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The Dysphoric Component of Stress Is Encoded by Activation of the Dynorphin κ-Opioid System
TLDR
The convergence of stress-induced aversive inputs on the Dynorphin system was unexpected, implicates dynorphin as a key mediator of dysphoria, and emphasizes κ-receptor antagonists as promising therapeutics. Expand
Injectable, Cellular-Scale Optoelectronics with Applications for Wireless Optogenetics
TLDR
The ability of these ultrathin, mechanically compliant, biocompatible devices to afford minimally invasive operation in the soft tissues of the mammalian brain foreshadow applications in other organ systems, with potential for broad utility in biomedical science and engineering. Expand
The dynorphin/kappa opioid system as a modulator of stress-induced and pro-addictive behaviors
TLDR
Results suggest that activation of the dynorphin/kappa opioid receptor (KOR) system is likely to play a major role in the pro-addictive effects of stress and novel insight to neuropeptide systems that regulate affective state is provided. Expand
Molecular mechanisms of opioid receptor-dependent signaling and behavior.
TLDR
There is a continued need for more translational work on opioid receptors in vivo and the authors put into context how opioid receptor signaling leads to the modulation of behavior with the potential for therapeutic intervention. Expand
Activation of the kappa opioid receptor in the dorsal raphe nucleus mediates the aversive effects of stress and reinstates drug seeking
TLDR
The results suggest that the adverse effects of stress may converge on the serotonergic system and offers an approach to controlling stress-induced dysphoria and relapse. Expand
Stress-Induced p38 Mitogen-Activated Protein Kinase Activation Mediates κ-Opioid-Dependent Dysphoria
TLDR
It is shown that repeated swim stress caused activation of both κ-opioid receptor (KOR) and p38 mitogen-activated protein kinase (MAPK) coexpressed in GABAergic neurons in the nucleus accumbens, cortex, and hippocampus, and this constitutes a key component of the molecular mechanisms mediating the aversive properties of stress. Expand
Kinase cascades and ligand-directed signaling at the kappa opioid receptor
TLDR
The current status of KOR signal transduction research is discussed and the data that support two novel hypotheses are discussed: (1) KOR selective partial agonists that do not efficiently activate p38 MAPK may be useful analgesics without producing the dysphoric or hallucinogenic effects of selective, highly efficacious KOR agonists and (2) Kor antagonists thatDo not activate JNK may be effective short-acting drugs that may promote stress-resilience. Expand
Selective p38α MAPK Deletion in Serotonergic Neurons Produces Stress Resilience in Models of Depression and Addiction
TLDR
It is suggested that stress initiates a cascade of molecular and cellular events in which p38α MAPK induces a hyposerotonergic state underlying depression-like and drug-seeking behaviors. Expand
Kappa Opioid Receptor Activation of p38 MAPK Is GRK3- and Arrestin-dependent in Neurons and Astrocytes*
TLDR
The results suggest that KOR may activate p38 MAPK in brain by a GRK3 and arrestin-dependent mechanism. Expand
Ligand-directed c-Jun N-terminal kinase activation disrupts opioid receptor signaling
TLDR
It is found that the μ-opioid receptor (MOR) could be similarly inactivated by a specific ligand class including the prototypical opioid, morphine, and acute analgesic tolerance to morphine and related opioids was blocked by JNK inhibition, but not by G protein receptor kinase 3 knockout. Expand
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