TrkB modulates parvalbumin interneuron excitability and spatial memory enhancement induced by long-term rhythmic light flicker.

Long-term 40 Hz light flicker stimulation enhances parvalbumin (PV) interneuron activity in the hippocampal dentate gyrus (DG), increasing GABA release, promoting adult neurogenesis, and improving spatial memory in mice. This stimulation upregulates brain-derived neurotrophic factor (BDNF) in the DG granule cells, while the expression of its receptor, TrkB, in PV interneurons remains unchanged. Knock-down TrkB expression in PV interneurons abolished the light flicker-evoked enhancement of PV excitability and inhibitory transmission to granule cells, highlighting the critical role of TrkB signaling in the function of PV interneurons. TrkB knockdown also reduced the increase in low gamma oscillations and blocked the improvement in spatial learning induced by light flicker. Mechanistically, TrkB modulates the flicker-evoked increase in sustained (I(K)) and transient (I(A)) components of the voltage-gated K(+) channels on PV interneurons. These findings demonstrate that mBDNF-TrkB signaling mediates the excitability of PV interneurons evoked by long-term rhythmic light flicker.