Neurodegeneration in the olfactory system in Niemann Pick type C1 disease.

GABAergic neurons of the cerebral cortex constitute a highly heterogeneous population that plays a crucial role in regulating neuronal network activity and mediating interactions among principal neurons (Skaggs et al., ; Somogyi & Klausberger, ). Accordingly, the coordination and integration of cortical functions depend not only on the overall proportion of GABAergic neurons, but also on their diversity. For many years, immunohistochemical detection of the calcium‐binding proteins—calbindin (CB), calretinin (CR), and parvalbumin (PV)—has been widely used to define the principal classes of cortical GABAergic neurons in primates. This classification is based on evidence that more than 80% of cortical GABAergic neurons express one of these three markers, with minimal overlap between them (Burkhalter, ; Gonchar et al., ; Gonchar & Burkhalter, ; Kubota et al., ; Tamamaki et al., ; Uematsu et al., ; van Brederode et al., ; Xu et al., ; Yan et al., ). This framework has, therefore, been widely adopted as a practical and robust approach for defining major interneuron classes in the primate cortex. Most calbindin‐positive (CB) neurons co‐express the neuropeptide somatostatin (SOM), which itself is present in a broader neuronal population (Gonchar & Burkhalter, ; Kawaguchi & Kubota, ; Kubota et al., ; Rogers, ). This partial overlap highlights a limitation of classical marker‐based classification and underscores the need to consider combined marker expression when defining interneuron subtypes. Approximately one third of SOM neurons do not express detectable levels of CB, including neurons expressing neuronal nitric oxide synthase (nNOS) and neuropeptide Y (Banovac et al., ). For this reason, SOM has been proposed as a more comprehensive marker than CB, as it encompasses a larger subset of cortical GABAergic neurons without overlapping with the other two major subpopulations. Together, PV, SOM and CR neurons are estimated to account for more than 90% of all cortical GABAergic neurons in primates (Hladnik et al., ).