# BDNF shapes the functional maturation of cortical interneurons

> **NIH NIH F31** · HARVARD MEDICAL SCHOOL · 2021 · $15,284

## Abstract

PROJECT SUMMARY/ABSTRACT
In the mammalian cerebral cortex, inhibitory interneurons sculpt the flow of excitatory information. This
complex task is carried out by a wide variety of interneuron subtypes which play distinct roles in cortical
function. However, the developmental origins of interneuron diversity is largely unknown. Two major classes of
interneurons, parvalbumin (PV)+ fast-spiking basket cells and somatostatin (SST)+ Martinotti cells, are both
derived from a common embryonic origin yet differentiate into highly specialized cell types. Mechanisms that
control the diversification of these cell types and specify their integration into their respective circuits are not
well understood. Increasing evidence suggests that this process depends not only on initial genetic
determinants of cell fate, but also activity-dependent signals once the interneurons invade the cortex and begin
for form synapses. One candidate signaling factor to mediate cortical interneuron maturation and synaptic
integration is brain-derived neurotrophic factor (BDNF), which is a neurotrophin critical for the development of
several cells types and has been shown to regulate inhibition in the developing cortex. However, the
contribution of the BDNF high-affinity receptor TrkB to interneuron development has never been tested.
Strikingly, BDNF also seems to influence the timing of visual critical period plasticity, which has long been
hypothesized to be controlled by the maturation of inhibition in visual cortex. Despite substantial evidence
supporting this hypothesis, the contributions of distinct subtypes of interneurons to the visual critical period
have not been fully explored. Furthermore, cell-autonomous signaling pathways that link interneuron
maturation with the developing visual network to control the precise timing of the visual critical period are not
known. This project aims to address these questions by 1) dissecting the requirement of the TrkB receptor in
PV and SST interneuron cellular and synaptic maturation and 2) assessing the contribution of BDNF signaling
onto PV and/or SST interneurons for the onset of the visual critical period. These goals will be accomplished
through a combination of longitudinal fate-mapping, molecular profiling, and electrophysiology both in vitro and
in vivo. This effort will provide insight into activity-dependent determinants of interneuron function and dissect
the roles of two major inhibitory subtypes in the onset of the critical period through a novel signaling pathway.

## Key facts

- **NIH application ID:** 10241312
- **Project number:** 5F31NS110120-03
- **Recipient organization:** HARVARD MEDICAL SCHOOL
- **Principal Investigator:** Elaine Fisher
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $15,284
- **Award type:** 5
- **Project period:** 2019-09-01 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10241312

## Citation

> US National Institutes of Health, RePORTER application 10241312, BDNF shapes the functional maturation of cortical interneurons (5F31NS110120-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10241312. Licensed CC0.

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