| Autor: | S B Ross, C Stenfors |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Synapsin I
medicine.medical_specialty Calmodulin biology Kinase Cyclin-dependent kinase 2 Mitogen-activated protein kinase kinase Tryptophan hydroxylase Psychiatry and Mental health Endocrinology Neurology Internal medicine Ca2+/calmodulin-dependent protein kinase medicine biology.protein Neurology (clinical) Protein kinase A Biological Psychiatry |
| Zdroj: | Journal of Neural Transmission. 109:1353-1363 |
| ISSN: | 0300-9564 |
| DOI: | 10.1007/s00702-002-0732-5 |
| Popis: | Inhibition of cAMP-dependent protein kinase (PKA) with N-[2-methylamino)ethyl]-5-isoquinolinesulfonamide (H-8) almost completely antagonized the increase in 5-HTP accumulation and 5-HIAA/5-HT ratio in hypothalamus induced by NAS-181, a 5-HT(1B) receptor antagonist, but had no effect when the mice were treated with NAS-181 together with WAY-100,635, a selective 5-HT(1A) receptor antagonist. Inhibition of Ca(2+)-calmodulin-dependent protein kinase (CaM kinase II) with the calmodulin antagonist N-(4-aminobutyl)-5-chloro-2-naphtalenesulfonamide (W-13) did not antagonise the effect of NAS-181 alone, but counteracted that evoked by the combined treatment with NAS-181 and WAY-100,635. The results indicate that activation of tryptophan hydroxylase by reducing the tone from terminal 5-HT(1B) receptors involves PKA whereas the depolarisation-induced activation of tryptophan hydroxylase involves CaM kinase II. The increase in the 5-HIAA/5-HT ratio may under the experimental conditions used suggest CaM kinase II-induced phosphorylation of synapsin I resulting in increased 5-HT release. |
| Databáze: | OpenAIRE |
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