Abstract

Somatostatin-expressing (SOM+), inhibitory interneurons represent a heterogeneous group of cells and given their remarkable diversity, classification of SOM+ interneurons remains a challenging task. Electrophysiological, morphological and neurochemical classes of SOM+ interneurons have been proposed in the past but it remains unclear as to what extent these classes are congruent. We performed whole-cell patch-clamp recordings from 127 GFP-labeled SOM+ interneurons ('GIN') of the superficial cingulate cortex with subsequent biocytin-filling and immunocytochemical labeling. Principal component analysis followed by k-means clustering predicted two putative subtypes of SOM+ interneurons, which we designated as group I and group II GIN. A key finding of our study is the fact that these electrophysiologically and morphologically distinct groups of SOM+ interneurons can be correlated with two neurochemical subtypes of SOM+ interneurons described recently in our laboratory. In particular, all SOM+ interneurons expressing calbindin but no calretinin could be classified as group I GIN, whereas all but one neuropeptide Y- and calretinin-positive interneurons were found in group II.

Highlights

  • Within the cerebral cortex, inhibitory modulation of excitatory information processing is crucial for proper network signaling

  • As previously reported [2], the so-called "green fluorescent protein (GFP) expressing interneurons" (GIN, [19]) of the mouse cingulate cortex represent a heterogeneous group of cells with respect to their neurochemical profile

  • We found that all SOM+ interneurons that were positive for CB but negative for CR (6 out of 6) were present in group I GFP-expressing inhibitory interneurons (GIN), whereas all but one GIN expressing neuropeptide Y (NPY) were present in group II GIN

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Summary

Introduction

Inhibitory modulation of excitatory information processing is crucial for proper network signaling. GABAergic interneurons represent around 10–20% of all neurons within the cerebral cortex. Somatostatin-expressing interneurons represent around one third of all GABAergic interneurons [1,2]. The cingulate cortex is a brain region that seems vulnerable to dysfunctions of GABAergic signaling and many neurological diseases are accompanied by a specific loss of somatostatin-expressing (SOM+) interneurons within this brain area [3,4,5]. In order to understand why a certain neurological disease is accompanied by a specific loss of one type of GABAergic interneurons, the specific properties and functions of these interneurons need to be determined. Efforts to classify GABAergic interneurons are faced with their enormous diversity in terms of morphology, neurochemistry and physiology.

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