Project description:Behavioral transitions Young infant rats paradoxically prefer odors paired with shock but older pups learn aversions. This transition is amygdala- and corticosterone-dependent. Microarray results showed downregulated dopaminergic presynaptic function in the amygdala with preference learning. Corticosterone injected 8-day-old pups and untreated 12-day-old pups learn aversions and had dopaminergic upregulation in the amygdala.
Project description:Behavioral transitions Young infant rats paradoxically prefer odors paired with shock but older pups learn aversions. This transition is amygdala- and corticosterone-dependent. Microarray results showed downregulated dopaminergic presynaptic function in the amygdala with preference learning. Corticosterone injected 8-day-old pups and untreated 12-day-old pups learn aversions and had dopaminergic upregulation in the amygdala. 8 day saline or corticosterone treated- or 12 day old untreated rat pups were trained with odor-shock pairings. Immediately after training pups were sacrificed and the amygdala dissected out. Controls were unpaired shock-odor groups.Paired and unpaired groups were processed together for each experimental condition. Paired and unpaired data were compared by ranked products.
Project description:We show that infant trauma, as modeled by infant paired odor-shock conditioning, results in later life depressive-like behavior that can be modulated by learned infant cues (i.e., odor previously paired with shock). We have previously shown that this infant attachment odor learning paradigm results in the creation of a new artificial maternal odor that is able to control pup behavior and retain its value throughout development. Here, we assess the mechanism by which this artificial maternal odor is able to rescue depressive-like behavior and show that this anti-depressant like effect results in glucocorticoid and serotonin (5-HT) related changes in amygdala gene expression and is dependent on amygdala 5-HT. Furthermore, increasing amygdala 5-HT and blocking corticosterone (CORT) in the absence of odor mimics the adult rescue effects elicited by the artificial maternal odor, suggesting a mechanism by which odor presentation exerts its repair effects. There are three experimental groups: 1: pups with no infant shock and the adult forced swim test (FST)with no odor; 2. pups with infant odor-shock pairing and the adult forced swim test (FST) with no odor; 3. pups with infant odor-shock pairing and adult forced swim test with infant odor.
Project description:We show that infant trauma, as modeled by infant paired odor-shock conditioning, results in later life depressive-like behavior that can be modulated by learned infant cues (i.e., odor previously paired with shock). We have previously shown that this infant attachment odor learning paradigm results in the creation of a new artificial maternal odor that is able to control pup behavior and retain its value throughout development. Here, we assess the mechanism by which this artificial maternal odor is able to rescue depressive-like behavior and show that this anti-depressant like effect results in glucocorticoid and serotonin (5-HT) related changes in amygdala gene expression and is dependent on amygdala 5-HT. Furthermore, increasing amygdala 5-HT and blocking corticosterone (CORT) in the absence of odor mimics the adult rescue effects elicited by the artificial maternal odor, suggesting a mechanism by which odor presentation exerts its repair effects.
Project description:Gene expression within the prefrontal cortex and amygdala in a developing model of high and low anixety and depression-like behavior in rats
