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Mitogen-activated Protein Kinase Phosphatase-2 Deletion Impairs Synaptic Plasticity And Hippocampal-Dependent Memory

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dc.contributor.authorNor Zaihana Abdul Rahmanen_US
dc.contributor.authorSam M. Greenwooden_US
dc.contributor.authorRos R. Bretten_US
dc.contributor.authorKyoko Tossellen_US
dc.contributor.authorMark A. Unglessen_US
dc.contributor.authorRobin Plevinen_US
dc.contributor.authorTrevor J. Bushellen_US
dc.date.accessioned2024-05-28T04:32:43Z
dc.date.available2024-05-28T04:32:43Z
dc.date.issued2015
dc.description.abstractMitogen-activated protein kinases (MAPKs) regulate brain function and their dysfunction is implicated in a number of brain disorders, including Alzheimer’s disease. Thus, there is great interest in understanding the signaling systems that control MAPK function. One family of proteins that contribute to this process, the mitogen-activated protein kinase phosphatases (MKPs), directly inactivate MAPKs through dephosphorylation. Recent studies have identified novel functions of MKPs in development, the immune system, and cancer. However, a significant gap in our knowledge remains in relation to their role in brain functioning. Here, using transgenic mice where the Dusp4 gene encoding MKP-2 has been knocked out (MKP-2 / mice), we show that long-term potentiation is impaired in MKP-2 / mice compared with MKP-2 / controls whereas neuronal excitability, evoked synaptic transmission, and paired-pulse facilitation remain unaltered. Furthermore, spontaneous EPSC (sEPSC) frequency was increased in acute slices and primary hippocampal cultures prepared from MKP-2 / mice with no effect on EPSC amplitude observed. An increase in synapse number was evident in primary hippocampal cultures, which may account for the increase in sEPSC frequency. In addition, no change in ERK activity was detected in both brain tissue and primary hippocampal cultures, suggesting that the effects of MKP-2 deletion were MAPK independent. Consistent with these alterations in hippocampal function, MKP-2 / mice show deficits in spatial reference and working memory when investigated using the Morris water maze. These data show that MKP-2 plays a role in regulating hippocampal function and that this effect may be independent of MAPK signaling.en_US
dc.identifier.doihttps://www.jneurosci.org/content/jneuro/36/8/2348.full.pdf
dc.identifier.epage2354
dc.identifier.issn1529-2401
dc.identifier.issue8
dc.identifier.spage2348
dc.identifier.urihttps://oarep.usim.edu.my/handle/123456789/5847
dc.identifier.volume36
dc.language.isoen_USen_US
dc.publisherSociety for Neuroscienceen_US
dc.relation.ispartofThe Journal of Neuroscienceen_US
dc.subjecthippocampal-dependent memory; MAPK; MKP-2; sEPSC; synaptic plasticityen_US
dc.titleMitogen-activated Protein Kinase Phosphatase-2 Deletion Impairs Synaptic Plasticity And Hippocampal-Dependent Memoryen_US
dc.typeArticleen_US
dspace.entity.typePublication

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