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N‐Methyl‐ d ‐Aspartate Induces Cortical Hyperemia through Cortical Spreading Depression‐Dependent and ‐Independent Mechanisms in Rats
Author(s) -
Lenti Laura,
Domoki Ferenc,
Gáspár Tamás,
Snipes James A.,
Bari Ferenc,
Busija David W.
Publication year - 2009
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1080/10739680903131510
Subject(s) - cortical spreading depression , nmda receptor , dilator , medicine , in vivo , electrophysiology , cerebral cortex , cerebral blood flow , anesthesia , somatosensory system , chemistry , biology , receptor , migraine , microbiology and biotechnology , psychiatry
Objective: N‐methyl‐ d ‐aspartate (NMDA) is a powerful cerebrovascular dilator in vivo . Cortical spreading depression (CSD) has recently been shown to contribute to the pial arteriolar dilation in mice. Our main aim was to examine the participation of CSD in the overall cerebrovascular response to NMDA in the rat. Methods: Anesthetized Wistar rats (eight weeks old) were equipped with a closed cranial window to allow topical application of NMDA (10 −5 –10 −3 M) to the parietal cortex. Cortical blood flow (CoBF) under and outside the cranial window was simultaneously monitored by using a two‐channel laser‐Doppler flowmeter. CSDs were detected by recording the changes in the cortical DC potential. Results: Concentrations of 10 −4 and 10 −3 M of NMDA evoked single CSDs associated with rapid, transient hyperemia, followed by a sustained, but reduced, increase in CoBF. The latency and magnitude of the CoBF responses were dose dependent. The higher dose resulted in shorter latency (100±5* vs. 146±11 seconds, * P <0.05; mean±standard error of the mean) and larger overall flow response (77±12* vs. 28±3% from baseline) under, but not outside, the cranial window. Conclusions : NMDA elicits dose‐dependent increases in CoBF that are composed of CSD‐dependent and ‐independent components in rats.