Abstract
Chronic pain damages the balance between excitation and inhibition in the sensory cortex. It has been confirmed that the activity of cortical glutamatergic pyramidal cells increases after chronic pain. However, whether the activity of inhibitory interneurons synchronized changed remains obscure, especially in in vivo conditions. In the present study, we checked the firing rate of pyramidal cells and interneurons in the anterior cingulate cortex, a main cortical area for the regulation of nociceptive information in mice with spared nerve injury by using in vivo multi-channel recording system. We found that the firing rate of pyramidal cells but not interneurons increased in the ACC, which was further confirmed by the increased FOS expression in pyramidal cells but not interneurons, in mice with neuropathic pain. Selectively high frequency stimulation of the ACC nociceptive afferent fibers only potentiated the activity of pyramidal cells either. Our results thus suggest that the increased activity of pyramidal cells contributes to the damaged E/I balance in the ACC and is important for the pain hypersensitivity in mice with neuropathic pain.
Highlights
Neuropathic pain (NP) is a chronic disease caused by a primary disease or lesion affecting the somatosensory nervous system [1, 2]
These behavioral tests results reveal that obvious mechanical allodynia, heat hyperalgesia and spontaneous pain are induced in spared nerve injury (SNI) mice
Spared nerve injury increased FOS expression in pyramidal cells but not interneurons Accumulating evidences show the involvement of anterior cingulate cortex (ACC) in the regulation of pain [3], we feel interest to check whether the ACC pyramidal cells and interneurons were simultaneously activated in SNI mice 7 days post-surgery
Summary
Neuropathic pain (NP) is a chronic disease caused by a primary disease or lesion affecting the somatosensory nervous system [1, 2]. It is well documented that anterior cingulate cortex (ACC), a forebrain structure, plays an important role for the process and regulation of neuropathic pain [3, 4]. In the ACC, it’s reported that selective activation of pyramidal neurons by using optogenetic methods decreases pain thresholds rapidly and induces allodynia, and specific inhibition of pyramidal neurons or activation of interneurons induces analgesic effects in mice [3, 9]. These results together indicate that the excitatory or inhibitory neuronal activity in the ACC significantly affect nociception and pain responses in mice
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