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"Calibration of olfactory sensory neuron excitability by NFAT transcription factors"

Award Number: F32DC023805
ORGANIZATION: NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/30/2026
PERIOD OF PERFORMANCE END DATE: 09/29/2027

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"Calibration of olfactory sensory neuron excitability by NFAT transcription factors" - PROJECT SUMMARY/ABSTRACT Animals live in complex environments with both constant environmental stimuli and novel, dynamic stimuli. To efficiently identify important novel stimuli, sensory systems must attenuate sensitivity to constant stimuli and heighten sensitivity to dynamic stimuli. Inability to perform this process of sensory calibration can lead to context-dependent sensory hypersensitivity or hyposensitivity, a core diagnostic feature of Autism Spectrum Disorder. Olfactory sensory neurons calibrate to the environment by reducing their excitability when chronically activated by a constant environmental odor and increased their excitability after sustained periods of low or no activity. Calibration of olfactory sensory neurons involves modulation of a transcriptional program that alters neuronal excitability by changing the expression of genes involved in processes including olfactory receptor signaling, calcium homeostasis, and regulation of membrane potential. Notably, many of these genes that support sensory calibration are Autism Spectrum Disorder risk genes. While it is known that neuronal activity alters expression of this transcriptional program, it is unclear how neuronal activity is paired to transcriptional modulation. Preliminary data suggests a role for the activity-dependent Nuclear Factor of Activated T cells (NFAT) in regulation of activity-dependent gene regulation in olfactory sensory neurons. The current proposal uses molecular biology, neurophysiology, and behavior to test the central hypothesis that the activity- dependent transcription factor NFAT is enables sensory calibration by modulating the transcription of genes that regulate neuronal excitability. First, the genomic binding sites of NFAT factors in olfactory sensory neurons will be identified. Second, the role of NFAT factors in sensory calibration will be tested by examining the consequences of inhibiting NFAT factors on the neurophysiological and behavioral response to odors after prolonged odor exposure. Finally, the role of NFAT factors in transcription of genes underlying sensory calibration will be examined using single-cell RNA sequencing in mice with inhibited NFAT activity. The studies in this proposal will identify mechanisms of sensory calibration which may be disrupted in neurodevelopmental disorders with sensory processing differences and may lead to novel therapies for sensory processing disorders. The research plan described will provide the applicant with additional technical and scientific training required to be a competitive independent investigator. The research plan will be executed in a stimulating, supportive scientific environment which is committed to the success of the applicant.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $76,780 )
2026	2026	RUTGERS, THE STATE UNIVERSITY	3 RUTGERS PLZ	NEW BRUNSWICK	NJ	08901	MIDDLESEX	USA	Research Related to Deafness and Communication Disorders	000	1	4/3/2026	NEW	$76,780
														Subtotal = $76,780

Grand Total All Awards = $76,780

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"Calibration of olfactory sensory neuron excitability by NFAT transcription factors"

Award Number: F32DC023805

ORGANIZATION: NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/30/2026

PERIOD OF PERFORMANCE END DATE: 09/29/2027

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