miR-7a alleviates the maintenance of neuropathic pain through regulation of neuronal excitability

• DOI: 10.1093/brain/awt191
• Publication Date: 2013-07-17T02:38:41Z
• Authors: Atsushi Sakai; Fumihito Saitow; Noriko Miyake; Koichi Miyake; Takashi Shimada; Hidenori Suzuki
• Keywords: Dorsal root ganglion; Nerve Injury; ATF3

Neuronal damage in the somatosensory system causes intractable chronic neuropathic pain. Plastic changes sensory neuron excitability are considered cellular basis of persistent Non-coding microRNAs modulate specific gene translation to impact on diverse functions and their dysregulation various diseases. However, significance adult neuronal disorders is still poorly understood. Here, we show that miR-7a a key functional RNA sustaining late phase pain through regulation rats. In pain, microarray analysis identified as most robustly decreased microRNA injured dorsal root ganglion. Moreover, local induction miR-7a, using an adeno-associated virus vector, neurons ganglion, suppressed established contrast, overexpression had no effect acute physiological or inflammatory Furthermore, downregulation was sufficient cause pain-related behaviours intact targeted β2 subunit voltage-gated sodium channel, associated with caused increased protein expression, independent messenger levels. Consistently, primary ganglion expression normalized long-lasting hyperexcitability nociceptive neurons. These findings demonstrate causally involved maintenance excitability, replenishment offers novel therapeutic strategy for