Intramuscular antagonism of the G-protein coupled estrogen receptor 1 partially affects dimorphic characteristics of the syrinx, but is ineffective within the neural song circuit of zebra finches
androgen receptor; behavior; brain; control nuclei; Drug delivery; estradiol; Estrogen receptor; expression; GPER1 antagonist; gpr30; growth; Sexual dimorphism; sexual-differentiation; Songbird; Syrinx; system
Within the zebra finch song system, robust sex differences exist that enable singing behavior in males, but not females. Estradiol is a potent contributor to this process, but how and through which receptor(s) it acts is not clear. Historically, pharmacological manipulations of nuclear estrogen receptors have yielded conflicting results possibly due to method of drug delivery. More recently, the membrane bound G-protein coupled estrogen receptor 1 (GPER1) has also been identified as a potential candidate, but its function has not been fully described. To further investigate the role of GPER1, and the importance of the route of drug administration, a specific antagonist (G-15) was intramuscularly administered to zebra finches for 25 days, starting on the day of hatching. G-15 significantly decreased muscle fiber sizes of ventralis and dorsalis in the syrinx of males only. Dimorphic characteristics of the neural song system were unaffected by this manipulation in either sex. These results contrast with a study in which G-15 was intracranially delivered. In males, select song nuclei were decreased in volume, and in females, syrinx muscle fiber size was increased. Together, these results support the hypothesis that estrogens acting through GPER1 influence dimorphic development of the song system, and that method of drug administration is important in this species.
Tehrani Mahtab Attarhaie; Veney Sean L
General and Comparative Endocrinology
2020
2020-07-01
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journalArticle
<a href="http://doi.org/10.1016/j.ygcen.2020.113492" target="_blank" rel="noreferrer noopener">10.1016/j.ygcen.2020.113492</a>
Knockdown Of Leptin A Expression Dramatically Alters Zebrafish Development
atlantic salmon; Auditory; bhlh genes; bone; carp cyprinus-carpio; cell fate specification; central-nervous-system; cloning; danio-rerio; differentiation; Endocrinology & Metabolism; gene; metabolism; n-cadherin; receptor; sensory ganglia; Visual; visual-system
Using morpholino antisense oligonucleotide (MO) technology, we blocked leptin A or leptin receptor expression in embryonic zebrafish, and analyzed consequences of leptin A knock-down on fish development. Embryos injected with leptin A or leptin receptor MOs (leptin A or leptin receptor morphants) had smaller bodies and eyes, undeveloped inner ear, enlarged pericardial cavity, curved body and/or tail and larger yolk compared to control embryos of the same stages. The defects persisted in 6-9 days old larvae. We found that blocking leptin A function had little effect on the development of early brain (1 day old), but differentiation of both the morphant dorsal brain and retinal cells was severely disrupted in older (2 days old) embryos. Despite the enlarged pericardial cavity, differentiation of cardiac cells appeared to be similar to control embryos. Formation of the morphants' inner ear is also severely disrupted, which corroborates existing reports of leptin receptor expression in inner ear of both zebrafish and mammals. Co-injection of leptin A MO and recombinant leptin results in partial rescue of the wild-type phenotype. Our results suggest that leptin A plays distinct roles in zebrafish development. (c) 2012 Elsevier Inc. All rights reserved.
Liu Q; Dalman M; Chen Y; Akhter M; Brahmandam S; Patel Y; Lowe J; Thakkar M; Gregory A V; Phelps D; Riley C; Londraville R L
General and Comparative Endocrinology
2012
2012-09
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/j.ygcen.2012.07.011" target="_blank" rel="noreferrer noopener">10.1016/j.ygcen.2012.07.011</a>