PT  - JOURNAL ARTICLE
AU  - TM Esterle
AU  - E Sanders-Bush
TI  - Serotonin agonists increase transferrin levels via activation of 5-HT1C receptors in choroid plexus epithelium
AID  - 10.1523/JNEUROSCI.12-12-04775.1992
DP  - 1992 Dec 01
TA  - The Journal of Neuroscience
PG  - 4775--4782
VI  - 12
IP  - 12
4099  - http://www.jneurosci.org/content/12/12/4775.short
4100  - http://www.jneurosci.org/content/12/12/4775.full
SO  - J. Neurosci.1992 Dec 01; 12
AB  - Choroid plexus epithelial cells are enriched in mRNA for proteins such as the iron carrier transferrin, which acts as a trophic factor in the brain. Choroid plexus epithelial cells also have a high density of 5- HT1C receptors linked to activation of the phosphoinositide (PI) hydrolysis second messenger system. The present studies show that the 5- HT1C/5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2- aminopropane (DOI) potently increases PI hydrolysis and the levels of transferrin in primary cultures of rat choroid plexus epithelial cells. These effects are blocked by the 5-HT1C/5-HT2 receptor antagonists mesulergine and mianserin, but not by the 5-HT2 receptor-selective antagonist spiperone. Similarly, mesulergine and mianserin, but not spiperone, block the increases in transferrin levels and PI hydrolysis elicited by 5-carboxamidotryptamine (5-CT), a 5-HT1 receptor-selective agonist, and by serotonin. We conclude, therefore, that 5-HT1C receptor activation in the choroid plexus leads to an increase in the production of transferrin. By promoting transferrin synthesis in the choroid plexus, 5-HT may indirectly influence brain development and differentiation.