PMID- 15869941
OWN - NLM
STAT- MEDLINE
DCOM- 20050715
LR  - 20220309
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 193
IP  - 2
DP  - 2005 Jun
TI  - Tumor necrosis-factor-alpha (TNF-alpha) induces rapid insertion of Ca2+-permeable 
      alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA)/kainate (Ca-A/K) 
      channels in a subset of hippocampal pyramidal neurons.
PG  - 384-93
AB  - The presence of cell surface Ca2+ permeable 
      alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA)/kainate (Ca-A/K) 
      channels on subsets of central neurons influences both normal physiological 
      function and vulnerability to excitotoxicity. Factors that regulate the formation 
      and membrane insertion of Ca-A/K channels, however, are poorly understood. 
      Recently, the cytokine tumor necrosis factor-alpha (TNF-alpha) was shown to 
      increase the cell surface expression of an AMPA receptor (AMPAR) subunit (GluR1) 
      and to potentiate vulnerability to AMPAR-mediated injury. In this study, we 
      examined the possibility that TNF-alpha might also increase numbers of functional 
      Ca-A/K channels. In acute hippocampal slice preparations, TNF-alpha appeared to 
      increase Ca-A/K channel numbers in pyramidal neurons (HPNs), as assessed using a 
      histochemical stain based on kainate-induced uptake of Co2+ ions (Co2+ labeling). 
      In dissociated hippocampal neuronal cultures, TNF-alpha exposure (6 nM, 15 min) 
      induced a rapid increase in cell surface levels not only of GluR1, but also of 
      the AMPAR subunit GluR2, on most neurons, without evident new protein synthesis. 
      Furthermore, consistent with the slice studies, fluorescence Ca2+ imaging 
      techniques revealed an increase in numbers of Ca-A/K channels on what appeared to 
      be a subset of HPNs. These observations are the first to provide evidence for the 
      rapid upregulation of neuronal Ca-A/K channels in response to a cytokine or any 
      other soluble factor, and provide a novel mechanism through which TNF-alpha may 
      modulate both synaptic function and neuronal vulnerability.
FAU - Ogoshi, Fumio
AU  - Ogoshi F
AD  - Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, 
      CA 92697-4292, USA.
FAU - Yin, Hong Zhen
AU  - Yin HZ
FAU - Kuppumbatti, Yuvarani
AU  - Kuppumbatti Y
FAU - Song, Bora
AU  - Song B
FAU - Amindari, Simin
AU  - Amindari S
FAU - Weiss, John H
AU  - Weiss JH
LA  - eng
GR  - 5T32NS07444/NS/NINDS NIH HHS/United States
GR  - AG00836/AG/NIA NIH HHS/United States
GR  - NS30884/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Aniline Compounds)
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Fluo 4)
RN  - 0 (Protein Subunits)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Glutamate)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Xanthenes)
RN  - 3G0H8C9362 (Cobalt)
RN  - 77521-29-0 (alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - EC 4.1.1.15 (Glutamate Decarboxylase)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Aniline Compounds/metabolism
MH  - Animals
MH  - Animals, Newborn
MH  - Blotting, Northern/methods
MH  - Blotting, Western/methods
MH  - Calcium/*metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2
MH  - Calcium-Calmodulin-Dependent Protein Kinases/metabolism
MH  - Cells, Cultured
MH  - Cobalt/pharmacokinetics
MH  - Diagnostic Imaging/methods
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Gene Expression Regulation/drug effects
MH  - Glutamate Decarboxylase/metabolism
MH  - Hippocampus/*cytology
MH  - Immunohistochemistry/methods
MH  - In Vitro Techniques
MH  - Mice
MH  - Protein Subunits/genetics/metabolism
MH  - Pyramidal Cells/*drug effects/metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Receptors, Glutamate/genetics/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Xanthenes/metabolism
MH  - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology
EDAT- 2005/05/05 09:00
MHDA- 2005/07/16 09:00
CRDT- 2005/05/05 09:00
PHST- 2004/09/20 00:00 [received]
PHST- 2004/12/17 00:00 [revised]
PHST- 2004/12/28 00:00 [accepted]
PHST- 2005/05/05 09:00 [pubmed]
PHST- 2005/07/16 09:00 [medline]
PHST- 2005/05/05 09:00 [entrez]
AID - S0014-4886(04)00540-0 [pii]
AID - 10.1016/j.expneurol.2004.12.026 [doi]
PST - ppublish
SO  - Exp Neurol. 2005 Jun;193(2):384-93. doi: 10.1016/j.expneurol.2004.12.026.