Developmental Postnatal Neuroplasticity of the Primate Amygdala: a Quantitative Analysis of Parvalbumin Neurons and Perineuronal Nets

Abstract

Neuroplasticity is implicated in the pathology of many psychiatric disorders, abnormal behaviors, and learning disabilities. Additionally, abnormalities in neuronal densities and regional volumes have been reported in psychiatric disorders such as schizophrenia (SZ) and Post Traumatic Stress Disorder (PTSD). Recent research shows parvalbumin (PVB) neurons and perineuronal nets (PNNs) play a crucial role in neuroplasticity. Current understanding of PVB or PNN development in humans, and the onset of their critical point (CP) of plasticity, has been limited to rodent models and human postmortem tissue. This study sought to address this informational gap through observation of the developmental trajectories of PVB neurons and PNNs in the primate amygdala. Tissue for this study was provided from Rhesus Macaques at 3 weeks, 3 months, and adulthood (+3 years) and processed via immunohistochemistry for each hemisphere. Left hemispheres were processed for PVB immunoreactive (IR) neurons, and the right hemispheres were processed using Wisteria floribunda Agglutinin (WFA) immunoreactive (IR) PNNs. After staining, each section of amygdala tissue was divided into subnuclei and we used quantitative microscopy to determine PVB and PNN densities. Our results show an anticipated increase in PVB neuronal density with age. However, we observed an unexpected and notable decrease in PNN density between 3 months and adulthood. We believe the decrease in PNN density may represent synaptic pruning that is occurring deep within brain regions such as the amygdala at this age and thus provides novel insight into the onset of the critical point in neuroplasticity in the primate amygdala. Overall our results suggest a more applicable model for the development of human neuronal plasticity and more research is required to confirm these findings.