ELECTROCORTICOGRAPHIC DESYNCHRONIZATION AFTER APPLICATION OF VISCERALAND SOMATIC NOXIOUS STIMULI IN URETHANE-ANESTHETIZED RATS - EFFECT OFINTRATHECAL ADMINISTRATION OF TACHYKININ (NK-1 OR NK-2) RECEPTOR ANTAGONISTS

We investigate the electrocortical (E.Co.G) correlates of visceral (to pical capsaicin application or overdistension of the urinary bladder) and somatic (perineal pinching) painful stimulation in urethane-anesth etized rats and their modulation by intrathecal application of selecti ve tachykinins receptors (NK 1 and NK 2) antagonists. Vesical overdist ension or topical capsaicin on the bladder serosal surface produced an immediate and lasting E.Co.G. desynchronization resembling a cortical arousal. A second application of capsaicin was ineffective. Bladder c ontraction induced by topical acetylcholine did not aler E.Co.G. A des ychronized E.Co.G. was also induced by pinching of the perineal area o f the rat. Intrathecal administration of lidocanie at lumbosacral leve l abolished the E.Co.G. desynchronization induced by both visceral and somatic noxious stimulation. On the other had capsaicin-induced or ov er-distension (but not pinching-induced) E.Co.G. desynchronization dis appeared in animals systemically pretreated with capsaicin or after in trathecal administration of NK 1 tachykinin receptor antagonists such as the peptide GR 82334 or the nonpeptide RP 67580, whereas the inacti ve enantiomer RP 68651 or the nonpeptide NK 2 antagonists SR 48968 wer e ineffective, In conclusion, the experimental model described herein, allowing a quantitative analysis of the E.Co.G. correlates of viscera l and somatic noxious stimulation in urethane-anesthetized rats, provi des evidence for a specific neural pathway carrying bladder-arising vi sceral (both mechanical and chemical) nociception that uses pelvic cap saicin-sensitive afferents projecting to NK I (but not NK 2) bearing s pinal neurons and that ultimately leads to activation of cortical area s.