Abstract
Perineuronal nets (PNNs) are specialized structures of extracellular matrix that are aggregated into mesh-like structures, preferentially ensheathing parvalbumin-expressing (PV+) interneurons. PV+ neurons fire action potentials at high frequencies and innervating the cell somata of excitatory neurons, they provide strong inhibitory control of neural networks. Moreover, evidence suggests that they are important regulators of critical period plasticity as well as synchronizing neural activity in the adult brain. It is, however, still unknown how PNNs influence the electrophysiology of these PV+ neurons. Previous studies have found varying results on the effects of removing PNNs, including increased membrane capacitance and decreased firing rate. However, most of these experiments were performed in young mice in which the PNNs may not be fully developed. Using acute brain slices of the primary visual cortex from adult (>P100) animals of the AcanKO mouse line, I opted to clarify the effects of PNNs on electrophysiology. The AcanKO mice are deficient of aggrecan, a core protein in PNNs, specifically in the CNS, and never develop PNNs. Whole-cell patch-clamp recordings of acute slices show that mice deficient of PNNs from birth have significantly increased membrane capacitance, although there are no differences in action potential frequencies or excitatory input to the PV+ interneurons. Although the full functions of PNNs remain elusive, this study has found that PNNs decrease the membrane capacitance of PV+ interneurons. The results also suggest that there might be compensatory mechanisms in mice deficient of PNNs from birth. Furthermore, this study also proposes methodological comparisons of PNN removal for example by chABC or Cre-lox inactivation of critical PNN components.