TY - JOUR
T1 - NF-κB p50 subunit knockout impairs late LTP and alters long term memory in the mouse hippocampus
AU - Oikawa, Kensuke
AU - Odero, Gary L.
AU - Platt, Eric
AU - Neuendorff, Melanie
AU - Hatherell, Avril
AU - Bernstein, Michael J.
AU - Albensi, Benedict C.
N1 - Funding Information:
This work was funded by the National Sciences and Engineering Research Council (to B.C.A.). In addition, salary support (to K.O.) and establishment funding was supplied by the Manitoba Health Research Council (to B.C.A.) . B.C.A. is a Research Affiliate at the University of Manitoba’s Centre on Aging. We thank Drs. P. Fernyhough and F. Parkinson for a critical reading of the manuscript.
PY - 2012/5/3
Y1 - 2012/5/3
N2 - Background: Nuclear factor kappa B (NF-κB) is a transcription factor typically expressed with two specific subunits (p50, p65). Investigators have reported that NF-κB is activated during the induction of in vitro long term potentiation (LTP), a paradigm of synaptic plasticity and correlate of memory, suggesting that NF-κB may be necessary for some aspects of memory encoding. Furthermore, NF-κB has been implicated as a potential requirement in behavioral tests of memory. Unfortunately, very little work has been done to explore the effects of deleting specific NF-κB subunits on memory. Studies have shown that NF-κB p50 subunit deletion (p50 -/-) leads to memory deficits, however some recent studies suggest the contrary where p50 -/- mice show enhanced memory in the Morris water maze (MWM). To more critically explore the role of the NF-κB p50 subunit in synaptic plasticity and memory, we assessed long term spatial memory in vivo using the MWM, and synaptic plasticity in vitro utilizing high frequency stimuli capable of eliciting LTP in slices from the hippocampus of NF-κB p50 -/- versus their controls (p50 +/+).Results: We found that the lack of the NF-κB p50 subunit led to significant decreases in late LTP and in selective but significant alterations in MWM tests (i.e., some improvements during acquisition, but deficits during retention).Conclusions: These results support the hypothesis that the NF-κ p50 subunit is required in long term spatial memory in the hippocampus.
AB - Background: Nuclear factor kappa B (NF-κB) is a transcription factor typically expressed with two specific subunits (p50, p65). Investigators have reported that NF-κB is activated during the induction of in vitro long term potentiation (LTP), a paradigm of synaptic plasticity and correlate of memory, suggesting that NF-κB may be necessary for some aspects of memory encoding. Furthermore, NF-κB has been implicated as a potential requirement in behavioral tests of memory. Unfortunately, very little work has been done to explore the effects of deleting specific NF-κB subunits on memory. Studies have shown that NF-κB p50 subunit deletion (p50 -/-) leads to memory deficits, however some recent studies suggest the contrary where p50 -/- mice show enhanced memory in the Morris water maze (MWM). To more critically explore the role of the NF-κB p50 subunit in synaptic plasticity and memory, we assessed long term spatial memory in vivo using the MWM, and synaptic plasticity in vitro utilizing high frequency stimuli capable of eliciting LTP in slices from the hippocampus of NF-κB p50 -/- versus their controls (p50 +/+).Results: We found that the lack of the NF-κB p50 subunit led to significant decreases in late LTP and in selective but significant alterations in MWM tests (i.e., some improvements during acquisition, but deficits during retention).Conclusions: These results support the hypothesis that the NF-κ p50 subunit is required in long term spatial memory in the hippocampus.
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U2 - 10.1186/1471-2202-13-45
DO - 10.1186/1471-2202-13-45
M3 - Article
C2 - 22553912
AN - SCOPUS:84860375179
VL - 13
JO - BMC Neuroscience
JF - BMC Neuroscience
SN - 1471-2202
IS - 1
M1 - 45
ER -