IFEC   20925
INSTITUTO DE FARMACOLOGIA EXPERIMENTAL DE CORDOBA
Unidad Ejecutora - UE
artículos
Título:
HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons.
Autor/es:
CALFA G, CHAPLEAU CA, CAMPBELL S, INOUE T, MORSE SJ, LUBIN FD, POZZO-MILLER L
Revista:
HIPPOCAMPUS
Editorial:
WILEY-LISS, DIV JOHN WILEY & SONS INC
Referencias:
Año: 2012 p. 1 - 8
ISSN:
1050-9631
Resumen:
Molecular mechanisms involved in the strengthening and
formation of synapses include the activation and repression of specific
genes or subsets of genes by epigenetic modifications that do not alter the
genetic code itself. Chromatin modifications mediated by histone acetylation
have been shown to be critical for synaptic plasticity at hippocampal
excitatory synapses and hippocampal-dependent memory formation.
Considering that brain-derived neurotrophic factor (BDNF) plays an
important role in synaptic plasticity and behavioral adaptations, it is not
surprising that regulation of this gene is subject to histone acetylation
changes during synaptic plasticity and hippocampal-dependent memory
formation. Whether the effects of BDNF on dendritic spines and quantal
transmitter release require histone modifications remains less known. By
using two different inhibitors of histone deacetylases (HDACs), we describe
here that their activity is required for BDNF to increase dendritic spine density
and excitatory quantal transmitter release onto CA1 pyramidal neurons
in hippocampal slice cultures. These results suggest that histone acetylation/
deacetylation is a critical step in the modulation of hippocampal
synapses by BDNF. Thus, mechanisms of epigenetic modulation of synapse
formation and function are novel targets to consider for the amelioration
of symptoms of intellectual disabilities and neurodegenerative disorders
associated with cognitive and memory deficits. VVC 2011 Wiley Periodicals, Inc.