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Regulation of serotonin-stimulated phosphoinositide hydrolysis: relation to the serotonin 5-HT-2 binding site

PJ Conn and E Sanders-Bush
Journal of Neuroscience 1 December 1986, 6 (12) 3669-3675; DOI: https://doi.org/10.1523/JNEUROSCI.06-12-03669.1986
PJ Conn
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E Sanders-Bush
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Abstract

The hypothesis that serotonin (5-HT)-stimulated phosphoinositide hydrolysis is mediated by the 5-HT-2 binding site in cerebral cortex was tested by comparing antagonist Kd values determined by Schild analyses with Ki values at the 5-HT-2 binding site. A significant correlation was found between Kd values and Ki values at competing for 3H-ketanserin binding (R = 0.98), suggesting that the phosphoinositide- linked receptor and the 5-HT-2 site are identical. The 5-HT-2-mediated phosphoinositide response was then used as a measure of 5-HT-2 receptor sensitivity after in vivo treatments that alter the availability of 5- HT. Chronic treatment with the 5-HT-2 antagonist mianserin resulted in a significant decrease (52%) in the density of 5-HT-2 binding sites and a significant decrease (49%) in the maximal phosphoinositide hydrolysis response to 5-HT. Depletion of 5-HT levels with para- chlorophenylalanine or chemical denervation of serotonergic neurons with 5,7-dihydroxytryptamine had no significant effect upon 5-HT-2 receptor density or upon the phosphoinositide response to 5-HT. These data suggest that changes or lack of changes in 5-HT-2 receptor density following in vivo manipulations reflect the functional state of the receptor.

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The Journal of Neuroscience: 6 (12)
Journal of Neuroscience
Vol. 6, Issue 12
1 Dec 1986
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Regulation of serotonin-stimulated phosphoinositide hydrolysis: relation to the serotonin 5-HT-2 binding site
PJ Conn, E Sanders-Bush
Journal of Neuroscience 1 December 1986, 6 (12) 3669-3675; DOI: 10.1523/JNEUROSCI.06-12-03669.1986

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Regulation of serotonin-stimulated phosphoinositide hydrolysis: relation to the serotonin 5-HT-2 binding site
PJ Conn, E Sanders-Bush
Journal of Neuroscience 1 December 1986, 6 (12) 3669-3675; DOI: 10.1523/JNEUROSCI.06-12-03669.1986
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