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303636 occurrences (No.74 in the rank) during 5 years in the PubMed. [no cache] 500 found

378) The ACC synaptic strengthening in chronic visceral pain may engage signal transduction pathways that are in common with those activated by electrical stimulation, and serves as an attractive cellular model of functional visceral pain.

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PMID:24108805 DOI:10.1093/cercor/bht273

2015 Cerebral cortex (New York, N.Y. : 1991)

* Facilitation of synaptic transmission in the anterior cingulate cortex in viscerally hypersensitive rats.

- Electrophysiological studies have shown the enhanced response of anterior cingulate cortex (ACC) to colorectal distension in viscerally hypersensitive (VH) rats, which can be observed up to 7 weeks following colonic anaphylaxis, independent of colon inflammation, suggesting a mechanism for learning and triggering of pain memories in the ACC neuronal circuitry. Activity-dependent plasticity in synaptic strength may serve as a key mechanism that reflects cortical plasticity. However, only a few reports have indicated the synaptic plasticity of ACC in vivo. In the present study, electrophysiological recording showed long-lasting potentiation of local field potential in the medial thalamus (MT)-ACC synapses in VH rats. Theta burst stimulation in the MT reliably induced long-term potentiation in the MT-ACC pathway in normal rats, but was occluded in the VH state. Further, repeated tetanization of MT increased ACC neuronal activity and visceral pain responses of normal rats, mimicking VH rats. In conclusion, we demonstrated for the first time that visceral hypersensitivity is associated with alterations of synaptic plasticity in the ACC. The ACC synaptic strengthening in chronic visceral pain may engage signal transduction pathways that are in common with those activated by electrical stimulation, and serves as an attractive cellular model of functional visceral pain.

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