Open AccessChandelier Cartridge Density Is Reduced in the Prefrontal Cortex in Autism
Author(s) -
Sarwat Amina,
Carmen Falcone,
Tiffany Hong,
Marisol Wendy Wolf-Ochoa,
Gelareh Vakilzadeh,
Erik Allen,
Rosalia Perez-Castro,
Mehdi Kargar,
Stephen C. Noctor,
Verónica MartínezCerdeño
Publication year - 2021
Publication title -
cerebral cortex
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.694
H-Index - 250
eISSN - 1460-2199
pISSN - 1047-3211
DOI - 10.1093/cercor/bhaa402
Subject(s) - autism , prefrontal cortex , parvalbumin , neuroscience , excitatory postsynaptic potential , interneuron , cerebral cortex , dorsolateral prefrontal cortex , neurodevelopmental disorder , biology , inhibitory postsynaptic potential , psychology , cognition , psychiatry
An alteration in the balance of excitation-inhibition has been proposed as a common characteristic of the cerebral cortex in autism, which may be due to an alteration in the number and/or function of the excitatory and/or inhibitory cells that form the cortical circuitry. We previously found a decreased number of the parvalbumin (PV)+ interneuron known as Chandelier (Ch) cell in the prefrontal cortex in autism. This decrease could result from a decreased number of Ch cells, but also from decreased PV protein expression by Ch cells. To further determine if Ch cell number is altered in autism, we quantified the number of Ch cells following a different approach and different patient cohort than in our previous studies. We quantified the number of Ch cell cartridges-rather than Ch cell somata-that expressed GAT1-rather than PV. Specifically, we quantified GAT1+ cartridges in prefrontal areas BA9, BA46, and BA47 of 11 cases with autism and 11 control cases. We found that the density of GAT1+ cartridges was decreased in autism in all areas and layers. Whether this alteration is cause or effect remains unclear but could result from alterations that take place during cortical prenatal and/or postnatal development.