PMID- 26526227
OWN - NLM
STAT- MEDLINE
DCOM- 20161221
LR  - 20161230
IS  - 1532-2785 (Electronic)
IS  - 0143-4179 (Linking)
VI  - 56
DP  - 2016 Apr
TI  - Mystixin-7 mini-peptide protects ionotropic glutamatergic mechanisms against 
      oxygen-glucose deprivation in vitro.
PG  - 51-7
LID - S0143-4179(15)00111-0 [pii]
LID - 10.1016/j.npep.2015.10.004 [doi]
AB  - The aim of the present study was to explore the neuroprotective effects of the 
      mystixin-7 mini-peptide (MTX, a synthetic corticotropin-releasing-factor-like, 
      7-amino-acid peptide) on an in vitro oxygen glucose deprivation model (OGD, 
      10min). The study used a technique of on-line monitoring of changes in 
      alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor (AMPAR) and 
      N-methyl-d-aspartic acid receptor (NMDAR)-mediated field excitatory postsynaptic 
      potentials (fEPSPs) in the olfactory cortex slices in the OGD model. OGD resulted 
      in an irreversible blockade of both AMPAR and NMDAR activity. Pretreatment of 
      slices by MTX and their subsequent exposure to OGD resulted in decreased activity 
      of these postsynaptic mechanisms (AMPARs, 71%; NMDARs, 68% as compared to 
      baseline), but they were not blocked altogether. The degree protection of 
      activity of both AMPARs and NMDARs had dose-dependent manner, with a maximal 
      effect at 100mg/mL. These protective effects were retained after the removal of 
      MTX from the bathing medium. To evaluate the protective efficacy of MTX on 
      NMDARs, the slices were pretreated by MTX and exposed to OGD and then treated 
      with l-glutamate (1mM). NMDARs' response to application of l-glutamate was 
      minimal at higher concentrations of MTX and maximal at lower concentrations. 
      These findings indicate that the molecules of MTX interact with a certain amount 
      of NMDARs, and thereby protect them from the OGD. Pretreatment of slices with MTX 
      contributed to the protection of network activity against OGD and promoted the 
      development of the learning process in the form of long-term potentiation. To 
      specify the protective effects of MTX, it was denatured by trypsin. The 
      proteolytic cleavage of MTX resulted to a significant decrease in the activity of 
      both AMPARs and NMDARs against OGD as compared with that of the native peptide. 
      Together, these findings provide further insight into the protective potential of 
      the MTX mini-peptide. We believe that the data presented can be the basis for the 
      development of therapeutics MTX-based medications for the treatment of the 
      ischemic stroke.
CI  - Copyright (c) 2015 Elsevier Ltd. All rights reserved.
FAU - Mokrushin, Anatoly A
AU  - Mokrushin AA
AD  - I. P. Pavlov Institute of Physiology, Russian Academy of Science, 199034, nab. 
      Makarova, 6, Saint-Petersburg, Russia. Electronic address: mok@inbox.ru.
LA  - eng
PT  - Journal Article
DEP - 20151028
PL  - Netherlands
TA  - Neuropeptides
JT  - Neuropeptides
JID - 8103156
RN  - 0 (Oligopeptides)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (mystixin 7)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Cell Hypoxia
MH  - Corticotropin-Releasing Hormone/analogs & derivatives
MH  - Dose-Response Relationship, Drug
MH  - Excitatory Postsynaptic Potentials/drug effects
MH  - Glucose/metabolism
MH  - Hypoxia/*physiopathology/prevention & control
MH  - In Vitro Techniques
MH  - Neurons/*drug effects/*physiology
MH  - Olfactory Cortex/*drug effects/*physiology
MH  - Oligopeptides/*administration & dosage
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, AMPA/*physiology
MH  - Receptors, N-Methyl-D-Aspartate/*physiology
OTO - NOTNLM
OT  - AMPARs
OT  - Mystixin-7 mini-peptide
OT  - NMDARs
OT  - OGD
EDAT- 2015/11/04 06:00
MHDA- 2016/12/22 06:00
CRDT- 2015/11/04 06:00
PHST- 2015/05/20 00:00 [received]
PHST- 2015/10/22 00:00 [revised]
PHST- 2015/10/22 00:00 [accepted]
PHST- 2015/11/04 06:00 [entrez]
PHST- 2015/11/04 06:00 [pubmed]
PHST- 2016/12/22 06:00 [medline]
AID - S0143-4179(15)00111-0 [pii]
AID - 10.1016/j.npep.2015.10.004 [doi]
PST - ppublish
SO  - Neuropeptides. 2016 Apr;56:51-7. doi: 10.1016/j.npep.2015.10.004. Epub 2015 Oct 
      28.