PMID- 25796564 OWN - NLM STAT- MEDLINE DCOM- 20160106 LR - 20171116 IS - 1095-953X (Electronic) IS - 0969-9961 (Linking) VI - 77 DP - 2015 May TI - Evaluation of TrkB and BDNF transcripts in prefrontal cortex, hippocampus, and striatum from subjects with schizophrenia, bipolar disorder, and major depressive disorder. PG - 220-7 LID - S0969-9961(15)00083-2 [pii] LID - 10.1016/j.nbd.2015.03.011 [doi] AB - Brain-derived neurotrophic factor (BDNF) signaling is integral to a range of neural functions, including synaptic plasticity and exhibits activity-dependent regulation of expression. As altered BDNF signaling has been implicated in multiple psychiatric diseases, here we report a quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis of mRNAs encoding TrkB, total BDNF, and the four most abundant BDNF transcripts (I, IIc, IV, and VI) in postmortem tissue from matched tetrads of subjects with schizophrenia, bipolar disorder, or major depressive disorder (MDD) and healthy comparison subjects. In all three regions examined, dorsolateral prefrontal cortex (DLPFC), associative striatum and hippocampus, total BDNF mRNA levels did not differ in any disease state. In DLPFC, BDNF IIc was significantly lower in schizophrenia relative to healthy comparison subjects. In hippocampus, BDNF I, IIc, and VI were lower in subjects with both schizophrenia and bipolar disorder relative to comparison subjects. In striatum, TrkB mRNA was lower in bipolar disorder and MDD, while BDNF IIc was elevated in MDD, relative to comparison subjects. These data highlight potential alterations in BDNF signaling in the corticohippocampal circuit in schizophrenia, and within the striatum in mood disorders. Novel therapies aimed at improving BDNF-TrkB signaling may therefore have potential to impact on a range of psychiatric disorders. CI - Copyright (c) 2015 Elsevier Inc. All rights reserved. FAU - Reinhart, Veronica AU - Reinhart V AD - Neuroscience, Pfizer Inc., Cambridge, MA, USA. FAU - Bove, Susan E AU - Bove SE AD - Life Technologies, New London, CT, USA. FAU - Volfson, Dmitri AU - Volfson D AD - Research Statistics, Pfizer Inc., Cambridge, MA, USA. FAU - Lewis, David A AU - Lewis DA AD - Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA. FAU - Kleiman, Robin J AU - Kleiman RJ AD - Translational Neuroscience Center, Boston Children's Hospital, Boston, MA, USA. FAU - Lanz, Thomas A AU - Lanz TA AD - Neuroscience, Pfizer Inc., Cambridge, MA, USA. Electronic address: Thomas.a.lanz@pfizer.com. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20150318 PL - United States TA - Neurobiol Dis JT - Neurobiology of disease JID - 9500169 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Membrane Glycoproteins) RN - 0 (RNA, Messenger) RN - EC 2.7.10.1 (Protein-Tyrosine Kinases) RN - EC 2.7.10.1 (Receptor, trkB) RN - EC 2.7.10.1 (tropomyosin-related kinase-B, human) SB - IM MH - Adult MH - Bipolar Disorder/*pathology MH - Brain/*metabolism MH - Brain-Derived Neurotrophic Factor/genetics/*metabolism MH - Corpus Striatum/metabolism MH - Depressive Disorder, Major/*pathology MH - Female MH - Hippocampus/metabolism MH - Humans MH - Male MH - Membrane Glycoproteins/*metabolism MH - Middle Aged MH - Prefrontal Cortex/metabolism MH - Protein-Tyrosine Kinases/*metabolism MH - RNA, Messenger/genetics/metabolism MH - Receptor, trkB MH - Schizophrenia/*pathology OTO - NOTNLM OT - BDNF OT - Bipolar disorder OT - Postmortem OT - RT-PCR OT - Schizophrenia OT - TrkB EDAT- 2015/03/23 06:00 MHDA- 2016/01/07 06:00 CRDT- 2015/03/23 06:00 PHST- 2014/10/30 00:00 [received] PHST- 2015/01/12 00:00 [revised] PHST- 2015/03/12 00:00 [accepted] PHST- 2015/03/23 06:00 [entrez] PHST- 2015/03/23 06:00 [pubmed] PHST- 2016/01/07 06:00 [medline] AID - S0969-9961(15)00083-2 [pii] AID - 10.1016/j.nbd.2015.03.011 [doi] PST - ppublish SO - Neurobiol Dis. 2015 May;77:220-7. doi: 10.1016/j.nbd.2015.03.011. Epub 2015 Mar 18.