Abstract
The most typical and well known inhibitory action in the cortical microcircuit is a strong inhibition on the target neuron by axo-somatic synapses. However, it has become clear that synaptic inhibition in the cortex is much more diverse and complicated. Firstly, at least ten or more inhibitory non-pyramidal cell subtypes engage in diverse inhibitory functions to produce the elaborate activity characteristic of the different cortical states. Each distinct non-pyramidal cell subtype has its own independent inhibitory function. Secondly, the inhibitory synapses innervate different neuronal domains, such as axons, spines, dendrites and soma, and their inhibitory postsynaptic potential (IPSP) size is not uniform. Thus, cortical inhibition is highly complex, with a wide variety of anatomical and physiological modes. Moreover, the functional significance of the various inhibitory synapse innervation styles and their unique structural dynamic behaviors differ from those of excitatory synapses. In this review, we summarize our current understanding of the inhibitory mechanisms of the cortical microcircuit.
Highlights
Reviewed by: Michael Higley, Yale School of Medicine, USA Alex M
We summarize our current understanding of the inhibitory mechanisms of the cortical microcircuit
The inhibitory synapse of the dually innervated spines (DiS) expresses GABAA alpha 1 and beta 2&3 receptors and the excitatory synapse has AMPA GluR2&3 receptors (Figures 5D,E; Kubota et al, 2007). These findings suggest that the DiS is a mature, stable spine (Matsuzaki et al, 2001; Holtmaat et al, 2006; Isshiki et al, 2014; Villa et al, 2016)
Summary
Yoshiyuki Kubota 1,2,3*, Fuyuki Karube 4, Masaki Nomura 3,5† and Yasuo Kawaguchi 1,2,3. At least ten or more inhibitory non-pyramidal cell subtypes engage in diverse inhibitory functions to produce the elaborate activity characteristic of the different cortical states. The microcircuit of the neocortex is a very complex, composed of excitatory neurons (including pyramidal cells and spiny stellate cells), inhibitory non-pyramidal interneurons (Jones, 1975; Kawaguchi and Kubota, 1997; Somogyi et al, 1998; Markram et al, 2004; DeFelipe et al, 2013), glutamatergic afferent axons arising from other cortical areas and from subcortical structures such as the thalamus (Jones, 2001; Kuramoto et al, 2009, 2015) as well as non-glutamatergic neuromodulatory afferents from many different brainstem nuclei (Gulledge and Stuart, 2005; Puig et al, 2014, 2015). They include parvalbumin (PV) positive fast spiking (FS) basket cells (Figures 3A,D–H), non-FS cholecystokinin (CCK) positive large basket cells (Figure 3C) which have a large perikaryon, and non-FS vasoactive intestinal polypeptide (VIP)/corticotrophin
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