Mystixin-7 mini-peptide protects ionotropic glutamatergic mechanisms against oxygen–glucose deprivation in vitro

Mokrushin, A. A.

doi:10.1016/j.npep.2015.10.004

Cited by 2 publications

(2 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This conclusion is supported by data on the protection of ionotropic glutamate receptors by using MTX in pentylenetetrazole model of ictogenesis. In this model of the glutamate excitotoxicity, the peptide reliably blocked both ictal and interictal epileptic-like activity in slices [ 21 ] and in another model has protected nerve cells against oxygen-glucose deprivation [ 22 ]. Together these data indicate that MTX possesses a broader protective potential.…”

Section: Discussionmentioning

confidence: 99%

“…Likely, due to these properties, the peptide safely blocked ictal- and interictal-like events in dose- and time-dependent manner in the pentylenetetrazole (PTZ) model of ictogenesis in brain slices [ 21 ] and protected ionotropic glutamatergic mechanisms against oxygen-glucose deprivation [ 22 ]. Based on these data, we hypothesized that MTX has a wider range of protective action on a variety of disorders of the brain, which associated with the development of glutamate excitotoxicity.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mystixin-7 Peptide Protects Ionotropic Glutamatergic Mechanisms against Glutamate-Induced Excitotoxicity In Vitro

Mokrushin

2016

International Journal of Peptides

Self Cite

View full text Add to dashboard Cite

Hyperactivation of the N-methyl-D-aspartic acid type glutamate receptors (NMDARs) causes glutamate excitotoxicity, a process potentially important for many neurological diseases. This study aims to investigate protective effects of the synthetic corticotrophin-releasing factor-like peptide, mystixin-7 (MTX), on model glutamate-induced excitotoxicity in vitro. The technique online monitoring of electrophysiological parameters (excitatory glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPAR) and NMDAR-dependent postsynaptic mechanisms) in the olfactory cortex slices was used. Application of L-glutamate in toxic concentration (20 mM) on slices evoked hyperactivation of NMDARs and weaker activation of the AMPARs. Upon further action agonist, the excessive activation of glutamate receptors was replaced by their irreversible blockade. Pretreatment of the slices using MTX in different concentrations (50 and 100 mg/mL) protected both NMDARs and AMPARs from glutamate-induced damage. An enzymatic treatment of MTX reduced hyperactivation of both NMDARs and AMPARs. The present study demonstrated that MTX minipeptide protected the functioning of both NMDARs and AMPARs against glutamate-induced damage. The MTX peptide is a prospective candidate for elaborated medication in treatment of neurological diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%