PMID- 30738184
OWN - NLM
STAT- MEDLINE
DCOM- 20190411
LR  - 20190411
IS  - 1095-9327 (Electronic)
IS  - 1044-7431 (Linking)
VI  - 95
DP  - 2019 Mar
TI  - Interleukin-16 inhibits sodium channel function and GluA1 phosphorylation via 
      CD4- and CD9-independent mechanisms to reduce hippocampal neuronal excitability 
      and synaptic activity.
PG  - 71-78
LID - S1044-7431(18)30174-X [pii]
LID - 10.1016/j.mcn.2019.01.002 [doi]
AB  - Interleukin 16 (IL-16) is a cytokine that is primarily associated with CD4(+) T 
      cell function, but also exists as a multi-domain PDZ protein expressed within 
      cerebellar and hippocampal neurons. We have previously shown that 
      lymphocyte-derived IL-16 is neuroprotective against excitotoxicity, but evidence 
      of how it affects neuronal function is limited. Here, we have investigated 
      whether IL-16 modulates neuronal excitability and synaptic activity in mouse 
      primary hippocampal cultures. Application of recombinant IL-16 impairs both 
      glutamate-induced increases in intracellular Ca(2+) and sEPSC frequency and 
      amplitude in a CD4- and CD9-independent manner. We examined the mechanisms 
      underlying these effects, with rIL-16 reducing GluA1 S831 phosphorylation and 
      inhibiting Na(+) channel function. Taken together, these data suggest that IL-16 
      reduces neuronal excitability and synaptic activity via multiple mechanisms and 
      adds further evidence that alternative receptors may exist for IL-16.
CI  - Copyright (c) 2019 Elsevier Inc. All rights reserved.
FAU - Hridi, Shehla U
AU  - Hridi SU
AD  - Strathclyde Institute of Pharmacy and Biomedical Sciences, University of 
      Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
FAU - Franssen, Aimee J P M
AU  - Franssen AJPM
AD  - Strathclyde Institute of Pharmacy and Biomedical Sciences, University of 
      Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
FAU - Jiang, Hui-Rong
AU  - Jiang HR
AD  - Strathclyde Institute of Pharmacy and Biomedical Sciences, University of 
      Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
FAU - Bushell, Trevor J
AU  - Bushell TJ
AD  - Strathclyde Institute of Pharmacy and Biomedical Sciences, University of 
      Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK. Electronic address: 
      trevor.bushell@strath.ac.uk.
LA  - eng
PT  - Journal Article
DEP - 20190207
PL  - United States
TA  - Mol Cell Neurosci
JT  - Molecular and cellular neurosciences
JID - 9100095
RN  - 0 (CD4 Antigens)
RN  - 0 (Interleukin-16)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Sodium Channels)
RN  - 0 (Tetraspanin 29)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - SY7Q814VUP (Calcium)
RN  - TFZ3H25BS1 (glutamate receptor ionotropic, AMPA 1)
SB  - IM
MH  - Animals
MH  - CD4 Antigens/metabolism
MH  - Calcium/metabolism
MH  - Cells, Cultured
MH  - *Excitatory Postsynaptic Potentials
MH  - Glutamic Acid/toxicity
MH  - Hippocampus/cytology
MH  - Interleukin-16/*pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurons/*drug effects/metabolism/physiology
MH  - Neuroprotective Agents/*pharmacology
MH  - Phosphorylation
MH  - Receptors, AMPA/*metabolism
MH  - Sodium Channels/*metabolism
MH  - Tetraspanin 29/metabolism
OTO - NOTNLM
OT  - CD4
OT  - Calcium signalling
OT  - IL-16
OT  - Na(+) channel
OT  - Neuron
OT  - sEPSCs
EDAT- 2019/02/10 06:00
MHDA- 2019/04/12 06:00
CRDT- 2019/02/10 06:00
PHST- 2018/06/06 00:00 [received]
PHST- 2019/01/04 00:00 [revised]
PHST- 2019/01/07 00:00 [accepted]
PHST- 2019/02/10 06:00 [pubmed]
PHST- 2019/04/12 06:00 [medline]
PHST- 2019/02/10 06:00 [entrez]
AID - S1044-7431(18)30174-X [pii]
AID - 10.1016/j.mcn.2019.01.002 [doi]
PST - ppublish
SO  - Mol Cell Neurosci. 2019 Mar;95:71-78. doi: 10.1016/j.mcn.2019.01.002. Epub 2019 
      Feb 7.