RT Journal Article
SR Electronic
T1 Selective Inhibition of Kindling Development by Intraventricular Administration of TrkB Receptor Body
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1424
OP 1436
DO 10.1523/JNEUROSCI.19-04-01424.1999
VO 19
IS 4
A1 Devin K. Binder
A1 Mark J. Routbort
A1 Terence E. Ryan
A1 George D. Yancopoulos
A1 James O. McNamara
YR 1999
UL http://www.jneurosci.org/content/19/4/1424.abstract
AB 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.