Deletion of TrkB in parvalbumin interneurons alters cortical neural dynamics

Signaling by neurotrophins such as the brain-derived neurotrophic factor (BDNF) is known to modulate development of interneurons, but the circuit effects of this modulation remain unclear. Here, we examined the impact of deleting TrkB, a BDNF receptor, in parvalbumin-expressing (PV) interneurons on the balance of excitation and inhibition (E-I) in cortical circuits. In the mouse olfactory cortex, TrkB deletion impairs multiple aspects of PV neuronal function including synaptic excitation, intrinsic excitability, and the innervation pattern of principal neurons. Impaired PV cell function resulted in aberrant spiking patterns in principal neurons in response to stimulation of sensory inputs. Surprisingly, dampened PV neuronal function leads to a paradoxical decrease in overall excitability in cortical circuits. Our study demonstrates that, by modulating PV circuit plasticity and development, TrkB plays a critical role in shaping the evoked pattern of activity in a cortical network.

Automated summary

The deletion of the BDNF receptor TrkB in PV interneurons in the mouse olfactory cortex impairs multiple aspects of PV neuronal function, leading to aberrant spiking patterns in principal neurons and a paradoxical decrease in overall excitability in cortical circuits. This study demonstrates the critical role of TrkB in shaping the evoked pattern of activity in a cortical network by modulating PV circuit plasticity and development.