PMID- 22858595
OWN - NLM
STAT- MEDLINE
DCOM- 20130501
LR  - 20141120
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 223
DP  - 2012 Oct 25
TI  - Tumor suppressor menin mediates peripheral nerve injury-induced neuropathic pain 
      through potentiating synaptic plasticity.
PG  - 473-85
LID - S0306-4522(12)00761-0 [pii]
LID - 10.1016/j.neuroscience.2012.07.036 [doi]
AB  - Synaptic plasticity is a crucial step in the development of central sensitization 
      in the pathogenesis of neuropathic hyperalgesia. Menin, the product of the 
      multiple endocrine neoplasia type 1 (MEN1) gene, possesses the property of 
      synaptogenesis which plays an essential role in neuronal activity. We tested the 
      contributing role of spinal menin in peripheral nerve injury-induced neuropathic 
      hypersensitivity through modulating neuronal synaptic plasticity. After approval 
      by the Institutional Animal Care and Use Committee, nociceptive responses were 
      detected with von Frey filaments and thermal plate after spared nerve injury in 
      C57BL/6 mice who were treated with either intrathecal antisense oligonucleotide 
      of MEN1 (ASO) or vehicle. Extracellular spontaneous discharge frequency, field 
      excitatory postsynaptic potential (fEPSP), and monosynaptic excitatory 
      postsynaptic currents (EPSCs) were measured electrophysiologically. Intrathecal 
      ASO alleviated nerve injury-induced mechanical and thermal hypersensitivity. 
      Upregulated spinal menin after nerve injury colocalized with NeuN in the 
      superficial laminae; genetic knockdown of spinal menin reduced nerve injury 
      induced in vivo spontaneous activity and instantaneous frequency and in vitro 
      field potentials; ASO decreased the frequency and amplitude of monosynaptic 
      EPSCs, and reduced synaptic strength and total charge. Collectively, these 
      findings highlight the role of upregulated neuronal menin in the spinal cord in 
      potentiating spinal synaptic plasticity in peripheral nerve injury-induced 
      neuropathic hypersensitivity.
CI  - Copyright (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Xu, S
AU  - Xu S
AD  - State Key Laboratory of Reproductive Medicine, Department of Anesthesiology and 
      Critical Care Medicine, Nanjing Maternity and Child Health Care Hospital, Nanjing 
      Medical University, Nanjing 210004, China.
FAU - Wu, H
AU  - Wu H
FAU - Wang, X
AU  - Wang X
FAU - Shen, X
AU  - Shen X
FAU - Guo, X
AU  - Guo X
FAU - Shen, R
AU  - Shen R
FAU - Wang, F
AU  - Wang F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120731
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Men1 protein, mouse)
RN  - 0 (Oligonucleotides, Antisense)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - EC 4.2.1.11 (Phosphopyruvate Hydratase)
SB  - IM
MH  - Action Potentials/drug effects/genetics
MH  - Analysis of Variance
MH  - Animals
MH  - Area Under Curve
MH  - Disease Models, Animal
MH  - Drug Delivery Systems
MH  - Electric Stimulation
MH  - Embryo, Mammalian
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Gene Expression Regulation/drug effects/*physiology
MH  - Hyperalgesia/drug therapy/etiology
MH  - In Vitro Techniques
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neuralgia/drug therapy/*etiology/*metabolism
MH  - Neurons/physiology
MH  - Oligonucleotides, Antisense/therapeutic use
MH  - Pain Measurement
MH  - Pain Threshold/drug effects
MH  - Peripheral Nerve Injuries/*complications
MH  - Phosphopyruvate Hydratase/metabolism
MH  - Proto-Oncogene Proteins/genetics/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Spinal Cord/cytology/drug effects/metabolism
EDAT- 2012/08/04 06:00
MHDA- 2013/05/02 06:00
CRDT- 2012/08/04 06:00
PHST- 2012/05/17 00:00 [received]
PHST- 2012/07/21 00:00 [revised]
PHST- 2012/07/24 00:00 [accepted]
PHST- 2012/08/04 06:00 [entrez]
PHST- 2012/08/04 06:00 [pubmed]
PHST- 2013/05/02 06:00 [medline]
AID - S0306-4522(12)00761-0 [pii]
AID - 10.1016/j.neuroscience.2012.07.036 [doi]
PST - ppublish
SO  - Neuroscience. 2012 Oct 25;223:473-85. doi: 10.1016/j.neuroscience.2012.07.036. 
      Epub 2012 Jul 31.