Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin (SST) is a multifunctional peptide and involves in several neurodegenerative diseases. N-Methyl-D-asparate (NMDA) receptor agonist quinolinic acid (QUIN)-induced neurotoxicity mimics an experimental model of Huntington's disease that is characterized by the selective preservation of medium-sized aspiny interneurons and degeneration of medium-sized spiny projection neurons in striatum. In QUIN- and NMDA-induced neurotoxicity, increased expression of SST and messenger RNA levels along with SST release in culture medium is generally observed. However, the molecular mechanisms and the functional consequences of increased SST are still obscure. In the present study, the role of SST was determined using immunoneutralization and immunoblockade of SST in cultured striatal neurons upon QUIN- and NMDA-induced neurotoxicity. The immunoblockade of SST with antisense oligonucleotides and immunoabsorption of released SST with specific antibodies potentiate QUIN- and NMDA-induced neuronal cell death. NADPH-diaphorase positive neurons that are selectively spared in several processes of neurodegeneration result in severe damage upon immunoblockade or immunoabsorption of SST. In addition, exogenous SST along with QUIN and NMDA provides selective preservation of projection neurons, which are selectively susceptible in excitotoxicity. Neuroprotective effect of SST is completely blocked by pertussis toxins, suggesting the role of somatostatin receptors. Taken together, these results provide first evidence that the presence of SST is a unique feature for the selective sparing of medium sized aspiny interneurons in excitotoxicity.
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PMID:Somatostatin in medium-sized aspiny interneurons of striatum is responsible for their preservation in quinolinic acid and N-methyl-D-asparate-induced neurotoxicity. 1848 77

Orexin A and B are hypothalamic peptides with a wide variety of effects such as anti-inflammation and neuroprotection. Impaired function of orexin system has been reported in some neurodegenerative diseases like Parkinson, Huntington and Alzheimer. In this study, the mRNA expression levels of some hypothalamic peptides were investigated in C57BL/6 female mice with experimental autoimmune encephalomyelitis (EAE). Animals were randomly divided into two control and EAE groups. EAE was induced by administration of myelin oligodendrocyte glycoprotein (MOG) with complete Ferund's adjuvant and pertussis toxin. Twenty-first days following immunization, mice were decapitated to remove the brains. Then, the expression profiles of prepro-orexin, orexin 1 receptors (OX1R) and orexin 2 receptors (OX2R) in hypothalamic region were assessed using real-time PCR method. In this study, we found a considerable increase in the mRNA expression of OX1R and OX2R following EAE induction in C57BL/6 mice. Elevation levels of OX1R and OX2R following EAE induction suggest that alteration in orexinergic system may involve in pathogenesis of multiple sclerosis.
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PMID:Increase in mRNA Level of Orexin1 and 2 Receptors Following Induction of Experimental Autoimmune Encephalomyelitis in Mice. 2699 8