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J Neurophysiol 94: 1751-1760, 2005. First published May 18, 2005; doi:10.1152/jn.00223.2005
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Endogenous ATP Involvement in Mustard-Oil-Induced Central Sensitization in Trigeminal Subnucleus Caudalis (Medullary Dorsal Horn)

C. Y. Chiang 1,*, S. Zhang1,*, Y. F. Xie1, J. W. Hu1, J. O. Dostrovsky2, M. W. Salter2,3 and B. J. Sessle1,2,*

1Faculty of Dentistry and 2Department of Physiology, Faculty of Medicine, University of Toronto; and 3Programme in Brain and Behaviour, The Hospital of Sick Children, Toronto, Ontario, Canada

Submitted 1 March 2005; accepted in final form 6 May 2005

Central sensitization represents a sustained hypersensitive state of dorsal horn nociceptive neurons that can be evoked by peripheral inflammation or injury to nerves and tissues. It reflects neuroplastic changes such as increases in neuronal spontaneous activity, receptive field size, and responses to suprathreshold stimuli and a decrease in activation threshold. We recently demonstrated that purinergic receptor mechanisms in trigeminal subnucleus caudalis (Vc; medullary dorsal horn) are also involved in the initiation and maintenance of central sensitization in brain stem nociceptive neurons of trigeminal subnucleus oralis. The aim of the present study was to investigate whether endogenous ATP is involved in the development of central sensitization in Vc itself. The experiments were carried out on urethan/{alpha}-chloralose anesthetized and immobilized rats. Single neurons were recorded and identified as nociceptive-specific (NS) in the deep laminae of Vc. During continuous saline superfusion (0.6 ml/h it) over the caudal medulla, Vc neuronal central sensitization was readily induced by mustard oil application to the tooth pulp. However, this mustard-oil-induced central sensitization could be completely blocked by continuous intrathecal superfusion of the wide-spectrum P2X receptor antagonist pyridoxal-phosphate-6-azophenyl-2, 4-disulphonic acid tetra-sodium (33–100 µM) and by apyrase (an ectonucleotidase enzyme, 30 units/ml). Superfusion of the selective P2X1, P2X3 and P2X2/3 receptor antagonist 2',3'-O-(2,4,6-trinitrophenyl) adenosine 5'-triphosphate (6–638 µM) partially blocked the Vc central sensitization. The two P2X receptor antagonists did not significantly affect the baseline nociceptive properties of the Vc neurons. These findings implicate endogenous ATP as an important mediator contributing to the development of central sensitization in nociceptive neurons of the deep laminae of the dorsal horn.

Address for reprint requests and other correspondence: B. J. Sessle, Faculty of Dentistry, University of Toronto, 124 Edward St., Toronto, ON M5G 1G6, Canada (E-mail: barry.sessle{at}utoronto.ca)




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