Acute Hippocampal Brain-Derived Neurotrophic Factor Restores Motivational and Forced Swim Performance After Corticosterone

Gourley, Shannon L.; Kiraly, Drew D.; Howell, Jessica L.; Olausson, Peter; Taylor, Jane R.

doi:10.1016/j.biopsych.2008.06.016

Cited by 182 publications

(167 citation statements)

References 49 publications

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“…Figure 1d illustrates the total dose of CORT in mg/kg per rat per day consumed at days sampled during the 50 mg/ml phase of CORT exposure, indicating that the level of CORT the rats were exposed to ranged from approximately 12.5-7.5 mg/kg across days and decreased in direct relation to their increase in weight. The total dose at the end of the exposure period is similar to that previously reported for adult rats, and that maintains high levels of circulating CORT Gourley et al, 2008a).…”

Section: Corticosterone Exposuresupporting

confidence: 84%

Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

Torregrossa

Xie

Taylor

2012

Neuropsychopharmacol

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Chronic stress during adolescence is associated with an increased risk for alcoholism and addictive disorders. Addiction is also associated with increased impulsivity, and stress during adolescence could alter cortical circuits responsible for response inhibition. Therefore, the present study determined the effect of chronic exposure to the stress hormone corticosterone (CORT) during adolescence on tests of impulsivity in adulthood and examined possible biochemical mechanisms. Male Sprague-Dawley rats were exposed to CORT by their drinking water during adolescence (post-natal day 30-50). The rats were then tested in adulthood to assess behavior on the 5-choice serial reaction time task (5CSRTT), stop-signal reaction time task (SSRTT), and the delay-discounting task, which differentially assess attention, impulsive action, and impulsive choice. Yohimbine-induced impulsivity on the 5CSRTT and biochemical analysis of the lateral orbital frontal cortex (lOFC) was also assessed owing to the ability of yohimbine to activate the hypothalamic-pituitary-adrenal axis and influence impulsivity. Adolescent CORT-treated rats were found to behave largely like controls on the 5CSRTT, but did show reduced premature responses when the intertrial interval was increased. Nevertheless, the CORT-treated rats tended to have more yohimbineinduced impulsive responses at low doses on this task, which was not found to be due to increased pCREB in the lOFC, but could be related to a higher expression/activity of the AMPA receptor subunit GluR1. Adolescent CORT-treated rats performed more accurately on the SSRTT, but showed greater impulsivity on the delay-discounting task, as indicated by steeper discounting functions. Therefore, adolescent CORT exposure reduced impulsive action but increased impulsive choice, indicating that chronic stress hormone exposure in adolescence can have long-term consequences on behavior.

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Section: Corticosterone Exposuresupporting

confidence: 84%

Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

Torregrossa

Xie

Taylor

2012

Neuropsychopharmacol

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“…These and related findings suggest a role for BDNF in the etiology and treatment of depression. On the other hand, chronic stress exposure decreases hippocampal cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) phosphorylation (pCREB) (13). CREB, in turn, regulates several targets involved in activity-dependent neuronal plasticity, including BDNF (13).…”

Section: The Mechanisms Of Electroconvulsive Stimuli In Brdu-positivementioning

confidence: 99%

“…On the other hand, chronic stress exposure decreases hippocampal cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) phosphorylation (pCREB) (13). CREB, in turn, regulates several targets involved in activity-dependent neuronal plasticity, including BDNF (13). Finally, we reported that repeated electroconvulsive stimuli treatment increased BDNF protein levels in the hippocampus in rats repeatedly treated with ACTH (4).…”

Section: The Mechanisms Of Electroconvulsive Stimuli In Brdu-positivementioning

confidence: 99%

The Mechanisms of Electroconvulsive Stimuli in BrdU-Positive Cells of the Dentate Gyrus in ACTH-Treated Rats

et al. 2013

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Abstract. In clinical studies, electroconvulsive stimuli have been associated with improvements in both depression and treatment-resistant depression. In a previous study, treatment with adrenocorticotropic hormone (ACTH) for 14 days decreased adult hippocampal cell proliferation. Furthermore, electroconvulsive stimuli significantly decreased the duration of immobility following repeated administration of ACTH for 14 days in rats. The present study was undertaken to further characterize the mechanism of treatment-resistant antidepressant effects of electroconvulsive stimuli by measuring cell proliferation, brain-derived neurotrophic factor (BDNF) levels, and phosphorylated and total cyclic adenosine monophosphate (cAMP) response elementbinding protein (pCREB/CREB) levels in the hippocampus of ACTH-treated rats. Electroconvulsive stimuli increased cell proliferation in both saline-treated and ACTH-treated rats. Mature-BDNF protein levels showed a tendency to decrease in ACTH-treated rats. Electroconvulsive stimuli treatment increased mature-BDNF protein levels in the hippocampus of both saline-treated and ACTH-treated rats. Furthermore, electroconvulsive stimuli increased phospho-Ser133-CREB (pCREB) levels and the ratio of pCREB/CREB in both saline-treated and ACTH-treated rats. These findings suggest that the treatment-resistant antidepressant effects of electroconvulsive stimuli may be attributed, at least in part, to an enhancement of hippocampal cell proliferation.

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“…Human recombinant BDNF (Chemicon) dissolved in sterile saline in a concentration of 0.4 mg/mL (Gourley et al 2008b) was used, with 0.2 mL/site at AP +2.0, DV À2.5, ML 60.1 (Gourley et al 2008a) infused over 2 min with needles left in place for 2 min after infusion.…”

mentioning

confidence: 99%

“…Several studies indicate BDNF has behavioral effects for several days after infusion into the striatum (Horger et al 1999), ventral tegmental area (Lu et al 2004), hippocampus (Shirayama et al 2002;Gourley et al 2008b), and prefrontal cortex (Berglind et al 2007(Berglind et al , 2009). Therefore, we utilized a single-infusion protocol: Food restriction resumed on day 5 after surgery, at which point mice appeared active.…”

mentioning

confidence: 99%

Prelimbic cortex bdnf knock-down reduces instrumental responding in extinction

Gourley¹,

Howell²,

Rios³

et al. 2009

Learn. Mem.

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Anatomically selective medial prefrontal cortical projections regulate the extinction of stimulus–reinforcement associations, but the mechanisms underlying extinction of an instrumental response for reward are less well-defined and may involve structures that regulate goal-directed action. We show brain-derived neurotrophic factor (bdnf) knock-down in the prelimbic, but not orbitofrontal, cortex accelerates the initial extinction of instrumental responding for food and reduces striatal BDNF protein. When knock-down mice were provided with alternative response options to readily obtain reinforcement, extinction of the previously reinforced response was unaffected, consistent with the hypothesis that the prelimbic cortex promotes instrumental action, particularly when reinforcement is uncertain or unavailable.

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Acute Hippocampal Brain-Derived Neurotrophic Factor Restores Motivational and Forced Swim Performance After Corticosterone

Cited by 182 publications

References 49 publications

Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

The Mechanisms of Electroconvulsive Stimuli in BrdU-Positive Cells of the Dentate Gyrus in ACTH-Treated Rats

Prelimbic cortex bdnf knock-down reduces instrumental responding in extinction

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