Roles of Glial Cells in Sculpting Inhibitory Synapses and Neural Circuits.

Ji Won Um

doi:10.3389/fnmol.2017.00381

Abstract

Glial cells are essential for every aspect of normal neuronal development, synapse formation, and function in the central nervous system (CNS). Astrocytes secrete a variety of factors that regulate synaptic connectivity and circuit formation. Microglia also modulate synapse development through phagocytic activity. Most of the known actions of CNS glial cells are limited to roles at excitatory synapses. Nevertheless, studies have indicated that both astrocytes and microglia shape inhibitory synaptic connections through various mechanisms, including release of regulatory molecules, direct contact with synaptic terminals, and utilization of mediators in the extracellular matrix. This review summarizes recent investigations into the mechanisms underlying CNS glial cell-mediated inhibitory synapse development.

Highlights

Synapses are the fundamental information-processing units underlying neuronal networks in the brain
Treatment of organotypic slices from the avian auditory brainstem with astrocyte-conditioned media (ACM) enhances the number of inhibitory synaptic inputs onto nucleus laminaris (NL) neurons, suggesting that soluble factors secreted by astrocytes promote inhibitory synaptogenesis during embryonic development (Korn et al, 2012; Cramer and Rubel, 2016)
Genetic deletion of specific developmental populations of astrocytes in the spinal cord was shown to increase inhibitory synapse numbers, but decrease excitatory synapse numbers (Tsai et al, 2012). These results indicate that astrocytes are crucial for maintaining the appropriate excitatory to inhibitory (E/I) ratio at synapses and neural circuits in the spinal cord

Summary

Introduction

Synapses are the fundamental information-processing units underlying neuronal networks in the brain. Astrocyte-induced increases in the number of GABAA receptor clusters were shown to be compromised by scavenging BDNF, indicating that signaling pathways involving BDNF and its receptor, tropomyosin receptor kinase B (TrkB), are required for astrocyte-mediated facilitation of inhibitory synapse development (Elmariah et al, 2005; Figure 1).

Results

Conclusion