期刊
NEUROPHARMACOLOGY
卷 93, 期 -, 页码 164-170出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2015.01.028
关键词
Spreading depression; BOLD; fMRI; Glutamate; NMDA receptors
资金
- Academy of Finland [252511]
- University of Eastern Finland
- UEF-Brain strategic funding
- Center for International Mobility (CIMO) [TM-09-6241]
- program of competitive growth of Kazan Federal University
- Academy of Finland (AKA) [252511, 252511] Funding Source: Academy of Finland (AKA)
Cortical spreading depression (CSD) is a phenomenon implicated in migraine with aura and associated with other neurological disorders (e.g. stroke, brain trauma). Current evidence points to the essential role of NMDA receptors in CSD mechanisms. However, the roles of multiple subunits of NMDA receptors expressed in neurons, glia and blood vessels in vivo, are little explored. Using BOLD fMRI of urethane anesthetized rats as an integrative CSD readout, we tested the involvement of different NMDA receptor subtypes in CSD induction and propagation. Rats were treated with a non-selective NMDA blocker (MK-801), NR2B antagonist (ifenprodil) or a NR2A selective antagonist (TCN-201). CSD was induced during fMRI scanning by application of KCl onto the cerebral cortex and fMRI data were collected by 9.41 MRI. The non-specific NMDA antagonist MK-801 coinpletely blocked CSD, which was not observed in the NR2A group where TCN-201 did not alter the CSD features. Unexpectedly, the NR2B specific antagonist ifenprodil largely promoted the initial negative phase of the BOLD CSD response, likely due to altered neurovascular coupling. Our data suggest key roles and differential involvement of NMDA receptor subtypes in CSD generation and propagation, highlighting an important role for the NR2B subtype. (C) 2015 Elsevier Ltd. All rights reserved.
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