Synaptic Plasticity and Excitation-Inhibition Balance in the Dentate Gyrus: Insights from In Vivo Recordings in Neuroligin-1, Neuroligin-2, and Collybistin Knockouts

Neural Plast. 2018 Feb 18:2018:6015753. doi: 10.1155/2018/6015753. eCollection 2018.

Abstract

The hippocampal dentate gyrus plays a role in spatial learning and memory and is thought to encode differences between similar environments. The integrity of excitatory and inhibitory transmission and a fine balance between them is essential for efficient processing of information. Therefore, identification and functional characterization of crucial molecular players at excitatory and inhibitory inputs is critical for understanding the dentate gyrus function. In this minireview, we discuss recent studies unraveling molecular mechanisms of excitatory/inhibitory synaptic transmission, long-term synaptic plasticity, and dentate granule cell excitability in the hippocampus of live animals. We focus on the role of three major postsynaptic proteins localized at excitatory (neuroligin-1) and inhibitory synapses (neuroligin-2 and collybistin). In vivo recordings of field potentials have the advantage of characterizing the effects of the loss of these proteins on the input-output function of granule cells embedded in a network with intact connectivity. The lack of neuroligin-1 leads to deficient synaptic plasticity and reduced excitation but normal granule cell output, suggesting unaltered excitation-inhibition ratio. In contrast, the lack of neuroligin-2 and collybistin reduces inhibition resulting in a shift towards excitation of the dentate circuitry.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Adhesion Molecules, Neuronal / deficiency*
  • Cell Adhesion Molecules, Neuronal / genetics
  • Dentate Gyrus / physiology*
  • Excitatory Postsynaptic Potentials / physiology*
  • Gene Knockout Techniques
  • Humans
  • Nerve Net / physiology
  • Nerve Tissue Proteins / deficiency*
  • Nerve Tissue Proteins / genetics
  • Neural Inhibition / physiology
  • Neuronal Plasticity / physiology*
  • Rho Guanine Nucleotide Exchange Factors / deficiency*
  • Rho Guanine Nucleotide Exchange Factors / genetics
  • Synapses / genetics
  • Synapses / metabolism

Substances

  • ARHGEF9 protein, human
  • Cell Adhesion Molecules, Neuronal
  • Nerve Tissue Proteins
  • Rho Guanine Nucleotide Exchange Factors
  • neuroligin 1
  • neuroligin 2