BDNF/TRKB signaling is required for amphetamine-induced spinogenesis

DANELON VICTOR; HELGUERA PABLO; FERNÁNDEZ GUILLERMO; MASCO DANIEL; FERRERAS SOLEDAD; PAGLINI GABRIELA

BsAs

Congreso; 2nd FALAN Congress (Federación de Asociaciones Latinoamericanas y del Caribe de Neurociencias); 2016

Changes in behavior, which occur as a function of experience, involve the reorganization of synaptic connections (structural plasticity). Psychostimulant-induced structural plasticity has been studied in many brain regions, being the dendritic spines one of the targets of such phenomena. Our previous studies have demonstrated that Amphetamine (Amph) increases dendritic spine density in CA1 hippocampal pyramidal neurons, both in vivo and in vitro conditions; besides, Amph-induced spinogenesis require intact Cdk5 activity. Several studies suggest that neurotrophins and their receptors play an important role in synaptic plasticity and memory. BDNF and TrkB have been implicated in the regulation of dendritic spine formation and its signaling capability involves Cdk5 activity. Considering these facts, in the present study we investigated the involvement of BDNF/TrkB in Amph-induced spinogenesis. Using eYFP-expressing hippocampal pyramidal neurons maintained in culture for 17 days, we demonstrated a significant increase in dendritic spines density 1 hour after exposure to Amph. Using the TrkB-Fc approach, a BDNF extracellular scavenger, we found that Amph-induced spinogenesis requires BDNF. Blocking TrkB receptor, with K252a, abolished the Amph-increased in dendritic spine density. Taken together our results demonstrate an important role of BDNF/TrkB signaling in Amph-induced structural plasticity in hippocampus.