Acute neuroestrogen blockade attenuates song-induced immediate early gene expression in auditory regions of male and female zebra finches.
Amanda A KrentzelMaaya Z IkedaTessa J OliverEra KoroveshiLuke Remage-HealeyPublished in: Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology (2019)
Neuron-derived estrogens are synthesized by aromatase and act through membrane receptors to modulate neuronal physiology. In many systems, long-lasting hormone treatments can alter sensory-evoked neuronal activation. However, the significance of acute neuroestrogen production is less understood. Both sexes of zebra finches can synthesize estrogens rapidly in the auditory cortex, yet it is unclear how this modulates neuronal cell signaling. We examined whether acute estrogen synthesis blockade attenuates auditory-induced expression of early growth response 1 (Egr-1) in the auditory cortex of both sexes. cAMP response element-binding protein phosphorylation (pCREB) induction by song stimuli and acute estrogen synthesis was also examined. We administered the aromatase inhibitor fadrozole prior to song exposure and measured Egr-1 across several auditory regions. Fadrozole attenuated Egr-1 in the auditory cortex greater in males than females. Females had greater expression and clustering of aromatase cells than males in high vocal center (HVC) shelf. Auditory-induced Egr-1 expression exhibited a large sex difference following fadrozole treatment. We did not observe changes in pCREB expression with song presentation or aromatase blockade. These findings are consistent with the hypothesis that acute neuroestrogen synthesis can drive downstream transcriptional responses in several cortical auditory regions, and that this mechanism is more prominent in males.
Keyphrases
- liver failure
- drug induced
- working memory
- binding protein
- hearing loss
- poor prognosis
- respiratory failure
- gene expression
- aortic dissection
- high glucose
- diabetic rats
- single cell
- functional connectivity
- long non coding rna
- transcription factor
- induced apoptosis
- dna methylation
- cell proliferation
- estrogen receptor
- protein kinase
- cerebral ischemia
- rna seq
- heat shock protein