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Pancreatic polypeptide inhibits somatostatin secretion
Kim, W.,Fiori, J.L.,Shin, Y.K.,Okun, E.,Kim, J.S.,Rapp, P.R.,Egan, J.M. North-Holland Pub ; Elsevier Science Ltd 2014 FEBS letters Vol.588 No.17
Pancreatic polypeptide (PP) is a major agonist for neuropeptide Y4 receptors (NPY4R). While NPY4R has been identified in various tissues, the cells on which it is expressed and its function in those cells has not been clearly delineated. Here we report that NPY4R is present in all somatostatin-containing cells of tissues that we tested, including pancreatic islets, duodenum, hippocampus, and hypothalamus. Its agonism by PP decreases somatostatin secretion from human islets. Mouse embryonic hippocampal (mHippo E18) cells expressed NPY4Rs and their activation by PP consistently decreased somatostatin secretion. Furthermore, central injection of PP in mice induced c-Fos immunoreactivity in somatostatin-containing cells in the hippocampus compared with PBS-injected mice. In sum, our results identify PP as a pivotal modulator of somatostatin secretion.
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Leonardo Almeida,Daniel Martinez-Ramirez,Peter J. Rossi,Zhongxing Peng,Aysegul Gunduz,Michael S. Okun 대한신경과학회 2015 Journal of Clinical Neurology Vol.11 No.2
Tourette syndrome is a childhood-onset disorder characterized by a combination of motor andvocal tics, ofen associated with psychiatric comorbidities including attention defcit and hyperactivity disorder and obsessive-compulsive disorder. Despite an onset early in life, half of patients may present symptoms in adulthood, with variable degrees of severity. In select cases,the syndrome may lead to signifcant physical and social impairment, and a worrisome riskfor self injury. Evolving research has provided evidence supporting the idea that the pathophysiology of Tourette syndrome is directly related to a disrupted circuit involving the cortexand subcortical structures, including the basal ganglia, nucleus accumbens, and the amygdala. Tere has also been a notion that a dysfunctional group of neurons in the putamen contributes to an abnormal facilitation of competing motor responses in basal ganglia structures ultimately underpinning the generation of tics. Surgical therapies for Tourette syndrome have beenreserved for a small group of patients not responding to behavioral and pharmacological therapies, and these therapies have been directed at modulating the underlying pathophysiology. Lesion therapy as well as deep brain stimulation has been observed to suppress tics in at leastsome of these cases. In this article, we will review the clinical aspects of Tourette syndrome, aswell as the evolution of surgical approaches and we will discuss the evidence and clinical responses to deep brain stimulation in various brain targets. We will also discuss ongoing research and future directions as well as approaches for open, scheduled and closed loop feedback-driven electrical stimulation for the treatment of Tourette syndrome.
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Cheng, Y.L.,Park, J.S.,Manzanero, S.,Choi, Y.,Baik, S.H.,Okun, E.,Gelderblom, M.,Fann, D.Y.W.,Magnus, T.,Launikonis, B.S.,Mattson, M.P.,Sobey, C.G.,Jo, D.G.,Arumugam, T.V. Blackwell Science ; Academic Press 2014 Neurobiology of disease Vol.62 No.-
Recent findings suggest that Notch-1 signaling contributes to neuronal death in ischemic stroke, but the underlying mechanisms are unknown. Hypoxia inducible factor-1α (HIF-1α), a global regulator of cellular responses to hypoxia, can interact with Notch and modulate its signaling during hypoxic stress. Here we show that Notch signaling interacts with the HIF-1α pathway in the process of ischemic neuronal death. We found that a chemical inhibitor of the Notch-activating enzyme, γ-secretase, and a HIF-1α inhibitor, protect cultured cortical neurons against ischemic stress, and combined inhibition of Notch-1 and HIF-1α further decreased neuronal death. HIF-1α and Notch intracellular domain (NICD) are co-expressed in the neuronal nucleus, and co-immunoprecipitated in cultured neurons and in brain tissue from mice subjected to focal ischemic stroke. Overexpression of NICD and HIF-1α in cultured human neural cells enhanced cell death under ischemia-like conditions, and a HIF-1α inhibitor rescued the cells. RNA interference-mediated depletion of endogenous NICD and HIF-1α also decreased cell death under ischemia-like conditions. Finally, mice treated with inhibitors of γ-secretase and HIF-1α exhibited improved outcome after focal ischemic stroke, with combined treatment being superior to individual treatments. Additional findings suggest that the NICD and HIF-1α collaborate to engage pro-inflammatory and apoptotic signaling pathways in stroke.
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