Changes in gene expression of D2 and D5 receptors in the thalamus and midbrain caused by a persistent painful stimulus in Parkinsonian rats

Abstract

Pain is the most common and underdiagnosed non-motor symptom in Parkinson’s disease. Dopaminergic receptors D2 and D5 have been implicated in pain modulation. In this study, the expression of D2 and D5 receptors in the midbrain and thalamus in response to a painful stimulus was evaluated. The animals were assigned to a 6-OHDA group, a Sham group and a Control group. 6-OHDA was administered to the experimental group and 2 μl of 1 % ascorbic acid to the Sham group in the substantia nigra pars compacta. The midbrain and thalamus were dissected for RT-qPCR. In the formalin test, phase 1 showed significant differences between the Sham, 6-OHDA and Control groups, while in phase 2 the 6-OHDA group presented a greater nociceptive response. In the cylinder test, the 6-OHDA group showed a reduction in the use of the left limb and both limbs. In the open-field test, the 6-OHDA group spent more time in corners and showed less exploration in the periphery and center. An increasing trend for D5 was observed in the midbrain of the 6-OHDA group and in the thalamus of the Sham group. Dopaminergic injury induced by 6-OHDA as part of the parkinsonian model alters motor function, increases anxiety, and increases nociceptive response in the persistent phase of the formalin model. In addition, a non-significant increase in D5 receptor expression in the midbrain and thalamus may suggest an adaptive response of dopaminergic signaling to persistent pain.