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Several studies have demonstrated that estrogen modulates brain‐derived neurotrophic factor (BDNF) mRNA and protein within the adult hippocampus and cortex. However, mechanisms underlying this regulation are unknown. Although an estrogen response element (ERE)‐like sequence has been identified within the BDNF gene, such a classical mechanism of estrogen‐induced transcriptional activation requires the colocalized expression of estrogen receptors within cells that produce BDNF. Developmental studies have demonstrated such a relationship, but to date no studies have examined colocalization of estrogen receptors and BDNF within the adult brain. By utilizing double‐label immunohistochemistry for BDNF, estrogen receptor‐α (ER‐α), and estrogen receptor‐β (ER‐β), we found only sparse colocalization between ER‐α and BDNF in the hypothalamus, amygdala, prelimbic cortex, and ventral hippocampus. Furthermore, ER‐β and BDNF do not colocalize in any brain region. Given the recent finding that cortical ER‐β is almost exclusively localized to parvalbumin‐immunoreactive GABAergic neurons, we performed BDNF/parvalbumin double labeling and discovered that axons from cortical ER‐β‐expressing inhibitory neurons terminate on BDNF‐immunoreactive pyramidal cells. Collectively, these findings support a potential transsynaptic relationship between estrogen state and cortical BDNF: By directly modulating GABAergic interneurons, estrogen may indirectly influence the activity and expression of BDNF‐producing cortical neurons. J. Comp. Neurol. 468:347–360, 2004. © 2003 Wiley‐Liss, Inc.

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Adding uPA to NMP22 and cytology improves their ability to predict bladder TCC by a statistically and prognostically substantial margin. An approach using multiple biomarkers may improve the diagnostic accuracy of voided urinary diagnostic tests.

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