Disinhibition in learning and memory circuits: New vistas for somatostatin interneurons and long-term synaptic plasticity

Brain Res Bull. 2018 Jul;141:20-26. doi: 10.1016/j.brainresbull.2017.11.012. Epub 2017 Nov 23.

Abstract

Neural circuit functions involve finely controlled excitation/inhibition interactions that allow complex neuronal computations and support high order brain functions such as learning and memory. Disinhibition, defined as a transient brake on inhibition that favors excitation, recently appeared to be a conserved circuit mechanism implicated in various functions such as sensory processing, learning and memory. Although vasoactive intestinal polypeptide (VIP) interneurons are considered to be the main disinhibitory cells, recent studies highlighted a pivotal role of somatostatin (SOM) interneurons in inhibiting GABAergic interneurons and promoting principal cell activation. Interestingly, long-term potentiation of excitatory input synapses onto hippocampal SOM interneurons is proposed as a lasting mechanism for regulation of disinhibition of principal neurons. Such regulation of network metaplasticity may be important for hippocampal-dependent learning and memory.

Publication types

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

MeSH terms

  • Animals
  • Brain / physiology
  • Interneurons / physiology*
  • Learning / physiology*
  • Neural Inhibition / physiology
  • Neural Pathways / physiology
  • Neuronal Plasticity / physiology*
  • Somatostatin / metabolism

Substances

  • Somatostatin