Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/12652
Title: Role of the brain-derived neurotrophic factor at glutamatergic synapses
Authors: Carvalho, A. L. 
Caldeira, M. V. 
Santos, S. D. 
Duarte, C. B. 
Keywords: BDNF; TrkB; Glutamate; AMPA receptors; NMDA receptors; Spine density; Synaptic plasticity
Issue Date: Mar-2008
Publisher: Nature Publishing Group
Citation: British Journal of Pharmacology. 153 (2008) S310-S324
Abstract: The neurotrophin brain-derived neurotrophic factor (BDNF) plays an important role in the activity-dependent regulation of synaptic structure and function, particularly of the glutamatergic synapses. BDNF may be released in the mature form, which activates preferentially TrkB receptors, or as proBDNF, which is coupled to the stimulation of the p75(NTR). In the mature form BDNF induces rapid effects on glutamate release, and may induce short- and long-term effects on the postsynaptic response to the neurotransmitter. BDNF may affect glutamate receptor activity by inducing the phosphorylation of the receptor subunits, which may also affect the interaction with intracellular proteins and, consequently, their recycling and localization to defined postsynaptic sites. Stimulation of the local protein synthesis and transcription activity account for the delayed effects of BDNF on glutamatergic synaptic strength. Several evidences show impaired synaptic plasticity of glutamatergic synapses in diseases where compromised BDNF function has been observed, such as Huntington's disease, depression, anxiety, and the BDNF polymorphism Val66Met, suggesting that upregulating BDNF-activated pathways may be therapeutically relevant. This review focuses on recent advances in the understanding of the regulation of the glutamatergic synapse by BDNF, and its implications in synaptic plasticity
URI: http://hdl.handle.net/10316/12652
ISSN: 0007-1188
Rights: openAccess
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais

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