Serotonergic stimulation of @entity3318 and XXXX gene expression.

@entity9210 @entity905 @entity50568 @entity10463 @entity14919 @entity2476 @entity3318 @entity750 @entity29235 @entity35
The neurotransmitter @entity750 ( @entity750 ) stimulates adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary gland via activation of central 5-HT1 and 5-HT2 receptors. The effect of @entity750 is predominantly indirect and may be mediated via release of hypothalamic @entity3318 ( @entity3318 ). We therefore investigated the possible involvement of @entity3318 in the serotonergic stimulation of ACTH secretion in male @entity35 . Increased neuronal @entity750 content induced by systemic administration of the precursor @entity2476 ( @entity2476 ) in combination with the @entity750 reuptake inhibitor @entity905 raised @entity3318 mRNA expression in the paraventricular nucleus (PVN) by 64%, increased @entity9210 ( @entity9210 ) mRNA in the anterior pituitary lobe by 17% and stimulated ACTH secretion five-fold. Central administration of @entity750 agonists specific to @entity10463 , @entity29235 , @entity14919 or @entity50568 receptors increased @entity3318 mRNA in the PVN by 15-50%, @entity9210 mRNA in the anterior pituitary by 15-27% and ACTH secretion three- to five-fold, whereas a specific 5-HT3 agonist had no effect. Systemic administration of a specific anti- @entity3318 antiserum inhibited the ACTH response to @entity2476 and @entity905 and prevented the @entity2476 and @entity905 -induced @entity9210 mRNA response in the anterior pituitary lobe. Central or systemic infusion of @entity750 increased ACTH secretion seven- and eight-fold, respectively. Systemic pretreatment with the anti- @entity3318 antiserum reduced the ACTH responses to @entity750 by 80% and 64%, respectively. It is concluded that @entity750 via activation of @entity10463 , @entity14919 , @entity50568 and possibly also @entity29235 receptors increases the synthesis of @entity3318 in the PVN and @entity9210 in the anterior pituitary lobe, which results in increased ACTH secretion. Furthermore, the results indicate that @entity3318 is an important mediator of the ACTH response to @entity750 .
