Absence of parvalbumin increases mitochondria volume and branching of dendrites in inhibitory Pvalb neurons in vivo: a point of convergence of autism spectrum disorder (ASD) risk gene phenotypes.

ABSTRACT:

Background

In fast firing, parvalbumin (PV)-expressing (Pvalb) interneurons, PV acts as an intracellular Ca²⁺ signal modulator with slow-onset kinetics. In Purkinje cells of PV^-/- mice, adaptive/homeostatic mechanisms lead to an increase in mitochondria, organelles equally capable of delayed Ca²⁺ sequestering/buffering. An inverse regulation of PV and mitochondria likewise operates in cell model systems in vitro including myotubes, epithelial cells, and oligodendrocyte-like cells overexpressing PV. Whether such opposite regulation pertains to all Pvalb neurons is currently unknown. In oligodendrocyte-like cells, PV additionally decreases growth and branching of processes in a cell-autonomous manner.

Methods

The in vivo effects of absence of P

SUBMITTER: Janickova L 

PROVIDER: S-EPMC7285523 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature