ABSTRACT
Nitric oxide is thought to control transmitter release and neuronal activity in the spinal dorsal horn and the spinal trigeminal nucleus, where nociceptive information from extra- and intracranial tissues is processed. Extracellular impulse activity was recorded from neurons in the rat spinal trigeminal nucleus with afferent input from the cranial dura mater. In contrast to the inactive isomer D-NAME, infusion of the nitric oxide synthase inhibitor L-NAME (20 mg/kg) significantly reduced neuronal activity and increased systemic blood pressure. It is concluded that nitric oxide production contributes to the ongoing activity of sensitized neurons in the spinal trigeminal nucleus. The results suggest that nitric oxide may be involved in the generation and maintenance of primary headaches such as migraine.
Subject(s)
Action Potentials/physiology , Meninges/enzymology , Neurons/enzymology , Nitric Oxide Synthase/antagonists & inhibitors , Trigeminal Nucleus, Spinal/enzymology , Action Potentials/drug effects , Animals , Enzyme Inhibitors/pharmacology , Male , Meninges/drug effects , NG-Nitroarginine Methyl Ester/pharmacology , Neurons/drug effects , Nitric Oxide Synthase/metabolism , Rats , Rats, Wistar , Trigeminal Nucleus, Spinal/drug effectsABSTRACT
In acute experiments on nembutal-urethan-anaesthetized rats, a slow infusion of subseptic dose of lipopolysaccharide (LPS) Escherichia coli (1 mg/ml) via the right jugular vein immediately led to bradycardia and extrasystoles. Preliminary administration of 20 mg/kg N(G)-nitro-L-arginine methyl ester (L-NAME) or 30 mg/kg aminoguanidine hydrochloride prevented the LPS-induced extrasystoles but did not affect the pattern of bradycardia. We conclude that nitric oxide (NO)-ergic mechanisms are involved in provoking electrical instability of the heart in conditions of endotoxemia.
