Journal
ENDOCRINOLOGY
Volume 144, Issue 7, Pages 3031-3036Publisher
ENDOCRINE SOC
DOI: 10.1210/en.2002-220995
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Funding
- NICHD NIH HHS [HD 33441, HD 08630-02] Funding Source: Medline
- NIMH NIH HHS [MH 57748] Funding Source: Medline
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In mature central neurons, chloride extrusion mediated by the K-Cl cotransporter KCC2 appears to be largely responsible for the Cl- driving force that allows gamma-aminobutyric acid(A) (GABA(A)) receptor activation to trigger a hyperpolarization. In its absence, GABA's effect is typically depolarizing and often excitatory. We examined the colocalization of KCC2 and GnRH in adult male and female mice using a combined in situ hybridization-immunofluorescence procedure. We found that KCC2 was localized to approximately 34% of GnRH neurons. This proportion was similar in females and males. However, females exhibited a marked rostrocaudal gradient of colocalization that was not seen in males. By contrast, KCC2 was localized to nearly all vasopressin neurons of the supraoptic nucleus. These results indicate that a substantial fraction of GnRH neurons may be depolarized and excited by GABA(A) receptor activation throughout life, supporting the existence of functionally heterogeneous subpopulations.
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