Detail of "143896-17-7"

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Galanin inhibits tyrosine hydroxylase expression in midbrain dopaminergic neurons

Galanin inhibits tyrosine hydroxylase expression in midbrain dopaminergic neurons. Counts, Scott E.; McGuire, Susan O.; Sortwell, Caryl E.; Crawley, Jacqueline N.; Collier, Timothy J.; Mufson, Elliott J. (Department of Neurological Sciences, Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612, USA). Journal of Neurochemistry, 83(2), 442-451 (English) 2002 Blackwell Science Ltd. CODEN: JONRA9. ISSN: 0022-3042. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Galanin (GAL) inhibits midbrain dopamine (DA) activity in several exptl.There are some reagents with their cas registry numbers 7440-09-7 and 143896-17-7 are used in this study. paradigms, yet the mechanism underlying this inhibition is unclear. The authors examd. the effects of GAL on the expression of tyrosine hydroxylase (TH) in primary cultures of rat embryonic (E14) ventral mesencephalon (VM). One micromolar GAL had no effect on the no. of TH-immunoreactive (ir) neurons in VM cultures. However, 1 mM GAL reduced an approx. 100% increase in TH-ir neurons in 1 mM dibutyryl cAMP (dbcAMP)-treated cultures by ~50%. TH-ir neuron no. in dbcAMP-treated VM cultures was dose-responsive to GAL and the GAL receptor antagonist M40 blocked GAL effects. Semi-quant. RT-PCR and quant. immunoblotting expts. revealed that GAL had no effect on TH mRNA levels in VM cultures but reduced TH protein. VM cultures expressed GALR1, GALR2, and GALR3 receptor mRNA. However, dbcAMP treatment resulted in a specific ~200% increase in GALR1 mRNA. GALR1 activity is linked to a pertussis toxin (PTX)-sensitive opening of G protein-gated K+ channels (GIRKs). GAL redn. of TH-ir neuron no. in dbcAMP + GAL-treated cultures was sensitive to both PTX and tertiapin, a GIRK inhibitor. GAL inhibition of midbrain DA activity may involve a GALR1-mediated redn. of TH in midbrain dopaminergic neurons. .

Compounds and methods for increasing neurogenesis by administering an agent that elevates intracellular cAMP

Compounds and methods for increasing neurogenesis by administering an agent that elevates intracellular cAMP. Bertilsson, Goran; Erlandsson, Rikard; Frisen, Jonas; Haegerstrand, Anders; Heidrich, Jessica; Hellstrom, Nina; Haggblad, Johan; Jansson, Katarina; Kortesmaa, Jarkko; Lindquist, Per; Lundh, Hanna; McGuire, Jacqueline; Mercer, Alex; Nyberg, Karl; Ossoinak, Amina; Patrone, Cesare; Ronnholm, Harriet; Wikstrom, Lilian; Zachrisson, Olof ( Neuronova AB, Swed.). U.S. Pat. Appl. Publ. US 2005009742 A1 13 Jan 2005, 45 pp., Cont.-in-part of U.S. Ser. No. 718,071. (English). (United States of America). CODEN: USXXCO. CLASS: ICM: A61K038-17. ICS: A61K038-12. APPLICATION: US 2004-850055 19 May 2004. PRIORITY: US 2003-2003/718071 20 Nov 2003; US 2002-2002/PV427912 20 Nov 2002. DOCUMENT TYPE: Patent CA Section: 1 (Pharmacology) The invention is directed to methods of promoting neurogenesis by contacting neuronal tissue with neurogenesis modulating agents. Novel methods for treating neurol. disorders using neurogenesis modulating agents are disclosed. At least one agent that elevates intracellular cAMP levels in the tissue is administered. Rats given i. 137110-97-5 and 143896-17-7 which are cas registry numbers of substances are two of reagents here.p. infusion of exendin-4 or calcitonin co-administered with BrdU twice daily showed a significant increase in the no. of newborn cells (BrdU pos. compared to sham injected) in highly neurogenic regions including the sub ventricular zone and the dentate gyrus in the hippocampus. These data indicate that exendin-4 and calcitonin exhibit an unexpected neural stem cell proliferative effect pointing to neurogenesis. .