Recombinant BDNF Rescues Deficits in Basal Synaptic Transmission and Hippocampal LTP in BDNF Knockout Mice

TLDR

BDNF is highly expressed in hippocampal neurons and activity‑dependent, and knockout mice are used to probe its role in synaptic plasticity, though developmental absence can confound adult phenotypes. The study uses rescue experiments to separate developmental from acute BDNF requirements. Recombinant BDNF fully restores LTP and markedly improves basal synaptic transmission in BDNF knockout hippocampal slices, demonstrating an acute role for BDNF in synaptic function.

Abstract

Brain-derived neurotrophic factor (BDNF) is expressed at high levels in hippocampal neurons, and its expression is modulated by neural activity. Knockout mice can be used to study the roles of molecules like BDNF in synaptic plasticity with more molecular specificity than is possible using pharmacological approaches. Because in conventional knockouts the disrupted gene product is absent in all tissues throughout the life of the animal, developmental effects may complicate the interpretation of deficits in the adult. Rescue experiments can help to distinguish between developmental and acute requirements for the missing gene product. We here demonstrate that treatment of hippocampal slices from BDNF knockout mice with recombinant BDNF completely reverses deficits in long-term potentiation and significantly improves deficits in basal synaptic transmission at the Schaffer collateral–CA1 synapse. Thus, BDNF has an acute role in hippocampal synaptic function.