Abstract

Experiencing stress during adolescence can severely impact appropriate adult stress responsiveness. Our lab utilizes a mouse model in which peripubertal (P30) mice are subjected to repeated aggressive social defeats, followed by tests for social interaction. When peripubertal animals are tested 24 hours after defeat, all defeated mice interact at levels similar to non-defeated controls. However, when the same mice are tested again, in adulthood, defeated mice show a split in behavior; some display social avoidance (susceptible), whereas others display normal social interaction (resistant). Furthermore, our lab found that the stress hormone, corticosterone, plays a role in shaping this divergent behavior, and increased levels during peripubertal interactions is associated with increased adult social interaction. We hypothesized that high corticosterone during the peripubertal period ameliorates the adult deficits in social behavior. To confirm this, peripubertal mice received corticosterone in their drinking water over night prior to social interaction testing at P32. Corticosterone at P32 ameliorates the deficits in adult social behavior caused by peripubertal social defeat. Pharmacologically blocking glucocorticoid receptors (GR) blocks the enhanced social behavior produced by corticosterone administration. Surprisingly, mice administered corticosterone, but not subjected to a social interaction test at P32, do not display increased social behavior as adults. These data suggest that corticosterone interacts with re-exposure to ameliorate the social behavior deficits caused by peripubertal social defeat. Therefore, corticosterone in combination with exposure therapy may be useful to combat against the long term, detrimental effects of early life social stress.

Modified Abstract

Our lab exposes peripubertal (P30) mice to repeated aggressive social defeats, followed by tests for social interaction. When mice are tested 24 hours after defeat, all defeated mice display interaction. When the same mice are tested in adulthood (P62), some display social avoidance, whereas others display normal social interaction. Corticosterone over night prior to social interaction testing at P32 ameliorates the deficits in adult social behavior caused by peripubertal social defeat. Pharmacologically blocking glucocorticoid receptors blocks enhanced social behavior produced by corticosterone administration. Mice administered corticosterone, but not subjected to a social interaction test at P32, do not display increased social behavior as adults. This data suggests that corticosterone interacts with re-exposure to ameliorate the social behavior deficits caused by peripubertal social defeat.

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

21-3-2017 1:00 PM

Research Area

Behavioral Neurobiology | Developmental Biology | Developmental Neuroscience | Molecular and Cellular Neuroscience

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Mar 21st, 1:00 PM

Corticosterone ameliorates the adult social behavior deficits caused by peripubertal social defeat

Experiencing stress during adolescence can severely impact appropriate adult stress responsiveness. Our lab utilizes a mouse model in which peripubertal (P30) mice are subjected to repeated aggressive social defeats, followed by tests for social interaction. When peripubertal animals are tested 24 hours after defeat, all defeated mice interact at levels similar to non-defeated controls. However, when the same mice are tested again, in adulthood, defeated mice show a split in behavior; some display social avoidance (susceptible), whereas others display normal social interaction (resistant). Furthermore, our lab found that the stress hormone, corticosterone, plays a role in shaping this divergent behavior, and increased levels during peripubertal interactions is associated with increased adult social interaction. We hypothesized that high corticosterone during the peripubertal period ameliorates the adult deficits in social behavior. To confirm this, peripubertal mice received corticosterone in their drinking water over night prior to social interaction testing at P32. Corticosterone at P32 ameliorates the deficits in adult social behavior caused by peripubertal social defeat. Pharmacologically blocking glucocorticoid receptors (GR) blocks the enhanced social behavior produced by corticosterone administration. Surprisingly, mice administered corticosterone, but not subjected to a social interaction test at P32, do not display increased social behavior as adults. These data suggest that corticosterone interacts with re-exposure to ameliorate the social behavior deficits caused by peripubertal social defeat. Therefore, corticosterone in combination with exposure therapy may be useful to combat against the long term, detrimental effects of early life social stress.