Critical role of trkB receptors in reactive axonal sprouting and hyperexcitability after axonal injury.
MouseTBIPenetrating / ballistictrkB(F616A) knock-in miceSystemic administrationAdministered for 7 days after the lesion
Model: Penetrative traumatic brain injury modelled by transection of the Schaffer collateral pathway
1NMPP1 given for 7 days after the lesion reduced trkB activation, GAP43 upregulation and injury-induced hyperexcitability, but also prevented the recovery of CA3 to CA1 synaptic transmission seen in untreated lesioned mice.
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