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Chronic BDNF deficiency permanently modifies excitatory synapses in the piriform cortex.

Nanobashvili, Avtandil LU ; Jakubs, Katherine LU and Kokaia, Merab LU (2005) In Journal of Neuroscience Research 81(5). p.696-705
Abstract
Brain-derived neurotrophic factor (BDNF), aside from its classic neurotrophic role in development and survival of neurons, has been shown to be involved in modification and plasticity of central synapses. In mice with BDNF gene deletion (BDNF+/-), deficits in synaptic transmission are often observed but are reversed readily by administration of BDNF, suggesting its acute effect. In support, blockade of BDNF signaling in wild-type hippocampal slices by TrkB-IgG closely reproduces synaptic alterations observed in BDNF+/- mice. We demonstrate that in BDNF+/- mice, lateral olfactory tract (LOT) synapses exhibit decreased release probability of glutamate, suggested by increased paired-pulse facilitation (PPF) of field excitatory postsynaptic... (More)
Brain-derived neurotrophic factor (BDNF), aside from its classic neurotrophic role in development and survival of neurons, has been shown to be involved in modification and plasticity of central synapses. In mice with BDNF gene deletion (BDNF+/-), deficits in synaptic transmission are often observed but are reversed readily by administration of BDNF, suggesting its acute effect. In support, blockade of BDNF signaling in wild-type hippocampal slices by TrkB-IgG closely reproduces synaptic alterations observed in BDNF+/- mice. We demonstrate that in BDNF+/- mice, lateral olfactory tract (LOT) synapses exhibit decreased release probability of glutamate, suggested by increased paired-pulse facilitation (PPF) of field excitatory postsynaptic potentials (fEPSPs), as well as by slower blocking rate of N-methyl-D-aspartate (NMIDA) receptor-mediated excitatory postsynaptic currents (EPSCs) by MK-801 in the pyramidal neurons of the piriform cortex. The changes in PPF were not mimicked in wild-type mice by acute blockade of BDNF signaling by TkrB-IgG. These data imply that BDNF deficit during development might lead to chronic changes of excitatory transmission in LOT synapses. Modification of the LOT synapses in BDNF+/- mice was associated with altered inhibitory drive onto the mitral cells from the granule and glomerular neurons, which in turn exhibited decreased renewal rate compared to that in wild-type mice. Taken together, these data suggest that BDNF deficiency can have both acute and more permanent effects on synaptic function, particularly when BDNF signaling is compromised during the early stages of brain development. In the latter case, altered synaptic properties in BDNF+/- mice could be secondary to other complex changes in the brain, e.g., cell survival/proliferation. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
patch-clamp techniques, olfactory bulb, fast PSPs, neurogenesis, synaptic plasticity
in
Journal of Neuroscience Research
volume
81
issue
5
pages
696 - 705
publisher
John Wiley & Sons
external identifiers
  • pmid:16035106
  • wos:000231580500010
  • scopus:27244445804
ISSN
1097-4547
DOI
10.1002/jnr.20578
language
English
LU publication?
yes
id
f28b40ce-a60b-4423-b0e6-d67432a59269 (old id 142001)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16035106&dopt=Abstract
date added to LUP
2007-07-16 13:46:55
date last changed
2017-01-01 07:16:24
@article{f28b40ce-a60b-4423-b0e6-d67432a59269,
  abstract     = {Brain-derived neurotrophic factor (BDNF), aside from its classic neurotrophic role in development and survival of neurons, has been shown to be involved in modification and plasticity of central synapses. In mice with BDNF gene deletion (BDNF+/-), deficits in synaptic transmission are often observed but are reversed readily by administration of BDNF, suggesting its acute effect. In support, blockade of BDNF signaling in wild-type hippocampal slices by TrkB-IgG closely reproduces synaptic alterations observed in BDNF+/- mice. We demonstrate that in BDNF+/- mice, lateral olfactory tract (LOT) synapses exhibit decreased release probability of glutamate, suggested by increased paired-pulse facilitation (PPF) of field excitatory postsynaptic potentials (fEPSPs), as well as by slower blocking rate of N-methyl-D-aspartate (NMIDA) receptor-mediated excitatory postsynaptic currents (EPSCs) by MK-801 in the pyramidal neurons of the piriform cortex. The changes in PPF were not mimicked in wild-type mice by acute blockade of BDNF signaling by TkrB-IgG. These data imply that BDNF deficit during development might lead to chronic changes of excitatory transmission in LOT synapses. Modification of the LOT synapses in BDNF+/- mice was associated with altered inhibitory drive onto the mitral cells from the granule and glomerular neurons, which in turn exhibited decreased renewal rate compared to that in wild-type mice. Taken together, these data suggest that BDNF deficiency can have both acute and more permanent effects on synaptic function, particularly when BDNF signaling is compromised during the early stages of brain development. In the latter case, altered synaptic properties in BDNF+/- mice could be secondary to other complex changes in the brain, e.g., cell survival/proliferation.},
  author       = {Nanobashvili, Avtandil and Jakubs, Katherine and Kokaia, Merab},
  issn         = {1097-4547},
  keyword      = {patch-clamp techniques,olfactory bulb,fast PSPs,neurogenesis,synaptic plasticity},
  language     = {eng},
  number       = {5},
  pages        = {696--705},
  publisher    = {John Wiley & Sons},
  series       = {Journal of Neuroscience Research},
  title        = {Chronic BDNF deficiency permanently modifies excitatory synapses in the piriform cortex.},
  url          = {http://dx.doi.org/10.1002/jnr.20578},
  volume       = {81},
  year         = {2005},
}