• Kang Zheng, Juan Ji An, Feng Yang, Weifeng Xu, Zhi-Qing David Xu, Jianyoung Wu, Tomas G M Hökfelt, André Fisahn, Baoji Xu, and Bai Lu.
• Gene, Cognition and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892-3714, USA.
• Proc. Natl. Acad. Sci. U.S.A. 2011 Oct 11; 108 (41): 17201-6.

AbstractAlthough brain-derived neurotrophic factor (BDNF) is known to regulate circuit development and synaptic plasticity, its exact role in neuronal network activity remains elusive. Using mutant mice (TrkB-PV(-/-)) in which the gene for the BDNF receptor, tyrosine kinase B receptor (trkB), has been specifically deleted in parvalbumin-expressing, fast-spiking GABAergic (PV+) interneurons, we show that TrkB is structurally and functionally important for the integrity of the hippocampal network. The amplitude of glutamatergic inputs to PV+ interneurons and the frequency of GABAergic inputs to excitatory pyramidal cells were reduced in the TrkB-PV(-/-) mice. Functionally, rhythmic network activity in the gamma-frequency band (30-80 Hz) was significantly decreased in hippocampal area CA1. This decrease was caused by a desynchronization and overall reduction in frequency of action potentials generated in PV+ interneurons of TrkB-PV(-/-) mice. Our results show that the integration of PV+ interneurons into the hippocampal microcircuit is impaired in TrkB-PV(-/-) mice, resulting in decreased rhythmic network activity in the gamma-frequency band.

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