Abstract
Recent evidence indicates that motor cortex stimulation (MCS) is a potentially effective treatment for chronic neuropathic pain. However, the neural mechanisms underlying the attenuated hyperalgesia after MCS are not completely understood. In this study, we investigated the neural mechanism of the effects of MCS using an animal model of neuropathic pain. After 10 daily sessions of MCS, repetitive MCS reduced mechanical allodynia and contributed to neuronal changes in the anterior cingulate cortex (ACC). Interestingly, inhibition of protein kinase M zeta (PKMζ), a regulator of synaptic plasticity, in the ACC blocked the effects of repetitive MCS. Histological and molecular studies showed a significantly increased level of glial fibrillary acidic protein (GFAP) expression in the ACC after peripheral neuropathy, and neither MCS treatment nor ZIP administration affected this increase. These results suggest that repetitive MCS can attenuate the mechanical allodynia in neuropathic pain, and that the activation of PKMζ in the ACC may play a role in the modulation of neuropathic pain via MCS.
Highlights
When the sensory nervous system is affected by injury or disease, it often leads to a sense of numbness or lack of sensation
To observe the effect of repetitive motor cortex stimulation (MCS) on neuropathic pain, 10 repetitive daily sessions of MCS were performed on NP and sham NP rats 14 days after the operation
The withdrawal latency of the pre-NP + MCS notably increased during repetitive MCS (σ value = 0.753, P = 0.03)
Summary
When the sensory nervous system is affected by injury or disease, it often leads to a sense of numbness or lack of sensation. Persistent chronic pain induces significant functional and structural changes in the nervous system[4] These new synaptic formations in the CNS underlie the plasticity of neurons. Recent studies have reported that pain relief occurs progressively after the onset of MCS and persists after the stimulation has stopped[11,12,13] This effect of MCS can last from minutes to days in some patients and suggests that MCS could potentially serve as a therapy for the treatment of resistant neuropathic pain[14, 15]. Our results implicate the potential role of cortical astrocytes and ACC structural synaptic plasticity in mechanical hyperalgesia and contribute to the understanding of the mechanism of MCS-induced analgesic effects in an animal model of neuropathic pain
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