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The Journal of Neuroscience, February 15, 1999, 19(4):1424-1436

Selective Inhibition of Kindling Development by Intraventricular Administration of TrkB Receptor Body

Devin K. Binder¹, Mark J. Routbort¹, Terence E. Ryan⁵, George D. Yancopoulos⁵, and James O. McNamara^{1, 2, 3, 4}

Departments of ¹ Neurobiology, ² Medicine (Neurology), ³ Pharmacology, and ⁴ Molecular Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, and ⁵ Regeneron Pharmaceuticals, Tarrytown, New York 10591

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.

Key words: neurotrophins; BDNF; kindling; epilepsy; epileptogenesis; trk receptors

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Copyright © 1999 Society for Neuroscience  0270-6474/99/1941424-13$05.00/0

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