Three populations of hypothalamic neuroendocrine dopaminergic (NEDA) neurons, arising from the arcuate and periventricular nuclei of the hypothalamus release @entity935 (DA) that acts at the pituitary gland to regulate the secretion of @entity3695 . It is generally accepted that NEDA neurons lack functional @entity18404 ( @entity18404 ), which are responsible for uptake of DA from the synaptic cleft into the presynaptic axon terminal. This study localized @entity18404 to the hypothalamo-pituitary axis and evaluated the effect of DAT blockade on the hypothalamo-pituitary regulation of @entity3695 . After 7 days of treatment with @entity2072 (a nonspecific @entity6115 transporter blocker) or @entity9015 (a specific DAT blocker), the relative abundance of @entity3695 messenger RNA (mRNA) in the anterior lobe (AL) of OVX @entity35 was significantly decreased, whereas the relative abundance of @entity669 hydroxylase mRNA in the hypothalamus was significantly increased. The effect of @entity2072 or @entity9015 administration on DA turnover and serum @entity3695 concentration was examined in @entity53 (E2)-treated OVX @entity35 . E2 administration (i.v.) resulted in a significant increase in serum @entity3695 within 4 h; however, @entity2072 or @entity9015 administration abolished the E2-induced increase of @entity3695 . @entity2072 or @entity9015 significantly increased the concentration of DA at the site of the axon terminals within the median eminence (ME), intermediate lobe (IL) and @entity1274 ( @entity1274 ), indicating blockade of uptake. Because formation of @entity4925 requires uptake of DA, concentrations of @entity4925 in the ME, IL and @entity1274 decreased following treatment with either @entity2072 or @entity9015 . These data, together with the presence of immunopositive DAT in the ME, pituitary stalk, IL, and @entity1274 , suggest that a functional DAT system is present within all three populations of NEDA neurons. Moreover, similarity between the effects of @entity2072 and @entity9015 treatment indicate that blockade of the DAT, but not other @entity6115 transporters, is responsible for suppression of @entity3695 gene expression and secretion. Blockade of @entity18404 prevent uptake of DA into NEDA neurons and consequently increases the amount of DA that diffuses into the portal vasculature and reaches the AL. These data provide evidence that @entity18404 play a physiological role in the regulation of DA release from and TH expression in NEDA neurons and consequently @entity3695 secretion and @entity3695 gene expression and further support our previous observation that the regulation of @entity3695 secretion involves all three populations of NEDA neurons.

XXXX transporters participate in the physiological regulation of prolactin.

@entity4925 :: ('MESH:D015102', 'Chemical') :: ['DOPAC'] @entity935 :: ('MESH:D004298', 'Chemical') :: ['dopamine'] @entity6115 :: ('CHEBI:32952', 'Chemical') :: ['amine'] @entity53 :: ('MESH:D004958', 'Chemical') :: ['estradiol'] @entity3695 :: ('24683(Tax:10116)', 'Gene') :: ['PRL'] @entity2072 :: ('MESH:D003042', 'Chemical') :: ['Cocaine', 'cocaine'] @entity1274 :: ('MESH:D006319', 'Disease') :: ['neural lobe', 'NL'] @entity18404 :: ('MESH:C567730', 'Disease') :: ['DA transporters', 'DATs'] @entity35 :: ('10116', 'Species') :: ['rats'] @entity669 :: ('CHEBI:18186', 'Chemical') :: ['tyrosine'] @entity9015 :: ('MESH:D008454', 'Chemical') :: ['mazindol']
@entity935 :: (MESH:D004298,Chemical) :: ['Dopamine']
