TNFRSF1A and acute pancreatitis: Since astrocytes are known to contribute to excess levels of TNF [79], and hippocampal TNF/TNFR1 activity is known to promote neuropathic pain [76, 78], it is plausible to suggest that hippocampal TNF/TNFR1 activity could be contributing to the induction of neuropathic pain in our model of acute pancreatitis.