Abstract

Adolescence is a critical developmental period during which stress reactivity is exacerbated compared to adulthood. This study utilized a mild repeated social defeat model to investigate the impact of early life social stress on subsequent social behavior. Social defeat in adults typically results in two phenotypic responses: social approach (resistance) and social avoidance (susceptibility). To investigate the development of these phenotypes, we followed neuroendocrine responses through defeat, social interaction, and adulthood. Our previous data showed that prepubertal defeated mice remaining resistant into adulthood had high levels of corticosterone at P32 compared to susceptible and control mice. The present study manipulates corticosterone after social interaction to determine if high early life corticosterone shaped adult social behavior. Prepubertal C57BL/6J (Post natal day 30, P30) mice were placed into the home cage of a territorial CD-1 aggressor for 3 attacks or 5 minutes followed by 55 minutes of sensory contact 4 times for 2 consecutive days. Twenty-four hours and 30 days later, mice completed a social test where amount of time spent interacting with a non-aggressive CD-1 mouse was measured. Following this test, mice were administered corticosterone or vehicle control. During prepubertal (P32) social interaction, mice were resistant. At P62, a split in phenotype was observed; some mice remained resistant and some became susceptible. We expect corticosterone administration to promote adult resistance to prepubertal social defeat. Data from these and future studies will help determine how neuroendocrine mechanisms interact with development to influence the ontogeny of responses to prepubertal social stress.

Modified Abstract

The current study utilized a mild repeated social defeat model to investigate the impact of early life social stress on subsequent social behavior. Social defeat in adults typically results in two phenotypic responses during a social interaction test: social approach (resistance) and social avoidance (susceptibility). To investigate the development of these phenotypes, we measured neuroendocrine response after social interaction. Our previous data showed that prepubertal defeated mice that remain resistant into adulthood showed high levels of prepubertal corticosterone compared to susceptible and control mice. The present study manipulates corticosterone immediately after social interaction to determine if high early life corticosterone shaped adult social behavior. These data will help determine how neuroendocrine mechanisms interact with development to influence the ontogeny of responses to perpubertal social stress.

Research Category

Psychology

Primary Author's Major

Psychology

Mentor #1 Information

Dr. Aaron Jasnow

Mentor #2 Information

Ms. Maeson Latsko

Presentation Format

Poster

Start Date

March 2016

Research Area

Biological Psychology

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Mar 15th, 1:00 PM

Does elevated corticosterone predict adult resistance to prepubertal social defeat?

Adolescence is a critical developmental period during which stress reactivity is exacerbated compared to adulthood. This study utilized a mild repeated social defeat model to investigate the impact of early life social stress on subsequent social behavior. Social defeat in adults typically results in two phenotypic responses: social approach (resistance) and social avoidance (susceptibility). To investigate the development of these phenotypes, we followed neuroendocrine responses through defeat, social interaction, and adulthood. Our previous data showed that prepubertal defeated mice remaining resistant into adulthood had high levels of corticosterone at P32 compared to susceptible and control mice. The present study manipulates corticosterone after social interaction to determine if high early life corticosterone shaped adult social behavior. Prepubertal C57BL/6J (Post natal day 30, P30) mice were placed into the home cage of a territorial CD-1 aggressor for 3 attacks or 5 minutes followed by 55 minutes of sensory contact 4 times for 2 consecutive days. Twenty-four hours and 30 days later, mice completed a social test where amount of time spent interacting with a non-aggressive CD-1 mouse was measured. Following this test, mice were administered corticosterone or vehicle control. During prepubertal (P32) social interaction, mice were resistant. At P62, a split in phenotype was observed; some mice remained resistant and some became susceptible. We expect corticosterone administration to promote adult resistance to prepubertal social defeat. Data from these and future studies will help determine how neuroendocrine mechanisms interact with development to influence the ontogeny of responses to prepubertal social stress.