Nitric oxide synthase inhibition does not affect somatosensory evoked potentials in the rat.
Nitric oxide synthase (NOS) inhibition reduces the regional cerebral blood flow (rCBF) responses to somatosensory stimulation. It is controversial whether this is caused by a signalling role of nitric oxide (NO) between neurons and vascular smooth muscle, or by effects of NOS inhibition on neuronal activity. We here report that more than 85% inhibition of NOS activity by topical application of the NOS inhibitor N omega-nitro-L-arginine (L-NNA) for 2 h does not affect somatosensory evoked potentials (SEPs) elicited by vibrissal deflection or electrical forepaw stimulation in choloralose anaesthetised rats equipped with a closed cranial window, whereas cerebral blood flow (CBF) responses due to these stimulation paradigms are reduced by approximately 60%. We conclude that the decrease of the regional vascular response to increased neuronal activity during NOS inhibition is not caused by a suppression of neuronal activity.
Lindauer
U
U
Department of Neurology, Humboldt University, Berlin, Germany. ulind@neuro.charite.hu-berlin.de
Megow
D
D
Schultze
J
J
Weber
J R
JR
Dirnagl
U
U
D000818:Animals; D002560:Cerebrovascular Circulation; D004558:Electric Stimulation; D005073:Evoked Potentials, Somatosensory / Q000502:physiology*; D005552:Forelimb / Q000502:physiology; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D019335:Nitroarginine / Q000494:pharmacology*; D010812:Physical Stimulation; D051381:Rats; D014738:Vibrissae / Q000502:physiology
D019335:Nitroarginine; D019001:Nitric Oxide Synthase