MicroRNA-mediated downregulation of potassium-chloride-cotransporter and vesicular γ-aminobutyric acid transporter expression in spinal cord contributes to neonatal cystitis-induced visceral pain in rats.

Pain

Authors: Zhang, Jian; Yu, James; Kannampalli, Pradeep; Nie, Linghui; Meng, Hui; Medda, Bidyut K; Shaker, Reza; Sengupta, Jyoti N; Banerjee, Banani;
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Publisher: NIH Public Access

Abstract

The neonatal period is a critical time for the development of the nociceptive neural pathways. Any alteration in the level of neuronal activity during this time may affect normal development. The intrinsic mechanism of early-life noxious stimuli-induced permanent alteration in nociceptive processing is not fully understood. It has been proposed that midbrain (RVM) descending inhibitory and facilitatory systems, which are involved in modulating pain behavior, are possibly affected. Impairment of the opioid inhibitory pathway has been implicated in the development of painful bladder disorders in animals that have experienced bladder inflammation early in life. In conjunction with these findings, we have recently reported a long-term visceral hyperalgesia and overexpression of spinal NMDA receptor subunit NR1 in adult rats following neonatally-induced cystitis. We have also documented that miRNA-mediated post-transcriptional dysregulation of GABAA-α1 receptor subunit expression in the lumbosacral (LS) spinal cord could play a role in the pathophysiology of cystitis-induced visceral pain.