Cellular mechanisms of learning and memory processes during postnatal development

At NBLab, we have delineated the maturation of intrinsic and synaptic properties of neurons in the prefrontal cortex (Konstantoudaki et al., 2018; Kalemaki et al., 2021 and on-going studies by Konstantinos Diskos and Angeliki Velli). Specifically, we have identified that the action potential properties of the pyramidal neurons completely mature to adult levels from the neonatal to the juvenile stage. Spontaneous excitatory currents remain relatively the same the neonatal to the juvenile and to the adolescent stage, then reduce in adulthood. The intrinsic properties of GABAergic interneurons mature from the neonatal to the juvenile stage and continue to mature until adolescent period. Spontaneous inhibitory postsynaptic currents increase from the neonatal to the juvenile period, then from the juvenile to the adolescent period, and finally reduce from the adolescent to the adult stage. Finally, I have identified that the shift of the GABA-A function from depolarizing to hyperpolarizing in prefrontal cortical neurons is delayed from postnatal day 7 in the hippocampus and primary sensory cortices to the second postnatal week (between 10^th and 20^th postnatal days). Furthermore, we have identified that long-term potentiation in the prefrontal cortex only emerges in the adult period and not before that. Increased expression of the NR2A subunit of the NMDA receptor contributes the emergence of long-term potentiation in adulthood
Ongoing current research at NBLab aims to study the cellular properties of neurons in the prefrontal cortex during development that belong to specific circuits (for example, neurons that project to the amygdala compared to neurons that project to the contralateral prefrontal cortex). This will allow us to delineate the developmental events in the neurons of the prefrontal cortex in a circuit-specific manner.
At NBLab, we have identified long-term potentiation, as an additional mechanism that contributes to working memory processes and enhances the function of the prefrontal cortex (Konstantoudaki et al., 2016; Konstantoudaki et al., 2018; Chalkiadaki et al., 2019; Stavroulaki et al., 2021; Velli et al., 2021). Specifically, the ability of synapses within the PFC to potentiate correlates with learning working memory tasks and with recency memory (Konstantoudaki et al., 2018; Chalkiadaki et al., 2019; Velli et al., 2021; Stavroulaki et al., 2021).
In collaboration with Vasiliki Nikoletopoulou, we have contributed to identifying autophagy as an important cellular mechanism in mediating synaptic plasticity processes (Kallergi et al., 2022; Nikoletopoulou et al., 2018).
We have identified the delayed afterdepolarization as a cellular mechanism that underlies persistent activity (the cellular correlate of working memory) and have shown that it interacts with the NMDA receptor (Sidiropoulou et al., 2009; Sidiropoulou and Poirazi, 2012; Konstantoudaki et al., 2014; Papoutsi et al., 2013; Papoutsi et al., 2014).