Calcitonin gene-related peptide (CGRP) acting within the bed nucleus of the stria terminalis (BNST) increases anxiety as well as neural activation in anxiety-related structures, and mediates behavioral stress responses. Similar effects have been described following intra-ventricular as well as intra-BNST infusions of the stress-responsive neuropeptide, corticotropin releasing factor (CRF). Interestingly, CGRP-positive terminals within the lateral division of the BNST form perisomatic baskets around neurons that express CRF, suggesting that BNST CGRP could exert its anxiogenic effects by increasing release of CRF from these neurons. With this in mind, the present set of experiments was designed to examine the role of CRFR1 signaling in the anxiogenic effects of CGRP within the BNST and to determine whether CRF from BNST neurons contributes to these effects. Consistent with previous studies, we found that 400 ng CGRP infused bilaterally into the BNST increased the acoustic startle response and induced anxiety-like behavior in the elevated plus maze compared to vehicle. Both of these effects were attenuated by 10 mg/kg PO of the CRFR1 antagonist, GSK876008. GSK876008 alone did not affect startle. An intra-BNST infusion of the CRFR1 antagonist CP376395 (2 μg) also blocked increases in acoustic startle induced by intra-BNST infusion of CGRP, as did virally-mediated siRNA knockdown of CRF expression locally within the BNST. Together, these results suggest that the anxiogenic effects of intra-BNST CGRP may be mediated by CRF from BNST neurons acting at local CRFR1 receptors.
Acute pancreatitis(AP) is one of the common causes of acute abdomen and known to be associated with high morbidity and mortality in severe cases. Though most common causes of AP are cholelithiasis and alcoholism, it has also been reported in association with diabetic ketoacidosis (DKA). Triad of AP, hypertriglyceridaemia (HTG) and DKA is rare co-association and here the causal factor of AP is still not fully established. We report a case of AP in a DKA patient with recent diagnosis of hyperlipidaemia and diabetes. Usually AP has been associated with severe HTG; interestingly, our patient showed only moderate raise in triglycerides but still suffered AP during DKA. Hence, it raises question about the real culprit in this enigmatic triad.
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