title: A block of spinal nitric oxide synthesis leads to increased background activity predominantly in nociceptive dorsal horn neurones in the rat.
abstract: Previous studies have shown that nitric oxide (NO) has a strong influence on the background (resting) activity of dorsal horn neurones. The background activity of dorsal horn neurones is generally assumed to be responsible for the presence of paraesthesia or spontaneous pain in patients depending on the functional type of neurones that are active. However, nothing is known about a possible selective action of NO - or a lack of NO - on a particular functional class of neurone. In the present study the background activity of lumbar dorsal horn neurones was examined in anaesthetized rats before and during spinal superfusion with L-NAME, an unspecific blocker of NO synthesis. The neurones were divided into five classes: (1) low-threshold mechanosensitive (LTM) cells with deep receptive fields (LTM deep units); (2) LTM cells with cutaneous receptive fields (LTM cutaneous units) (these two classes were considered to be non-nociceptive); (3) high-threshold mechanosensitive (HTM) deep cells; (4) HTM cutaneous cells; and (5) multireceptive (MR) cutaneous cells (the last three classes were assumed to be nociceptive). HTM neurones increased the frequency of their background activity significantly during L-NAME superfusion and 80% of the initially silent neurones became active after administration of the NOS blocker. MR neurones likewise increased their background activity. In contrast, the background activity of non-nociceptive (LTM) neurones was not significantly affected. The results support previous studies showing that NO has a tonic depressing effect on the background activity of dorsal horn neurones and demonstrate for the first time that this effect is largely restricted to nociceptive neurones. Therefore, a reduction in spinal NO synthesis which often occurs during a long-lasting peripheral lesion is likely to cause increased background activity in nociceptive neurones and thus might contribute to spontaneous pain in patients.
authors.affiliation: Institut für Pharmakologie im Klinikum der Universität Kiel, Hospitalstraße 4, D-24105 Kiel, Germany Institut für Anatomie und Zellbiologie III, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Hoheisel
authors.forename: T
authors.initials: T
authors.lastname: Unger
authors.forename: S
authors.initials: S
authors.lastname: Mense
mesh_terms: D000818:Animals; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D009619:Nociceptors / Q000187:drug effects / Q000378:metabolism*; D020671:Posterior Horn Cells / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019331:NG-Nitroarginine Methyl Ester