The temporoinsular projection system: an anatomical study

OBJECTIVEConnections between the insular cortex and the amygdaloid complex have been demonstrated using various techniques. Although functionally well connected, the precise anatomical substrate through which the amygdaloid complex and the insula are wired remains unknown. In 1960, Klingler briefly described the “fasciculus amygdaloinsularis,” a white matter tract connecting the posterior insula with the amygdala. The existence of such a fasciculus seems likely but has not been firmly established, and the reported literature does not include a thorough description and documentation of its anatomy. In this fiber dissection study the authors sought to elucidate the pathway connecting the insular cortex and the mesial temporal lobe.METHODSFourteen brain specimens obtained at routine autopsy were dissected according to Klingler’s fiber dissection technique. After fixation and freezing, anatomical dissections were performed in a stepwise progressive fashion.RESULTSThe insula is connected with the opercula of the frontal, parietal, and temporal lobes through the extreme capsule, which represents a network of short association fibers. At the limen insulae, white matter fibers from the extreme capsule converge and loop around the uncinate fasciculus toward the temporal pole and the mesial temporal lobe, including the amygdaloid complex.CONCLUSIONSThe insula and the mesial temporal lobe are directly connected through white matter fibers in the extreme capsule, resulting in the appearance of a single amygdaloinsular fasciculus. This apparent fasciculus is part of the broader network of short association fibers of the extreme capsule, which connects the entire insular cortex with the temporal pole and the amygdaloid complex. The authors propose the term “temporoinsular projection system” (TIPS) for this complex.

Regulation of adenosine A2Areceptor gene expression in a model of binge eating in the amygdaloid complex of female rats

Background:Pharmacological treatment approaches for eating disorders, such as binge eating disorder and bulimia nervosa, are currently limited.Methods and aims:Using a well-characterized animal model of binge eating, we investigated the epigenetic regulation of the A2AAdenosine Receptor (A2AAR) and dopaminergic D2 receptor (D2R) genes.Results:Gene expression analysis revealed a selective increase of both receptor mRNAs in the amygdaloid complex of stressed and restricted rats, which exhibited binge-like eating, when compared to non-stressed and non-restricted rats. Consistently, pyrosequencing analysis revealed a significant reduction of the percentage of DNA methylation but only at the A2AAR promoter region in rats showing binge-like behaviour compared to the control animals. Focusing thus on A2AAR agonist (VT 7) administration (which inhibited the episode of binge systemically at 0.1 mg/kg or intra-central amygdala (CeA) injection at 900 ng/side) induced a significant increase of A2AAR mRNA levels in restricted and stressed rats when compared to the control group. In addition, we observed a significant decrease in A2AAR mRNA levels in rats treated with the A2AAR antagonist (ANR 94) at 1 mg/kg. Consistent changes in the DNA methylation status of the A2AAR promoter were found in restricted and stressed rats after administration of VT 7 or ANR 94.Conclusion:We confirm the role of A2AAR in binge eating behaviours, and we underline the importance of epigenetic regulation of the A2AAR gene, possibly due to a compensatory mechanism to counteract the effect of binge eating. We suggest that A2AAR activation, inducing receptor gene up-regulation, could be relevant to reduction of food consumption.