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Acta Physiologica Congress

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Acta Physiologica 2012; Volume 206, Supplement 692
The 63rd National Congress of the Italian Physiological Society
9/21/2012-9/23/2012
Verona, Italy


MODULATION OF THE COUGH REFLEX WITHIN THE CAUDAL NUCLEUS TRACTUS SOLITARII BY ERK1/2 ACTIVATION IN THE RABBIT
Abstract number: P1.38

MUTOLO1 D, BONGIANNI1 F, CINELLI1 E, GIOVANNINI2 MG, PANTALEO1 T

1Dipartimento di Scienze Fisiologiche, Univ. degli Studi di Firenze, Firenze, Italy
2Dipartimento di Farmacologia Preclinica e Clinica, Univ. degli Studi di Firenze, Firenze, Italy

The caudal nucleus tractus solitarii (cNTS), the first relay medullary station of cough-related afferents, has been shown to be a site of action of some centrally acting antitussive agents. A role of ERK1/2 has been suggested in central processing of nociceptive inputs. Because pain and cough share similar features, we investigated whether ERK1/2 activation could also be involved in the central transduction of tussive inputs. The present research was undertaken on pentobarbitone anesthetized, spontaneously breathing rabbits by using microinjections (30-50 nl) of an inhibitor of ERK1/2 activation (U0126) into the cNTS. Bilateral microinjections of 25 mM U0126 caused rapid and reversible reductions in the cough responses induced by both mechanical and chemical (citric acid) stimulation of the tracheobronchial tree. At the higher concentration (50 mM), U0126 completely suppressed the cough reflex without affecting the Breuer-Hering inflation reflex, the pulmonary chemoreflex and the sneeze reflex. Bilateral microinjections of 50 mM U0126 into the caudal ventral respiratory group did not cause appreciable effects. This is the first study that provides evidence that ERK1/2 activation within the cNTS is required for the mediation of cough reflex responses in the anesthetized rabbit. These results suggest a role for ERK1/2 pathway in the processing of tussive inputs by nontranscriptional mechanisms, given the short time lapsed from ERK1/2 inhibition and cough response suppression.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 692 :P1.38

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