Calcium-Calmodulin-Dependent Protein Kinase Type 2

Publication Title: 
Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology

Chronic social defeat stress in mice produces a susceptible phenotype characterized by several behavioral abnormalities consistent with human depression that are reversed by chronic but not acute exposure to antidepressant medications. Recent work in addiction models demonstrates that the transcription factor ?FosB and protein kinase calmodulin-dependent protein kinase II (CaMKII) are co-regulated in nucleus accumbens (NAc), a brain reward region implicated in both addiction and depression models including social defeat.

Author(s): 
Robison, A. J.
Vialou, Vincent
Sun, Hao-Sheng
LabontÈ, Benoit
Golden, Sam A.
Dias, Caroline
Turecki, Gustavo
Tamminga, Carol
Russo, Scott
Mazei-Robison, Michelle
Nestler, Eric J.
Publication Title: 
British Journal of Pharmacology

BACKGROUND AND PURPOSE: Artemisinin is an antimalarial drug exerting pleiotropic effects, such as the inhibition of the transcription factor nuclear factor-kappa B and of the sarcoplasmic/endoplasmic reticulum Ca(++)-ATPase (SERCA) of P. falciparum.

Author(s): 
Riganti, C.
Doublier, S.
Viarisio, D.
Miraglia, E.
Pescarmona, G.
Ghigo, D.
Bosia, A.
Publication Title: 
The Journal of Pharmacology and Experimental Therapeutics

The limited data that currently exist for the role of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in neuropathic pain are conflicting. In the present study, we tested the hypothesis that CaMKII is required for the maintenance of neuropathic pain in a rodent model of experimental mononeuropathy. Spinal nerve L(5)/L(6) ligation (SNL) was found to increase the spinal activity of CaMKII (pCaMKII) on the ipsilateral (but not contralateral) side.

Author(s): 
Chen, Yan
Luo, Fang
Yang, Cheng
Kirkmire, Chelsea M.
Wang, Zaijie Jim
Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

Repeated administration of opioids not only leads to tolerance and dependence, but also results in nociceptive enhancement called opioid-induced hyperalgesia (OIH). Nociceptive mediators involved in OIH generation remain poorly understood. In the present study, we tested the hypothesis that Ca(2+)/calmodulin-depent protein kinase II (CaMKIIalpha) is critical for OIH. Opioid-induced hyperalgesia was produced by repeated morphine administration or pellet implantation in mice.

Author(s): 
Chen, Yan
Yang, Cheng
Wang, Zaijie Jim
Publication Title: 
The Biochemical Journal

IbeA in meningitic Escherichia coli K1 strains has been described previously for its role in invasion of BMECs (brain microvascular endothelial cells). Vimentin was identified as an IbeA-binding protein on the surface of HBMECs (human BMECs). In the present study, we demonstrated that vimentin is a primary receptor required for IbeA+ E. coli K1-induced signalling and invasion of HBMECs, on the basis of the following observations. First, E44 (IbeA+ E.

Author(s): 
Chi, Feng
Jong, Timothy D.
Wang, Lin
Ouyang, Yannan
Wu, Chunhua
Li, Wei
Huang, Sheng-He
Publication Title: 
Hematology / the Education Program of the American Society of Hematology. American Society of Hematology. Education Program

Pain is a frequent complaint of people living with sickle cell disease (SCD); however, the neurobiology of pain in SCD remains poorly understood. Whereas this pain has been thought to be primarily related to visceral and somatic tissue injury subsequent to vaso-occlusion events, emerging evidence from human and animal studies has suggested that a component of SCD pain may be related to neuropathic processes. Significant knowledge has been obtained from studies of molecular and neurobiological mechanisms leading to and maintaining neuropathic pain.

Author(s): 
Wang, Zaijie J.
Wilkie, Diana J.
Molokie, Robert
Publication Title: 
The Journal of Pharmacology and Experimental Therapeutics

Previous studies from our laboratory and others have implicated a critical role of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in opioid tolerance and dependence. Translational research targeting the CaMKII pathway is challenging, if not impossible, because of a lack of selective inhibitors. We discovered in a preliminary study that haloperidol, a butyrophenone antipsychotic drug, inhibited CaMKII, which led us to hypothesize that haloperidol can attenuate opioid tolerance and dependence by inhibiting CaMKII.

Author(s): 
Yang, Cheng
Chen, Yan
Tang, Lei
Wang, Zaijie Jim
Publication Title: 
American Journal of Physiology. Regulatory, Integrative and Comparative Physiology

Glucose in the gut lumen activates gut endocrine cells to release 5-HT, glucagon-like peptide 1/2 (GLP-1/2), and glucose-dependent insulinotropic polypeptide (GIP), which act to change gastrointestinal function and regulate postprandial plasma glucose. There is evidence that both release and action of incretin hormones is reduced in type 2 diabetes (T2D). We measured cellular activation of enteroendocrine and enterochromaffin cells, enteric neurons, and vagal afferent neurons in response to intestinal glucose in a model of type 2 diabetes mellitus, the UCD-T2DM rat.

Author(s): 
Lee, Jennifer
Cummings, Bethany P.
Martin, Elizabeth
Sharp, James W.
Graham, James L.
Stanhope, Kimber L.
Havel, Peter J.
Raybould, Helen E.
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