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ATP plays an important role as an endogenous pain mediator generating and/or modulating pain signaling from the periphery to the central nervous system. The aim of this study was to analyze the role of peripheral purinergic receptors in modulation of the nitroxidergic system at a trigeminal ganglia level by monitoring changes in nitric oxide synthase isoforms. We also evaluated Fos-positive neurons in brainstem (spinal trigeminal nucleus) and pain-related behavior. We found that local administration of the P2 purinergic receptor antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) decreased face-rubbing activity, nitric oxide synthase isoform expression in trigeminal ganglia, and Fos expression in spinal trigeminal nucleus after subcutaneous injection of formalin. These results suggest a role for peripheral P2 purinergic receptors in orofacial pain transmission through modulation of the nitroxidergic system. .

Glial cells coordinate the differentiation, metabolism, and excitability of neurons; they modulate synaptic transmission and integrate signals emanating from neurons and other glial cells. Several evidences underlying the relation between these pathways and the regulatory mechanisms of ion concentration, supporting the role of Aquaporins (AQPs) in these processes. The goal of this review is to summarize the localization of different isoforms of AQPs in relation to glial cells both in central and peripheral nervous system, underlying AQP involvement in physiological and in pathophysiological conditions such as brain edema, glioma and epilepsy.

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