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Cortical spreading depression confounds concentration-dependent pial arteriolar dilation during N-methyl-D-aspartate superfusion

¹Stroke and Neurovascular Regulation Laboratory, Department of Radiology; ²Stroke Service and Neuroscience Intensive Care Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts

Submitted 18 October 2005 ; accepted in final form 16 November 2005

Pial arterioles do not express N-methyl-D-aspartate (NMDA) receptors but dilate in response to topical NMDA application. We explored the mechanism underlying NMDA-mediated responses in murine pial arterioles (11–31 µm), using a closed cranial window preparation, and found that arteriolar dilation was not concentration dependent. Pial arteriolar diameter abruptly increased within 3 min of superfusing 50 or 100 µM NMDA. Dilation reached a peak within 1 min (46 ± 14%) and then declined to a plateau (28 ± 13%) for the duration of superfusion. Whereas a higher concentration (200 µM) did not produce further dilation, lower concentrations (1–10 µM) did not dilate the arterioles at all. MK-801 (10 µM) abrogated the dilation response, whereas N-nitro-L-arginine (1 mM) attenuated the peak and abolished the sustained dilation during NMDA superfusion. We determined that NMDA-induced pial arteriolar responses were evoked by cortical spreading depression, because abrupt vasodilation during 50 or 100 µM NMDA superfusion was associated with a large negative slow potential shift and electrocorticogram suppression that spread from the superfusion window to distant cortical areas. Our data suggest that the responses of pial arterioles to NMDA are caused in part by neurovascular coupling due to cortical spreading depression.

cranial window; pial arterioles; electrophysiology

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