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  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 306 (1979), S. 173-177 
    ISSN: 1432-1912
    Schlagwort(e): Serotonin turnover ; Kainic acid ; Corpus striatum ; Feedback regulation
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Kainic acid, a cyclic analog of glutamate, has been reported by other investigators to reduce the number of serotonin (5HT) binding sites in rat striatum following an intrastriatal injection. We found that kainic acid injected into the striatum caused a dose-dependent increase in ipsilateral striatal 5-hydroxyindoleacetic acid (5HIAA) content, while not affecting the level of 5HT. There was no detectable change in 5HT metabolism in the contralateral striatum. The increase of 5HIAA was a reflection of increased 5HT turnover in the injected striatum as measured from the decline of 5HIAA after pargyline treatment or the rise of 5-hydroxytryptophan after benserazide treatment. There was also a concomitant increase of tryptophan hydroxylase activity. Kainic acid treatment resulted in an apparent decrease of the K mand increase of the V max for the pteridine cofactor and an increase of the V max for tryptophan by tryptophan hydroxylase. Kainic acid injection into the dorsal raphe nucleus caused a dose-dependent decrease in 5HT content of the dorsal raphe nucleus and in both striata, which are dorsal raphe nucleus projection areas. Our results suggest that 5HT formation in the striatum is normally modulated by an inhibitory neuronal feedback loop. Interruption of the loop by injecting kainic acid causes 5HT formation and tryptophan hydroxylase activity to increase in the ipsilateral but not contralateral striatum. Kainic acid apparently destroys 5HT neurons when injected close to the cell soma.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Cellular and molecular neurobiology 11 (1991), S. 455-462 
    ISSN: 1573-6830
    Schlagwort(e): muscarinic receptors ; adenylate cyclase ; cyclic AMP ; phosphoinositide hydrolysis ; phorbol esters ; pertussis toxin ; cholera toxin ; rat retina
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie
    Notizen: Summary 1. Agonist activation of rat retina muscarinic receptors results in suppression of cyclic AMP (cAMP) generation and enhanced phosphoinositide hydrolysis. 2. Pharmacological manipulations that elevate cAMP or stable analogues of cAMP attenuate the acetylcholine (ACh)-induced enhancement of phosphoinositide hydrolysis. We postulate that cross-talk between adenylate cyclase and phospholipase C signal transducing systems probably exists in rat retina, as has been described for other systems. 3. Intraocular administration of pertussis toxin attenuated the response of both adenylate cyclase and phospholipase C to muscarinic stimulation, suggesting that some retinal muscarinic receptors are apparently coupled to their effector systems via pertussis toxin sensitive G proteins.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Cellular and molecular neurobiology 3 (1983), S. 17-26 
    ISSN: 1573-6830
    Schlagwort(e): dopamine ; opiates ; adenylate cyclase ; striatum
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie
    Notizen: Summary 1. Low-affinity (micromolar)3H-dopamine binding was measured under conditions which permitted dopamine activation and opiate inhibition of adenylate cyclase in rat striatal membranes. Opiate drugs and peptides inhibited the dopamine binding in the presence of both GTP5 and Gpp(NH)p. Opiate inhibition of adenylate cyclase was, however, observed only in the presence of GTP. 2. It is suggested that the dopamine D1 receptor in striatum may be modulated by the opiate delta receptor through a shared guanine nucleotide binding subunit.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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