Postnatal plasticity in the paralaminar nucleus of the pallial amygdala in juvenile swine brain.

The aim of this study was to investigate the presence of immature cells and their phenotype in the pallial amygdala of juvenile swine brains by way of immunoreactivity for the microtubule-associated protein doublecortin (DCX), combined with the cell proliferation marker Ki-67 and different neuronal markers, including NeuN and the transcription factor COUP-TFII (NR2F2, critical for amygdalar development and adult phenotype maintenance). Our results showed the existence of numerous DCX+ cells along the external border of the basal amygdalar complex, adjacent to the amygdalar capsule, in an area identified as the swine paralaminar nucleus. These cells showed a patchy distribution, with shell-like clusters of DCX+ cells partially surrounding islands of non-stained large cells of the basal amygdalar complex. The paralaminar nucleus and the other nuclei of the basal amygdalar complex also contained abundant neurons expressing COUP-TFII, but not the transcription factor FOXP2, which defines the clusters of intercalated amygdalar cells. Paralaminar patches of DCX+ cells were more abundant at posterior levels, where they were continuous with chains of DCX+ cells with migratory-like morphology that appear to come from the subventricular zone surrounding the temporal horn of the lateral ventricle. This part of the ventricular/subventricular zone (vz/svz) contained many cells coexpressing COUP-TFII/Ki-67 and DCX/Ki-67, suggesting that this might be the source of the immature cells found in the paralaminar nucleus. Overall, these results show that the swine pallial amygdala shows a prolonged postnatal plasticity and contains a reservoir of immature neurons mainly located in the paralaminar nucleus and related vz/svz, resembling the situation seen in humans. These findings also point to the swine as an excellent model to study mechanisms behind postnatal plasticity in the amygdala of gyrencephalic animals, and the role of this protracted plasticity in amygdala function and dysfunction. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00429-026-03106-8.