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Role of hippocampal HCN Channels in social avoidance

Award Number: R01MH134958
ORGANIZATION: NATIONAL INSTITUTE OF MENTAL HEALTH
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/10/2024
PERIOD OF PERFORMANCE END DATE: 02/28/2029

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Role of hippocampal HCN Channels in social avoidance - Contact PD/PI: Kim, Chung Sub Abstract Social stress in humans increases the risk of mental health problems. Individuals who experience physical and/or emotional bullying display anxiety, depression, and social avoidance. Despite the gender differences and individual variance in stress-related mental disorders, most preclinical research on the effects of social stress has been conducted on male subjects. Chronic social defeat stress (CSDS) is a rodent model of psychosocial stress that causes fear-based social avoidance and anhedonia. We have developed direct physical (i.e., inter- male and inter-female aggression) and witnessing mouse models of social avoidance. Using male and female mouse models of social avoidance, we find that hyperpolarization-activated cyclic nucleotide-gated nonselective cation (HCN) channels are increased in the dorsal hippocampus of susceptible male and female mice. Moreover, the levels of HCN protein expression and hyperpolarization-activated current (Ih) are higher in susceptible female mice than in susceptible male mice. Notably, behavioral responses to social defeat are different between male and female mice. Consistent with these preclinical findings, HCN1 mRNA expression in isolated CA1 areas is elevated in human patients with major depressive disorder. We hypothesize that hippocampal HCN channels mediate sex-dependent behavioral coping and individual differences in social avoidance. To test this hypothesis, we propose three specific aims. In Aim 1, we will test the hypothesis that the changes in neuronal activity mediated by the HCN channels in the hippocampal CA1 neurons affect behavioral susceptibility and resilience to social defeat. In Aim 2, we will test the hypothesis that the HCN channels in the hippocampal CA1 neurons affects sex differences in behavioral coping with social defeat and individual differences in social avoidance. In Aim 3, we will test the hypothesis that estradiol promotes sex-dependent behavioral susceptibility and passive coping with social defeat through HCN channels. Together, the results are expected to provide insights into the novel molecular and cellular mechanisms underlying dendritic HCN channels that regulate stress coping and individual differences in social defeat and offer novel therapeutic targets for stress-related mental disorders.


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 = $393,981 )
2026	2026	AUGUSTA UNIVERSITY RESEARCH INSTITUTE, INC	AUGUSTA UNIVERSITY 1120 15TH STREET	AUGUSTA	GA	30912	RICHMOND	USA	Mental Health Research Grants	000	3	3/26/2026	NON-COMPETING CONTINUATION	$393,981
														Subtotal = $393,981

Issue Date FY: 2025 ( Subtotal = $334,884 )
2025	2025	AUGUSTA UNIVERSITY RESEARCH INSTITUTE, INC	AUGUSTA UNIVERSITY 1120 15TH STREET	AUGUSTA	GA	30912	RICHMOND	USA	Mental Health Research Grants	000	2	3/18/2025	NON-COMPETING CONTINUATION	$334,884
														Subtotal = $334,884

Issue Date FY: 2024 ( Subtotal = $393,981 )
2024	2024	AUGUSTA UNIVERSITY RESEARCH INSTITUTE, INC	AUGUSTA UNIVERSITY 1120 15TH STREET	AUGUSTA	GA	30912	RICHMOND	USA	Mental Health Research Grants	000	1	7/10/2024	NEW	$393,981
														Subtotal = $393,981

Grand Total All Awards = $1,122,846

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Role of hippocampal HCN Channels in social avoidance

Award Number: R01MH134958

ORGANIZATION: NATIONAL INSTITUTE OF MENTAL HEALTH

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 07/10/2024

PERIOD OF PERFORMANCE END DATE: 02/28/2029

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