Induced juvenile-like plasticity (iPlasticity) by pharmacological and optogenetic manipulations
Gene and Cell technology, A.I.Virtanen Institute, University of Eastern Finland, Kuopio,
Finland, Neuroscience Center, HiLIFE, University of Helsinki, Helsinki, Finland.
We have demonstrated that antidepressants reopen or induce a critical period-like plasticity
(iPlasticity), which allows brain networks to better adapt to environmental stimuli, such as
training or rehabilitation, and consequently ameliorate neuropsychiatric symptoms. It is also
known that Brain-derived neurotrophic factor (BDNF), and its receptor tyrosine kinase TrkB
have pivotal roles in iPlasticity. We have developed an optically activatable TrkB receptor
(optoTrkB) and demonstrated that optoTrkB activation in Parvalbumin-positive interneurons
of the visual cortex and pyramidal neurons in the dorsal hippocampus induced behavioral
changes, shift of ocular dominance plasticity and promoted fear erasure, respectively
(Winkel et al., Mol Psychiatry, 2021; Umemori et al., BioRxiv, 2021). Recently, I started to
work at the University of Eastern Finland as an independent researcher, and attempt to
ameliorate symptoms of animal models of Alzheimer’s disease by manipulating TrkB activity
and reverse epigenomics on causative genes. I will introduce our iPlasticity studies and
discuss our future plans.