Open AccessLong-term down-regulation of BDNF mRNA in rat hippocampal CA1 subregion correlates with PTSD-like behavioural stress response
Author(s) -
Nitsan Kozlovsky,
Michael A. Matar,
Zeev Kaplan,
Moshe Kotler,
Joseph Zohar,
Hagit Cohen
Publication year - 2007
Publication title -
international journal of neuropsychopharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 107
eISSN - 1469-5111
pISSN - 1461-1457
DOI - 10.1017/s1461145707007560
Subject(s) - tropomyosin receptor kinase b , neurotrophic factors , hippocampus , brain derived neurotrophic factor , neuroscience , neuroplasticity , psychology , hippocampal formation , corticosterone , synaptic plasticity , chronic stress , medicine , receptor , hormone
Brain-derived neurotrophic factor (BDNF) and its intracellular kinase-activating receptor TrkB, have been implicated in the neurobiological mechanisms underlying the clinical manifestations of PTSD, especially those related to synaptic efficacy and neural plasticity. BDNF interacts with components of the stress response such as corticosterone, and plays an important role in growth, maintenance and functioning of several neuronal systems. This study employed an animal model of PTSD to investigate the relationship between prevalence rates of distinct patterns of behavioural responses to predator stress, circulating levels of corticosterone and local levels of mRNA for BDNF, TrkB and two other neurotrophic factors in selected brain areas. Animals whose behaviour was extremely disrupted by exposure selectively displayed significant down-regulation of mRNA for BDNF and up-regulation of TrkB mRNA in the CA1 subregion of the hippocampus, compared to animals whose behaviour was minimally or partially affected and to unexposed controls. The response was consistent throughout the entire study only in CA1. The consistent long-term the BDNF down-regulation and TrkB up-regulation associated with extreme behavioural compromise may be associated with chronic stress-induced psychopathological processes, especially in the hippocampus. The corresponding changes in neural plasticity and synaptic functioning may mediate clinical manifestations of PTSD.