AI Article Synopsis
- Several studies indicate that NMDA-receptor activation in the anterior cingulate cortex (ACC) is vital for managing visceral pain in rats with visceral hypersensitivity (VH).
- The research focused on the expression of NMDA subtypes (NR2A, NR2B) and AMPA receptor (GluR2) in the ACC of VH rats, particularly after inducing VH with mustard oil.
- Findings revealed that NR2B and GluR2 levels were significantly elevated in VH rats over time, suggesting their role in promoting long-term changes in synaptic function linked to visceral pain.
Article Abstract
Several studies have shown that N-methyl-D-aspartate (NMDA)-receptor activation in anterior cingulate cortex (ACC) neurons plays critical roles in modulating visceral pain responses in visceral hypersensitivity (VH) rats. However, there are few reports about the expressions of NMDA and α-amino-3-hydroxy-5-methyl-4-isox-azolepropionic-acid (AMPA) receptor subtypes in ACC of VH model rats at different time points. The current study was undertaken to investigate NR2A, NR2B and GluR2 expressions in ACC of VH rats that were induced by administration with 5% mustard oil. Our results indicated that NR2B, but not NR2A, was highly expressed in VH model group on day 15, 22, and 36 compared with normal group (p < 0.05). GluR2 expression was also higher in VH model group on day 15, 22, and 36 than that of normal group (p < 0.05). These findings suggested increased expression of NR2B and GluR2 might be key mechanisms for long-term synaptic plastic changes in VH rats.
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| http://dx.doi.org/10.1016/j.cellimm.2013.12.001 | DOI Listing |
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