioral plasticity in the adult mammalian brain.
摘要
最近的研究表明，在癫痫点燃模型中诱发癫痫发作后，神经营养因子基因表达会增加，但神经营养因子是否调节点燃发展尚不清楚。在本研究中，我们试图通过慢性脑室内注射trk受体体，在大鼠整个点燃发展过程中选择性阻断不同神经营养因子受体的激活。通过抑制嗜铬细胞瘤（PC12）细胞和皮质神经元原代培养物中神经营养因子诱导的trk受体磷酸化，确定了trk受体体的有效性和选择性。与生理盐水或人IgG对照、trkA-Fc或trkC-Fc相比，脑室内注入trkB受体体（trkB-Fc）可抑制点燃发展。这些结果表明，trkB受体的激活有助于点燃的发展，点燃是成年哺乳动物大脑中一种依赖活动的行为可塑性形式。
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