BDNF-TrkB signalling in fear learning: from genetics to neural networks
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Grabiele Musumeci
Abstract
Discovering the basic mechanisms in fear encoding and expression is important in many fields, including psychology, sociology, medicine, and neuroscience. Effective treatment for fear-based pathology depends on understanding how fear is learned and regulated. Among the molecular systems required for fear learning and amygdalar synaptic plasticity, brain derived neurtrophic factor (BDNF) and its high affinity receptor Ntrk2/TrkB have been shown to play essential roles. Therefore, we will focus this review on three main aspects; first of all, the impact of Bdnf polymorphism on fear related characteristics in humans and animal models. Secondly, we will discuss BDNF-TrkB activity regulation by epigenetic, transcriptional and post-translational events, and finally we will discuss TrkB-BDNF signalling in fear learning. BDNF-TrkB and the signalling activated in this particular form of plasticity are becoming crucial players in fear learning and memory thus highlighting these molecules as potential therapeutic targets in fear-related pathologies.
©2011 by Walter de Gruyter Berlin Boston
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- Synapses, NMDA receptor activity and neuronal Aβ production in Alzheimer’s disease
- Cytokines and depression: findings, issues, and treatment implications
- BDNF-TrkB signalling in fear learning: from genetics to neural networks
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Artikel in diesem Heft
- Publisher’s Note
- Impoverished environment, cognition, aging and dementia
- When is adult hippocampal neurogenesis necessary for learning? Evidence from animal research
- Synapses, NMDA receptor activity and neuronal Aβ production in Alzheimer’s disease
- Cytokines and depression: findings, issues, and treatment implications
- BDNF-TrkB signalling in fear learning: from genetics to neural networks
- Role of the basolateral amygdala and NMDA receptors in higher-order conditioned fear
- Allosteric modulation of ATP-gated P2X receptor channels
- Current perspectives on potential role of albumin in neuroprotection
- Spontaneously hypertensive rat (SHR) as an animal model for ADHD: a short overview
