Related Experiment Video
Updated: May 16, 2026
12:12
Irrelevant Stimuli and Action Control: Analyzing the Influence of Ignored Stimuli via the Distractor-Response Binding Paradigm
Published on: May 14, 2014
Action control is mediated by prefrontal BDNF and glucocorticoid receptor binding
Shannon L Gourley1, Andrew M Swanson, Andrea M Jacobs
1Department of Pediatrics, Graduate Program in Neuroscience, Yerkes National Primate Research Center, Emory School of Medicine, Atlanta, GA 30329, USA. shannon.l.gourley@emory.edu
Summary
Chronic stress impairs decision-making and motivation by affecting glucocorticoid receptors (GR) and brain-derived neurotrophic factor (BDNF). Riluzole may reverse these stress-induced deficits.
Area of Science:
- Neuroscience
- Behavioral Science
- Endocrinology
Background:
- Stressor exposure alters decision-making strategies, shifting from outcome-based to stimulus-response associations.
- Chronic stress desensitizes glucocorticoid receptors (GR) and reduces motivation, but causal links are unclear.
Purpose of the Study:
- To investigate the causal role of GR and brain-derived neurotrophic factor (BDNF) in stress-induced changes in decision-making and motivation.
- To explore potential therapeutic interventions for stress-related deficits.
Main Methods:
- Rodents were exposed to chronic corticosterone or acute GR blockade (RU38486).
- Medial prefrontal cortex (mPFC) BDNF was selectively knocked down.
- Behavioral tasks assessed decision-making and motivation (progressive-ratio task).
- Riluzole was administered to assess its effects on stress-induced deficits.
Main Results:
- GR activation is necessary for learning response-outcome associations.
- Medial prefrontal BDNF levels correlate with motivation, and its knockdown induces amotivation and RU38486 vulnerability.
- Riluzole reversed corticosterone-induced motivational deficits and restored mPFC BDNF.
Conclusions:
- Compromised prefrontal neurotrophin systems and desensitized GR feedback contribute to amotivation and inflexible strategies in chronic stress.
- These deficits are linked to stress-related mood disorders.
- Riluzole shows potential for reversing stress-induced motivational deficits.
More Related Videos
Related Concept Videos
01:37Hypothalamic-Pituitary Axis
The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
01:09GPCRs Regulate Adenylyl Cylase Activity
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Two...
01:31Sympathetic Signaling
Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...
01:25cAMP-dependent Protein Kinase Pathways
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
01:26Adrenergic Receptors: β Subtype
β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
02:04Co-activators and Co-repressors
Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...