<HashMap><database>biostudies-literature</database><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>57</viewCount><searchCount>0</searchCount></scores><additional><submitter>Zheng K</submitter><funding>Intramural NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>17201-6</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3193255</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>108(41)</volume><pubmed_abstract>Although 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.</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>TrkB signaling in parvalbumin-positive interneurons is critical for gamma-band network synchronization in hippocampus.</pubmed_title><pmcid>PMC3193255</pmcid><funding_grant_id>R01 NS073930</funding_grant_id><funding_grant_id>R21 NS066235</funding_grant_id><funding_grant_id>NS050596</funding_grant_id><funding_grant_id>R01 NS050596</funding_grant_id><funding_grant_id>R56 NS050596</funding_grant_id><pubmed_authors>Zheng K</pubmed_authors><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>An JJ</pubmed_authors><pubmed_authors>Hokfelt TG</pubmed_authors><pubmed_authors>Xu B</pubmed_authors><pubmed_authors>Xu ZQ</pubmed_authors><pubmed_authors>Xu W</pubmed_authors><pubmed_authors>Fisahn A</pubmed_authors><pubmed_authors>Yang F</pubmed_authors><pubmed_authors>Lu B</pubmed_authors><view_count>57</view_count></additional><is_claimable>false</is_claimable><name>TrkB signaling in parvalbumin-positive interneurons is critical for gamma-band network synchronization in hippocampus.</name><description>Although 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.</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Oct</publication><modification>2024-12-03T20:07:09.077Z</modification><creation>2019-03-27T00:44:58Z</creation></dates><accession>S-EPMC3193255</accession><cross_references><pubmed>21949401</pubmed><doi>10.1073/pnas.1114241108</doi></cross_references></HashMap>