Cortical inhibitory interneurons control sensory processing

Abstract

Inhibitory and excitatory neurons form intricate interconnected circuits in the mammalian sensory cortex. Whereas the function of excitatory neurons is largely to integrate and transmit information within and between brain areas, the inhibitory neurons are thought to shape the way excitatory neurons integrate information, and exhibit context-and behavior-specific responses. Over the last few years, work across sensory modalities has begun unraveling the function of distinct types of cortical inhibitory neurons in sensory processing, identifying their contribution to controlling stimulus selectivity of excitatory neurons and modulating information processing based on the behavioral state of the subject. Here, we review the results from recent studies, and discuss the implications for the contribution of inhibition to cortical circuit activity and information processing.

Effects of lorazepam and baclofen on short‐ and long‐latency afferent inhibition

“…Inhibition plays a large role in S1 with respect to modulating receptor response profiles, where networks of inhibitory interneurons shape the spatial and temporal profiles of excitatory pyramidal neurons (DiCarlo & Johnson, ; Wood et al . ). M1 is governed by a balance of excitation and inhibition, with excitation mainly governing motor output (Werhahn et al .…”

“…Although lorazepam acts globally within the cortex, lorazepam may increase GABA A receptor transmission on the dense inhibitory interneuron population within S1 that ultimately acts to disinhibit pyramidal neurons (DiCarlo & Johnson, ; Wood et al . ). Disinhibition of S1 pyramidal neurons would allow for excitation of M1 pyramidal neurons via long‐range connections throughout layers II/III (Amassian et al .…”

“…A main effect of ISI is shown on the right, where SAI was significantly stronger for N20 + 4 ms compared to N20 + 6 ms. D, mean ± SD SAI before and after administration of placebo. A main effect of ISI is shown on the right, where SAI was significantly stronger for N20 + 4 ms compared to N20 + 6 ms. (DiCarlo & Johnson, 2000;Wood et al 2017). M1 is governed by a balance of excitation and inhibition, with excitation mainly governing motor output (Werhahn et al 2007).…”

“…Asterisks indicate individuals who demonstrated reduction in SAI following lorazepam intake, reflecting the TIME main effect found in the two-way ANOVA. Long-latency afferent inhibition Baclofen ISI 1,9 = 0.631, P = 0.543 TIME 2,18 = 1.497, P = 0.252 ISI × TIME 2,18 = 1.125, P = 0.346 Placebo ISI 1,9 = 0.509, P = 0.610 TIME 2,18 = 0.896, P = 0.369 ISI × TIME 2,18 = 0.548, P = 0.588 Short-latency afferent inhibition Baclofen ISI 1,9 = 1.299, P = 0.284 TIME 1,9 = 0.884, P = 0.372 ISI × TIME 1,9 = 0.279, P = 0.610 Placebo ISI 1,9 = 0.297, P = 0.599 TIME 1,9 = 0.093, P = 0.767 ISI × TIME 1,9 = 2.557, P = 0.144 interneuron population within S1 that ultimately acts to disinhibit pyramidal neurons (DiCarlo & Johnson, 2000;Wood et al 2017). Disinhibition of S1 pyramidal neurons would allow for excitation of M1 pyramidal neurons via long-range connections throughout layers II/III (Amassian et al 1987) and V (Ferezou et al 2007;Aronoff et al 2010).…”

Robust perisomatic GABAergic self-innervation inhibits basket cells in the human and mouse supragranular neocortex

“…GABAergic inhibition at the perisomatic region efficiently controls spike output (Tremblay R et al 2016;Feldmeyer D et al 2018). Hence, pvBCs are key players synchronizing neuronal network activity through their inhibitory synapses (Cobb SR et al 1995;Pouille F and M Scanziani 2001;Wood KC et al 2017;Cardin JA 2018), and altered pvBC firing is often linked to pathological network activities (Palop JJ and L Mucke 2016;Dienel SJ and DA Lewis 2018). In addition, perisomatic inhibition through autapses can efficiently regulate pvBC firing (Bacci A and JR Huguenard 2006;Guo D et al 2016;Yilmaz E et al 2016).…”