Some forms of cAMP-mediated long-lasting potentiation are associated with release of BDNF and nuclear translocation of phospho-MAP kinase

Long-lasting forms of synaptic plasticity like the late phase of LTP (L-LTP ) typically require an elevation of cAMP, the recruitment of the cAMP-depen dent protein kinase (PKA), and ultimately the activation of transcription a nd translation; some forms also require brain-derived neurotrophic factor ( BDNF). Both cAMP and BDNF can activate mitogen-activated protein kinase (MA PK/ERK), which also plays a role in LTP. However, little is known about the mechanisms whereby cAMP, BDNF, and MAPK interact. We find that increases i n cAMP can rapidly activate the BDNF receptor TrkB and induce BDNF-dependen t long-lasting potentiation at the Schaffer collateral-CA1 synapse in hippo campus. Surprisingly, in these BDNF-dependent forms of potentiation, which are also MAPK dependent, TrkB activation is not critical for the activation of MAPK but instead appears to modulate the subcellular distribution and n uclear translocation of the activated MAPK.