Molecular motor KIF3B in the prelimbic cortex constrains the consolidation of contextual fear memory

Molecular and cellular mechanisms underlying the role of the prelimbic cortex in contextual fear memory remain elusive. Here we examined the kinesin family of molecular motor proteins (KIFs) in the prelimbic cortex for their role in mediating contextual fear, a form of associative memory. KIFs function as critical mediators of synaptic transmission and plasticity by their ability to modulate microtubule function and transport of gene products. However, the regulation and function of KIFs in the prelimbic cortex insofar as mediating memory consolidation is not known. We find that within one hour of contextual fear conditioning, the expression of KIF3B is upregulated in the prelimbic but not the infralimbic cortex. Importantly, lentiviral-mediated knockdown of KIF3B in the prelimbic cortex produces deficits in consolidation while reducing freezing behavior during extinction of contextual fear. We also find that the depletion of KIF3B increases spine density within prelimbic neurons. Taken together, these results illuminate a key role for KIF3B in the prelimbic cortex as far as mediating contextual fear memory.

Automated summary

The study reveals that KIF3B plays a crucial role in mediating contextual fear memory in the prelimbic cortex, as upregulation of KIF3B expression and lentiviral-mediated knockdown of KIF3B both have significant effects on memory consolidation and extinction behavior. Additionally, depletion of KIF3B leads to increased spine density in prelimbic neurons, further highlighting the importance of KIF3B in synaptic plasticity and memory formation.