Estrogen receptor‐beta colocalizes extensively with parvalbumin‐labeled inhibitory neurons in the cortex, amygdala, basal forebrain, and hippocampal formation of intact and ovariectomized adult rats

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Abstract
Estrogen has been reported to regulate the activity of γ‐aminobutyric acid (GABA)ergic interneurons within the hippocampus, basal forebrain, and hypothalamus of adult rodents. Although estrogen receptor‐alpha bearing GABAergic interneurons have been identified previously, the neurotransmitter phenotype of cells that express the more recently characterized estrogen receptor‐beta (ER‐β) has not been examined in vivo. We, therefore, have used fluorescent immunohistochemistry to further characterize the phenotype of ER‐β–bearing cells by double labeling for the GABAergic‐associated calcium‐binding protein, parvalbumin (PV). We find that a large proportion of ER‐β–immunoreactive cells within the cortex, amygdala, basal forebrain, and hippocampal formation of intact and ovariectomized (ovx) adult rats are PV‐immunoreactive. Within the infralimbic, agranular insular, primary motor, parietal association, perirhinal, and lateral entorhinal cortices, an average of 95.6% ± 0.8% (intact) and 94.5% ± 1.4% (ovx) of all ER‐β–immunoreactive cells coexpress parvalbumin, and this proportion is strikingly similar across these diverse cortical regions. ER‐β/PV double‐labeled cells represent 23.3% ± 1.6% (intact) and 25.8% ± 2.0% (ovx) of all PV‐labeled cells within these regions. ER‐β/PV double‐labeled cells are also observed within the lateral, accessory basal, and posterior cortical nuclei of the amygdala, and periamygdaloid cortex. Within the basal forebrain, 31.0% ± 3.1% (intact) and 26.0% ± 5.2 % (ovx) of ER‐β–immunoreactive cells coexpress PV. Almost all ER‐β–immunoreactive cells within the subiculum, a major output region of the hippocampal formation, double label for PV (intact = 97.2% ± 2.8%; ovx = 100% ± 0.0%). Thus, ER‐β exhibits extensive colocalization with a subclass of inhibitory neurons, suggesting a potential mechanism whereby estrogen can regulate neuronal excitability in diverse and broad brain regions by modulating inhibitory tone. J. Comp. Neurol. 452:276–287, 2002.