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Direct Involvement of Orexinergic Systems in the Activation of the Mesolimbic Dopamine Pathway and Related Behaviors Induced by Morphine
Findings provide new evidence that orexin-containing neurons in the VTA are directly implicated in the rewarding effect and hyperlocomotion induced by morphine through activation of the mesolimbic dopamine pathway in rodents. Expand
Selective p38α MAPK Deletion in Serotonergic Neurons Produces Stress Resilience in Models of Depression and Addiction
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
Ligand-directed c-Jun N-terminal kinase activation disrupts opioid receptor signaling
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
Direct evidence for the involvement of brain‐derived neurotrophic factor in the development of a neuropathic pain‐like state in mice
It is demonstrated here for the first time that the increase in intracellular Ca2+ concentration by application of BDNF in cultured mouse spinal neurons was abolished by pre‐treatment with either K‐252a or Ro‐32‐0432. Expand
Implication of protein kinase C in the orexin‐induced elevation of extracellular dopamine levels and its rewarding effect
In the present study, we investigated the role of orexinergic systems in the activation of midbrain dopamine neurons. In an in vitro study, exposure to either orexin A or orexin B under superfusionExpand
Duration of Action of a Broad Range of Selective κ-Opioid Receptor Antagonists Is Positively Correlated with c-Jun N-Terminal Kinase-1 Activation
This work used C57BL/6 wild type mice to determine the durations of antagonist action of novel κ-opioid receptor ligands and examined their efficacies for JNK1 activation compared with conventional competitive antagonists. Expand
Direct Evidence of Astrocytic Modulation in the Development of Rewarding Effects Induced by Drugs of Abuse
Direct evidence is provided that astrocytes may, at least in part, contribute to the synaptic plasticity induced by drugs of abuse during the development of rewarding effects induced by psychostimulants and opioids. Expand
Kappa opioids promote the proliferation of astrocytes via Gβγ and β‐arrestin 2‐dependent MAPK‐mediated pathways
Proliferative actions of both agonists were abolished by either inhibition of ERK1/2, Gβγ subunits or β‐arrestin 2, suggesting that both G protein‐dependent and ‐independent ERK pathways are required for this outcome. Expand
Direct evidence for spinal cord microglia in the development of a neuropathic pain‐like state in mice
The present data strongly support the idea that spinal cord astrocytes and microglia are activated under the neuropathic pain‐like state, and that the proliferated and activated micro glial cells directly contribute to the development of a neuropathicPain‐ like state in mice. Expand
Chronic pain‐induced emotional dysfunction is associated with astrogliosis due to cortical δ‐opioid receptor dysfunction
It is shown that mice with chronic pain exhibit anxiety‐like behavior and an increase of astrocytes in the cingulate cortex due to the dysfunction of cortical δ‐opioid receptor systems, which may lead to emotional disorders including aggravated anxiety under chronic pain‐like state. Expand