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Delayed Administration of Tat-HA-NR2B9c Promotes Recovery After Stroke in Rats.

Abstract：

BACKGROUND AND PURPOSE:Previous studies reported that Tat-NR2B9c, a peptide disrupting the N-methyl-d-aspartate receptor-postsynaptic density protein-95 interaction, reduced ischemic damage in the acute phase after stroke. However, its effect in the subacute phase is unknown. The aim of this study is to determine whether disrupting the N-methyl-d-aspartate receptor-postsynaptic density protein-95 interaction in the subacute phase promotes recovery after stroke. METHODS:Studies were performed on Sprague-Dawley rats or nNOS(-/-) mice, and experimental ischemic stroke was induced by middle cerebral artery occlusion. Animals were treated with drugs starting at day 4 after ischemia. Sensorimotor functions and spatial learning and memory ability were assessed after drug treatment. Then, rats were euthanized for morphological observation and biochemical tests. RESULTS:Disrupting the N-methyl-d-aspartate receptor-postsynaptic density protein-95 interaction with Tat-HA-NR2B9c significantly ameliorated the ischemia-induced impairments of spatial memory and sensorimotor functions in rats during subacute stage but did not improve stroke outcome in nNOS(-/-) mice. Consistent with the functional recovery, Tat-HA-NR2B9c substantially increased neurogenesis in the dentate gyrus and dendritic spine density of mature neurons in the motor cortex of rats, meanwhile, reversed the ischemia-induced formation of S-nitrosylation-cyclin-dependent kinase 5 and increased cyclin-dependent kinase 5 activity in ipsilateral hippocampus. However, directly blocking N-methyl-d-aspartate receptors with MK-801 or Ro 25-6981 did not show the beneficial effects above. CONCLUSIONS:Dissociating N-methyl-d-aspartate receptor-postsynaptic density protein-95 coupling by Tat-HA-NR2B9c in the subacute phase after stroke promotes functional recovery, probably because of that it increases neurogenesis and dendritic spine density of mature neurons via regulating cyclin-dependent kinase 5 in the ischemic brain.

journal_name

Stroke

journal_title

Stroke

authors

Zhou HH,Tang Y,Zhang XY,Luo CX,Gao LY,Wu HY,Chang L,Zhu DY

doi

10.1161/STROKEAHA.115.008886

subject

Has Abstract

pub_date

2015-05-01 00:00:00

pages

1352-8

issue

5

eissn

0039-2499

issn

1524-4628

pii

STROKEAHA.115.008886

journal_volume

46

pub_type

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