A diametric mode of neuronal circuitry-neurogenesis coupling in the adult hippocampus via parvalbumin interneurons

Abstract

Adult neurogenesis occurs within a specialized microenvironment (or niche), and is dynamically regulated by experience. However, the niche mechanism that couples neuronal circuitry activity to the production of new neurons is not well-understood. In our recent two studies published in Nature¹ and Nature Neuroscience,² we identified a novel niche mechanism involving parvalbumin (PV⁺) interneurons that couples local circuit activity to diametric regulation of the activation of quiescent neural stem cells (NSC) and the survival of their proliferating neural progeny, two critical early phases of adult hippocampal neurogenesis. Using a combination of optogenetics, lineage-tracing of adult NSCs, and retroviral mediated approach for birthdating of neural progenitors, we demonstrated that activation of PV⁺ interneurons, but not somatostatin (SST⁺) or vasoactive intestinal peptide (VIP⁺) interneurons, suppresses the activation of quiescent NSCs, while simultaneously promotes the survival of proliferative newborn progeny in the adult mouse dentate gyrus. In this commentary, we review our findings and discuss a potential role for PV⁺ neuron-mediated GABA signaling as a key neuronal activity sensor that translates animal's experience into regulation of adult hippocampal neurogenesis.

Keywords: :

• parvalbumin interneurons
• optogenetics
• GABAergic inputs
• adult hippocampal neurogenesis
• proliferating neural progenitors

This article refers to:

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Acknowledgments

The research in the authors’ laboratories was supported by UNC start-up fund (J.S.), NARSAD (J.S. and G.M.), Whitehall Foundation (J.S.), American Heart Association (J.S.), UNC BBSP and Neurobiology Curriculum training grant (A.J.C.), UNC Department of Pharmacology training grant (R.H.J.O.), NIH (G.M. and H.S.), and MSCRF (G.M.).