%0 Journal Article
%T Electrophysiological Study of the Antinociception Produced by the Coapplication of (¡À)-CPP and Propentofylline in Monoarthritic Rats
%A Claudio Laurido
%A Jos¨¦ L. Mart¨ªnez
%A Francisco Morales
%J ISRN Pain
%D 2013
%R 10.1155/2013/315626
%X The NMDA receptor is central in the generation and maintenance of chronic pain. This receptor has several sites of modulation. One is the glutamate recognition site that can be blocked by (¡À)-3-(2-carboxypiperazin-yl)propyl-1-phosphoric acid or (¡À)-CPP. We investigated whether the effect of glial inhibition produced by propentophylline (PPF) can be enhanced when combined with (¡À)-CPP. We used Sprague-Dawley rats with experimental monoarthritis, administering intrathecally the ED30 for both drugs (3.97£¿¦Ìg of (¡À)-CPP and 1.42£¿¦Ìg of PPF), since this combination produces an antinociceptive supra-additive effect when used in mechanical nociception (Randall-Selitto test). The combination of (¡À)-PPF and CPP produced an antinociceptive effect which was greater than that each drug alone as tested by both the C reflex and windup. We conclude that the antinociceptive effect of the combination of (¡À)-PPF and CPP possibly generates a supra additive interaction type in monoarthritic rats. 1. Introduction Pain continues to be a clinical problem difficult to solve for a significant proportion of patients due to the incomplete knowledge we have about the adaptive changes that occur in the neural substrates of the nociceptive system and glial cells in response to episodes of persistent pain. These changes primarily are associated with chronic inflammation processes or injury to peripheral and central nerves. In a chronic inflammatory process, tissue damage induces a persistent stimulation of nociceptors, which are peripheral nerve endings of primary afferent fibers responsible for pain transmission. Chronic activation of nociceptors by different chemical mediators induces hypersensitivity or nociceptive sensitization, which is reflected in changes in the basal activation levels of neurons and altered gene transcription (plasticity). This allows the appearance of hyperalgesia or an exaggerated response to a nociceptive stimulus and allodynia, or a nociceptive response against an innocuous stimulus [1]. Great advances in this field occurred in the 1980¡¯s when two groups demonstrated that NMDA receptor antagonists inhibit the hyperexcitability of nociceptive neurons in the spinal cord induced by stimulation of C fibers [2, 3]. As mentioned above, the NMDA receptor is important in the establishment of chronic pain. However, today we know other factors that may modulate this pain, such as glial cells [4]. In the last decade numerous studies have shown that glial cells of the spinal cord have close contact with neurons, and this led to the proposed term tripartite synapses
%U http://www.hindawi.com/journals/isrn.pain/2013/315626/