Recent developmental studies indicate that distinct neuronal subpopulations in the amygdala, including somatostatin (SOM)-containing neurons, originate from progenitor domains in the anterior entopeduncular area, thus suggesting a different origin from subpallial territories for amygdalar versus cortical SOM-expressing interneurons, the latter derived from the dorsal part of the medial ganglionic eminence. In this context, we carried out an immunohistochemical study analyzing spatiotemporal expression patterns for SOM- and neuropeptide Y (NPY)-containing neurons in the embryonic, postnatal, and adult mouse amygdala. Our results indicate that SOM- and NPY-immunoreactive cells are present in the amygdalar complex from embryonic day (E)12.5, and that these peptidergic cells seem to arise from the anterior entopeduncular area progenitor domain. From E12.5 on there was a notable increase in the number and immunoreactivity of cells containing these peptides in distinct territories of the amygdalar complex, reaching a peak around birth. The distribution pattern for NPY neurons was very similar to that of SOM neurons in most nuclei of the amygdala, although the number of NPY neurons was always lower than that of SOM. At postnatal ages a reduction in the number of immunoreactive cells is observed in most amygdalar nuclei, remaining then similar from P14 to the adult. We interpret this reduction of the number of immunoreactive neurons in relation to the increased immunoreactivity for axons that occurs postnatally. We also suggest that the anterior entopeduncular area-derived SOM- and NPY-containing neurons in pallial and subpallial amygdaloid nuclei become local interneurons and projection neurons, respectively.

Angiogenesis drives evolution and destabilisation of atherosclerotic plaques and the growth and expansion of tumour cells. Vascular endothelial growth factor (VEGF) is the main endogenous pro-angiogenic factor in humans. The aim was to provide insight into the anti-VEGF activity of bioactive compounds derived from aromatic amino acids (serotonin, melatonin, 3-indoleacetic acid, 5-hydroxytryptophol and hydroxytyrosol). Experiments involved endothelial cell migration (wound-healing assay), the molecular mechanisms (ELISA assay) and the downstream effects (phospholipase C gamma 1 (PLCγ1), protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS) by Western blot) on human umbilical vein endothelial cells (HUVECs). The data suggest for the first time that hydroxytyrosol interacts with surface components of the endothelial cell membrane (, preventing VEGF from activating its receptor. Serotonin and 5-hydroxytryptophol significantly inhibited HUVEC migration (98% and 50%, respectively) following the same mechanism. Conversely to other bioactive compounds, the anti-angiogenic effect of melatonin, serotonin, 3-indoleacetic acid and 5-hydroxytryptophol is not mediated via PLCγ1. However, hydroxytyrosol inhibits PLCγ1 phosphorylation. Additionally, melatonin and serotonin maintained eNOS phosphorylation and hydroxytyrosol significantly activated eNOS—all via Akt. These data provide new evidence supporting the interest in melatonin, serotonin, 3-indoleacetic acid, 5-hydroxytryptophol and hydroxytyrosol for their further exploitation as anti-VEGF ingredients in food.