There are a number of hypothetical explanations for the actions of ethanol on the exocrine pancreas; among them, the cholinergic hypothesis has received special attention. According to this hypothesis, chronic alcohol consumption induces alterations in the control of exocrine pancreatic function resulting in cholinergic hyperstimulation of pancreatic acinar cells and their muscarinic receptors. Our aim was to investigate the cholinergic control of pancreatic enzyme secretion and the number and affinity of muscarinic receptors in the pancreatic acinar cells of rats subjected to chronic ethanol ingestion. We also investigated whether a high-fibre diet modifies the actions of ethanol on these aspects of the exocrine pancreatic function. Four groups of rats received either a standard or a high fibre diet, and either water or 20% (v/v) ethanol. After 6 months of treatment, isolated pancreatic acini were used for the determination of carbachol-stimulated amylase secretion and for the analysis of muscarinic receptors, using 1-[N-methyl-3H]scopolamine as a radioligand. Neither chronic ethanol intake nor a high fibre diet caused any apparent alteration in pancreatic histology, neither did them modify plasmatic amylase levels. Chronic alcoholization resulted in a significant increase in the amylase released from pancreatic acini in response to carbachol stimulation, but it did not affect either the number or the affinity of pancreatic acinar muscarinic receptors. The actions of ethanol are not significantly modified by the simultaneous consumption of a high fibre diet.

Recent studies indicate that the brain neutrophic factor (BDNF) mRNA expression and release is increased in the SON by osmotic stress. The molecular mechanism of action of BDNF and its physiological significance for the vasopressin secretion after dehydration remains to be clarified. Our overall hypothesis is that BDNF release in the SON may produce its responses by phosphorylation of its cognate receptor TrkB. Following 48h water deprivation (48hWD), vasopressin positive neurons in the SON showed increased immunoreactivity for both c‐fos and the phosphorylated form of TrkB (pTrkBY515; abcam, ab51187) as compared to control, euhydrated rats. Brain punches taken from the SON were homogenized in modified RIPA buffer and 5 μg of the total lysate was subjected to Western Blot analysis of both TrkB (abcam, ab18987) and pTrkBY515 expression. Densitometric measurements of the immunoreactive bands for TrkB and pTrkBY515 were normalized using β‐actin as a standard. Although no changes were observed for the TrkB expression, pTrkBY515 expression was increased by 5 fold (P<0.01) in the SON of 48hWD animals compared to euhydrated animals. In conclusion, our data show that increased TrkB phosphorilation in the SON following acute dehydration may play a role in the intracellular signaling associated with vasopressin secretion. The increased TrkB phosphorilation may be at least in part mediated by BDNF. (HL62579)