Expression of Calbindin, a Marker of Gamma-Aminobutyric Acid Neurons, Is Reduced in the Amygdala of Oestrogen Receptor β-Deficient Female Mice

Abstract

Oestrogen receptor β (ERβ) knock-out female mice display increased anxiety and decreased threshold for synaptic plasticity induction in the basolateral amygdala. This may suggest that the γ-aminobutyric acid (GABA) inhibitory system is altered. Therefore, the immunoreactivity of main GABAergic markers—i.e., calbindin, parvalbumin, calretinin, somatostatin, α1 subunit-containing GABAA receptor and vesicular GABA transporter—were compared in the six subregions (LA, BL, BM, ME, CE and CO) of the amygdala of adult female wild-type and ERβ knock-out mice using immunohistochemistry and quantitative methods. The influence of ERβ knock-out on neuronal loss and glia was also elucidated using pan-neuronal and astrocyte markers. The results show severe neuronal deficits in all main amygdala regions in ERβ knock-out mice accompanied by astroglia overexpression only in the medial, basomedial and cortical nuclei and a decrease in calbindin-expressing neurons (CB+) in the amygdala in ERβ knock-out mice compared with controls, while other markers of the GABAergic system remain unchanged. Concluding, the lack of ERβ led to failure in the structural integrity of the CB+ subpopulation, reducing interneuron firing and resulting in a disinhibitory effect over pyramidal function. This fear-promoting excitatory/inhibitory alteration may lead to the increased anxiety observed in these mice. The impact of neuronal deficits and astroglia overexpression on the amygdala functions remains unknown.

SARS-CoV-2 S1 protein causes brain inflammation by reducing intracerebral acetylcholine production

“…In order to investigate the influence of systemic inflammation in brain inflammation, we administered lipopolysaccharide (LPS) intraperitoneally to the S1 mouse to enhance systemic inflammation and investigated expression of neural differentiation markers in the olfactory bulb and brain. As a result, the expression of calbindin, 48 , 49 a GABAergic neuron marker, was markedly decreased. ( Figures 2 I and 2J).…”

Does sex influence the natural history of idiopathic adult-onset dystonia?

“…The men's preponderance in those forms of dystonia like ULD that mainly develop before menopause, and the women's preponderance in those forms of dystonia, like cranial dystonia, that mostly develop at around or after menopause, would suggest a protective role of oestrogens on dystonia development. Supporting this view, oestrogens have been proposed as a protective factor for GABAergic systems and the nigrostriatal dopaminergic system, [17][18][19] both implicated in developing animal models of dystonia. 20 21 If oestrogens contribute to developing at least some forms of IAOD, there may be a complex interaction between hormonal influences and putative environmental risk factors.…”