Nucleus accumbens dopaminergic neurotransmission switches its modulatory action in chronification of inflammatory hyperalgesia. (8th August 2015)

• Record Type: Journal Article
• Authors: Dias, Elayne Vieira; Sartori, César Renato; Marião, Paula Ramos; Vieira, André Schwambach; Camargo, Lilian Calili; Athie, Maria Carolina Pedro; Pagliusi, Marco Oreste; Tambeli, Claudia Herrera; Parada, Carlos Amilcar
• Is Part Of: European journal of neuroscience. Volume 42:Number 7(2015:Oct.)
• Page Start: 2380
• Page End: 2389
• Publication Date: 2015-08-08
• Subjects: Nervous system -- Periodicals; 612.8
• DOI: 10.1111/ejn.13015
• Languages: English
• ISSNs: 0953-816X

Abstract

<abstract abstract-type="main" id="ejn13015-abs-0001"> <title>Abstract</title> <p>Dopaminergic neurotransmission in the nucleus accumbens, a central component of the mesolimbic system, has been associated with acute pain modulation. As there is a transition from acute to chronic pain ('chronification'), modulatory structures may be involved in chronic pain development. Thus, this study aimed to elucidate the role of nucleus accumbens dopaminergic neurotransmission in chronification of pain. We used a rat model in which daily subcutaneous injection of prostaglandin E<sub>2</sub> in the hindpaw for 14 days induces a long‐lasting state of nociceptor sensitization that lasts for at least 30 days following the end of the treatment. Our findings demonstrated that the increase of dopamine in the nucleus accumbens by local administration of GBR12909 (0.5 nmol/0.25 μL), a dopamine reuptake inhibitor, blocked prostaglandin E<sub>2</sub>‐induced acute hyperalgesia. This blockade was prevented by a dopamine D2 receptor antagonist (raclopride, 10 nmol/0.25 μL) but not changed by a D1 receptor antagonist (SCH23390, 0.5, 3 or 10 nmol/0.25 μL), both co‐administered with GBR12909 in the nucleus accumbens. In contrast, the induction of persistent hyperalgesia was facilitated by continuous infusion of GBR12909 in the nucleus accumbens (0.021 nmol/0.5 μL/h) over 7 days of prostaglandin E<sub>2</sub> treatment. The development of persistent hyperalgesia was impaired by SCH23390 (0.125 nmol/0.5 μL/h) and raclopride (0.416 nmol/0.5 μL/h), both administered continuously in the nucleus accumbens over 7 days. Taken together, our data suggest that the chronification of pain involves the plasticity of dopaminergic neurotransmission in the nucleus accumbens, which switches its modulatory role from antinociceptive to pronociceptive.</p> </abstract>