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Mechanisms of serotonergic signaling in the auditory midbrain in aging

Award Number: R01DC023215
ORGANIZATION: NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/28/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2031

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Mechanisms of serotonergic signaling in the auditory midbrain in aging - Abstract Age-related hearing loss (ARHL) is the most common form of hearing loss in older adults. Because ARHL causes difficulty understanding speech in noisy environments, it can lead to social isolation and depression. ARHL leads to a shift in the balance of excitatory and inhibitory (EI) circuits in the inferior colliculus (IC), favoring excitability. This homeostatic process, known as enhanced gain, is likely to compensate for the loss of drive from the periphery. When enhanced gain is exacerbated, it can result in pathological conditions such as tinnitus and impaired temporal processing. The mechanisms that regulate EI balance in the IC remain unclear. The serotonergic system has been shown to regulate EI balance in other brain regions, and it is an excellent target for interventions as it can influence excitability without directly altering basic neural functions. Serotonergic fibers from the dorsal raphe nuclei densely innervate the IC, and previous studies have shown that serotonin elicits diverse effects on IC neurons. However, the cellular and synaptic mechanisms of serotonergic modulation in the IC, and whether serotonergic inputs change in ARHL, remain largely unknown. In our recent study, we showed that GABAergic IC neurons primarily express excitatory serotonergic receptors. In contrast, glutamatergic IC neurons primarily express inhibitory serotonergic receptors, suggesting an inhibitory net effect of serotonin in the IC. Based on our past studies and new preliminary data, this proposal aims to determine (1) how does the expression of serotonergic receptors as well as serotonergic synapses to GABAergic and glutamatergic IC neurons change in young mice with normal hearing and older mice with ARHL, (2) how the effect of exogenously and endogenously released serotonin alters the activity of two distinct classes of IC GABAergic neurons as well as glutamatergic neurons in young mice with normal hearing and old mice with hearing loss and (3) how serotonin alter distinct sources of presynaptic inputs to two classes of GABAergic as well glutamatergic IC neurons. The proposed experiments represent a significant step toward our long-term goal of understanding how neuromodulation reconfigures neural networks in the central auditory pathway, thereby providing a mechanistic foundation for the development of neuromodulatory therapeutics aimed at improving hearing for individuals with hearing impairments.


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 = $466,462 )
2026	2026	THE UNIVERSITY OF TEXAS AT SAN ANTONIO	1 UTSA CIR	SAN ANTONIO	TX	78249	BEXAR	USA	Research Related to Deafness and Communication Disorders	000	1	7/30/2026	NEW	$466,462
														Subtotal = $466,462

Grand Total All Awards = $466,462

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Mechanisms of serotonergic signaling in the auditory midbrain in aging

Award Number: R01DC023215

ORGANIZATION: NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 07/28/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2031

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