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Reproductive Endocrine Unit, Massachusetts General Hospital/Harvard Medical School (S.M.L., W.F.C.), and Department of Biochemistry, University of Massachusetts Medical School (S.A.T.), Boston, Massachusetts 02114; and Department of Biosciences, University of Helsinki (K.K.), SF-00014 Helsinki, Finland
Address all correspondence and requests for reprints to: Dr. Sarah M. Leupen, Reproductive Endocrine Unit, BHX-519, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114. E-mail: leupen{at}world.oberlin.edu.
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
-aminobutyric acidA (GABAA) receptor activation to trigger a hyperpolarization. In its absence, GABAs 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 GABAA receptor activation throughout life, supporting the existence of functionally heterogeneous subpopulations.
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