# Role of fast spiking interneurons in network synchronization and development

> **NIH NIH F99** · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2021 · $39,593

## Abstract

SUMMARY
 The brain's ability to properly process information is dependent on the ability of neuronal networks to
synchronize and generate oscillations in the gamma band (30-80 Hz). The ability of neuronal networks to
generate proper gamma oscillations matures slowly. Developing networks are susceptible to environmental
insults that could alter their development leading to abnormal oscillations. Abnormalities in gamma oscillations
are implicated in the pathology of mental health disorders including schizophrenia and bipolar disorder. In many
of these disorders, dysregulated inhibition is thought to give rise to abnormalities in network function. Fast spiking
interneurons (FSI) are a subset of GABAergic inhibitory neurons known to be crucial for the proper generation
of gamma oscillations. Abnormal FSI function has been observed in multiple animal models of schizophrenia.
Rodent models using antagonists of N-methyl-D-aspartate receptors (NMDAR) mimic many of the phenotypes
observed in schizophrenia including the late age onset of cognitive deficits and abnormalities in gamma
oscillations. Inhibition of NMDARs can also lead to abnormalities in FSI maturation and physiology, but the impact
of NMDAR antagonists on the ability of FSIs' to generate coordinated network activity remains poorly understood.
 The objective of this proposal is to determine the role of NMDARs in the capacity of FSIs to generate
and sustain coordinated network activity. The short-term training goals for the F99 phase of this proposal are
to determine how NMDARs influence FSIs' maturation and physiology leading to impaired network function. This
will be achieved by using microelectrode arrays to measure and manipulate synchronous network activity in
brain sections obtained from adult animals after pharmacological blockade of NMDARs. I will use protein
quantification through western blots and immunohistochemistry to identify changes in proteins that could
contribute to the physiological impairment of FSIs. The F99 phase will provide a foundation for the K00 phase in
which I will focus on determining how the intrinsic properties of FSIs allow them to generate and maintain
synchronous network activity. A combination of single cell, network recordings, in vivo manipulation of FSIs'
activity, and in silico network modeling will be incorporated to identify the different properties that contribute to
synchronize network activity. The F99 and K00 training phases will provide a strong foundation for my long-term
goal of becoming an independent academic researcher focused on determining how neurons participate in
neuronal networks and the impact of environmental insults.
 This proposal will help build upon our understanding of the fundamental principles that govern how
neurons interact to form functional networks. Additionally, it will help advance our understanding of the link
between molecular and network alteration underlying complex mental health disorders like schizophrenia.

## Key facts

- **NIH application ID:** 10318693
- **Project number:** 1F99NS120645-01A1
- **Recipient organization:** UNIVERSITY OF MICHIGAN AT ANN ARBOR
- **Principal Investigator:** Jean Carlos Rodriguez Diaz
- **Activity code:** F99 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $39,593
- **Award type:** 1
- **Project period:** 2021-07-01 → 2023-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10318693

## Citation

> US National Institutes of Health, RePORTER application 10318693, Role of fast spiking interneurons in network synchronization and development (1F99NS120645-01A1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10318693. Licensed CC0.

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