Kainate postconditioning protects against neuronal dysfunction after global hypoperfusion in rat hippocampus
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1
University of Szeged, Department of Physiology, Anatomy and Neuroscience, Hungary
Ischemic postconditioning initially referred to a repetitious reperfusion performed after reperfusion for preventing ischaemic injury in both myocardial and cerebral infarction. It has evolved into a concept that can be induced by a broad range of stimuli or triggers after transient global cerebral hypoperfusion. The short and transient brain hypoperfusion resulted in an impaired LTP function in the hippocampal CA1 region. Additionally, hypoperfusion impairs memory and learning functions.
The present study was undertaken to evaluate possible neuroprotective effects of kainate against delayed neuronal death in neurons if applied two days after transient global hypoperfusion. Transient hypoperfusion was induced in rats by two-vessel occlusion (2VO) for 30 min. We used 5 groups of animals: control, 2VO 30 min and 72 hours of survival, i.p. injection of kainate (5mg/kg) 24 hours of survival, i.p. injection of kainate 48 hours of survival, 2VO 30 min and 72 hours of survival with i.p. injection of kainate applied 48 hours after 2VO.
We found neuronal disfunction at day 3 after hypoperfusion. The impaired LTP functions were also observable after i.p. kainate treatment and 24 hours as well as 48 hours of survival. If we apply the kainate 48 hours after the 2VO, the hippocampal dysfunction could be significantly averted. It is probable that de novo protein synthesis in the post-ischaemic cells play a principal role in the acquisition of the ischaemic tolerance. Hypoperfusion causes inhibition of protein synthesis in selectively vulnerable brain regions. It leads to the decrease of dendritic spine number and LTP functions.
From the results we can deduce that a sublethal second post-ischaemic event can be considered to be a trigger for the start of protein synthesis activity in post-ischaemic cells. Postconditioning probably causes a re-modulation of protective protein synthesis leading to a switch from pro-apoptotic to anti-apoptotic pathways.
Conference:
IBRO International Workshop 2010, Pécs, Hungary, 21 Jan - 23 Jan, 2010.
Presentation Type:
Poster Presentation
Topic:
Disorders of the nervous system
Citation:
Nagy
D,
Marosi
M,
Füzik
J,
Kocsis
K,
Antal
P,
Knapp
L,
Kiss
Z,
Farkas
T and
Toldi
J
(2010). Kainate postconditioning protects against neuronal dysfunction after global hypoperfusion in rat hippocampus.
Front. Neurosci.
Conference Abstract:
IBRO International Workshop 2010.
doi: 10.3389/conf.fnins.2010.10.00051
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Received:
20 Apr 2010;
Published Online:
20 Apr 2010.
*
Correspondence:
Dávid Nagy, University of Szeged, Department of Physiology, Anatomy and Neuroscience, Szeged, Hungary, david.nagy01@gmail.com