# Cortical and subcortical chandelier cell pathophysiology and symptomatology in autism

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA AT DAVIS · 2022 · $541,899

## Abstract

Abstract
The goal of our first funded R01 grant was to unravel the cell type(s), if any, altered in the human prefrontal
cortex (PFC) in autism spectrum disorder (ASD). We discovered a decreased number of Chandelier (Ch) cells
in the PFC of postmortem human tissue in ASD patients. In our first renewed R01 we proposed to define the role
of Ch cells in the PFC in ASD. We found an alteration of components of the GABA system in Ch cells in the PFC
in autism. Here, in our second R01 renewal application, we propose to follow up our studies by determining Ch
cell pathophysiology association to ASD symptomatology in PFC, other cortical areas, and in subcortical areas
known to be involved in ASD. Ch cells are the interneurons that regulates the final output of excitatory projection
neurons in the neocortex, hippocampus, and amygdala. Therefore, the loss of a single Ch cell may critically
impair proper function of projection neurons and the anatomical structure as a whole. This proposal will explore
the hypothesis that disturbances in Ch cell number in several areas of the cerebral cortex and subcortical areas
contribute to the altered function of the GABAergic system reported in the ASD brain. We also hypothesize that
a decreased number of Ch cells in dentate gyrus translates into a decreased rate of neurogenesis in ASD. We
will also test the hypothesis that there is a correlation between the pathophysiological alterations of Ch cells
and the severity of patient’s symptoms. We will test these hypotheses by quantifying the number of Ch cells in
specific areas of the neocortex (aim 1a,b), hippocampal formation (aim 2a,c), and amygdala (aim 3a,b) in ASD,
and correlating these numbers with patient behavior. We will also assess the number of progenitor cells and
immature neurons in the dentate gyrus in ASD (aim 2b). The number and function of Ch cells outside the PFC
has not yet been evaluated in ASD. Our proposal addresses this gap in knowledge. This project will greatly
expand our understanding of the GABAergic Ch system function in ASD, which will have a great impact on
translational research directed towards providing better treatment paradigms for individuals with ASD.

## Key facts

- **NIH application ID:** 10385289
- **Project number:** 2R01MH094681-11
- **Recipient organization:** UNIVERSITY OF CALIFORNIA AT DAVIS
- **Principal Investigator:** Veronica Martinez-Cerdeno
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $541,899
- **Award type:** 2
- **Project period:** 2011-06-02 → 2026-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10385289

## Citation

> US National Institutes of Health, RePORTER application 10385289, Cortical and subcortical chandelier cell pathophysiology and symptomatology in autism (2R01MH094681-11). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10385289. Licensed CC0.

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