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.

中文翻译：

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删除小白蛋白中间神经元中的 TrkB 会改变皮质神经动力学

已知神经营养因子如脑源性神经营养因子 (BDNF) 的信号传导可调节中间神经元的发育，但这种调节的电路效应仍不清楚。在这里，我们检查了在表达小白蛋白 (PV) 的中间神经元中删除 BDNF 受体 TrkB 对皮质电路中兴奋和抑制 (EI) 平衡的影响。在小鼠嗅觉皮层中，TrkB 缺失会损害 PV 神经元功能的多个方面，包括突触兴奋、内在兴奋性和主要神经元的神经支配模式。PV 细胞功能受损导致主要神经元响应感官输入的刺激而出现异常的尖峰模式。令人惊讶的是，受抑制的 PV 神经元功能会导致皮层回路中整体兴奋性的反常降低。我们的研究表明，