The Current Status of Somatostatin-Interneurons in Inhibitory Control of Brain Function and Plasticity

Abstract

The mammalian neocortex contains many distinct inhibitory neuronal populations to balance excitatory neurotransmission. A correct excitation/inhibition equilibrium is crucial for normal brain development, functioning, and controlling lifelong cortical plasticity. Knowledge about how the inhibitory network contributes to brain plasticity however remains incomplete. Somatostatin- (SST-) interneurons constitute a large neocortical subpopulation of interneurons, next to parvalbumin- (PV-) and vasoactive intestinal peptide- (VIP-) interneurons. Unlike the extensively studied PV-interneurons, acknowledged as key components in guiding ocular dominance plasticity, the contribution of SST-interneurons is less understood. Nevertheless, SST-interneurons are ideally situated within cortical networks to integrate unimodal or cross-modal sensory information processing and therefore likely to be important mediators of experience-dependent plasticity. The lack of knowledge on SST-interneurons partially relates to the wide variety of distinct subpopulations present in the sensory neocortex. This review informs on those SST-subpopulations hitherto described based on anatomical, molecular, or electrophysiological characteristics and whose functional roles can be attributed based on specific cortical wiring patterns. A possible role for these subpopulations in experience-dependent plasticity will be discussed, emphasizing on learning-induced plasticity and on unimodal and cross-modal plasticity upon sensory loss. This knowledge will ultimately contribute to guide brain plasticity into well-defined directions to restore sensory function and promote lifelong learning.

Somatostatin receptors (SSTR1-5) on inhibitory interneurons in the barrel cortex

“…Many studies have shown that the different subtypes of interneurons display different activation patterns in learned behaviours and characteristic behavioural states, and they are important players in neuroplasticity (Gentet et al 2012;Hensch 2005;Katona et al 2014;Lee et al 2012;Nys et al 2015;Pinto and Dan 2015;Sachidhanandam et al 2016;Schneider et al 2014). SST INs have been found to be involved in the cellular mechanisms of learning (Adler et al 2019;Chen et al 2015;Cichon and Gan 2015;Kato et al 2015;Letzkus et al 2011;Lovett-Barron et al 2014;McKay et al 2013;Pi et al 2013;Stefanelli et al 2016;Wolff et al 2014) and cortical plasticity (Fu et al 2015;Khan et al 2018;Scheyltjens and Arckens 2016). Our studies of learning-dependent plasticity in the barrel cortex point to the involvement of SST containing GABAergic neurons in the mechanism underlying the development of plastic changes (Cybulska-Klosowicz et al 2013).…”

A Neural “Tuning Curve” for Multisensory Experience and Cognitive-Perceptual Schizotypy

“…By putting a brake on cortical excitability, inhibitory neurons provide temporal precision to cortical firing in response to sensory inputs and enhance their saliency. 102 The current study is not without limitations. First, even though we selected biological predictors of TBW based on a strong a priori rationale, many additional factors not accounted for by our study are likely to contribute to this complex perceptual phenotype.…”

Impaired Tuning of Neural Ensembles and the Pathophysiology of Schizophrenia: A Translational and Computational Neuroscience Perspective

“…Fast-spiking neurons have higher AMPA/NMDA ratios and reduced sensitivity to the effects of NMDA-R antagonists than pyramidal neurons (120) or regular-spiking or low threshold-spiking interneurons (121, 122), i.e., firing patterns characteristic of SST interneurons (123). In visual cortex, layer IV SST neurons inhibit PV neurons while PV neurons do not prominently inhibit other interneuron populations (124, 125). As a result, SST inhibition by NMDA-R antagonists would increase PV activity and thereby increase γ oscillations.…”