Synaptic plasticity in the anterior cingulate cortex in acute and chronic pain

• Published in: Nature reviews. Neuroscience Vol. 17; no. 8; pp. 485 - 496
• Main Authors: Bliss, Tim V. P., Collingridge, Graham L., Kaang, Bong-Kiun, Zhuo, Min
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.08.2016; Nature Publishing Group
• Subjects: 631/378/1689/2610; 631/378/2591; 631/378/2620/410; Adaptation (Physiology); Animal Genetics and Genomics; Animals; Anxiety; Behavioral Sciences; Biological Techniques; Biomedicine; Care and treatment; Chronic pain; Chronic Pain - metabolism; Chronic Pain - physiopathology; Cingulate cortex; Gyrus Cinguli - metabolism; Gyrus Cinguli - physiopathology; Humans; Long-Term Potentiation - physiology; Memory; Neurobiology; Neuronal Plasticity - physiology; Neurons; Neurosciences; Physiological aspects; Physiology; Receptors, N-Methyl-D-Aspartate - metabolism; review-article; Risk factors; Rodents; Spinal cord; Synapses - metabolism; United Kingdom > UK; Toronto Ontario Canada; Canada
• ISSN: 1471-003X; 1471-0048; 1469-3178
• DOI: 10.1038/nrn.2016.68

Key Points The anterior cingulate cortex (ACC) plays an important part in chronic pain states. NMDA-receptor-dependent postsynaptic long-term potentiation (LTP) in the ACC sustains the affective component of the pain state. Kainate-receptor-dependent presynaptic LTP in the ACC contributes to pain-related anxiety. The mechanism for neuropathic pain is linked to the expression of LTP in the ACC. Upregulation of GluN2B-containing NMDA receptors is found in chronic neuropathic pain conditions. Calcium-stimulated adenylyl cyclase 1 is a potential target for future treatment of chronic pain and anxiety. Evidence suggests that activity in the anterior cingulate cortex (ACC) contributes to acute and chronic pain. In this article, Zhuo and colleagues review the different types of synaptic plasticity observed in the ACC and the implications of these forms of plasticity for pain processing. The anterior cingulate cortex (ACC) is activated in both acute and chronic pain. In this Review, we discuss increasing evidence from rodent studies that ACC activation contributes to chronic pain states and describe several forms of synaptic plasticity that may underlie this effect. In particular, one form of long-term potentiation (LTP) in the ACC, which is triggered by the activation of NMDA receptors and expressed by an increase in AMPA-receptor function, sustains the affective component of the pain state. Another form of LTP in the ACC, which is triggered by the activation of kainate receptors and expressed by an increase in glutamate release, may contribute to pain-related anxiety.