ABSTRACT
It is unknown whether the famous sex-related difference in emotion processing is accounted for by biological sex, gender role, or their interaction. To clarify the issue, in Study 1 we recorded event-related potentials in response to negative and positive images of diverse intensities when 47 masculine (26 males) and 47 feminine (22 males) subjects performed a non-emotional task. The occipital P1 and N1 amplitudes were larger in women than in men, while feminine subjects showed larger N1 amplitudes than masculine subjects, regardless of sex. Moreover, feminine subjects showed enhanced frontocentral N2 (210–270 ms) amplitudes for highly and mildly negative than for neutral stimuli, while masculine subjects showed an emotion effect only for highly negative stimuli. The feminine-specific effect for mildly negative stimuli was positively correlated to the feminine score, and this correlation was located to the anterior cingulate and the superior and medial frontal gyri. Furthermore, feminine but not masculine subjects showed enhanced parietal P3 (330–560 ms) amplitudes for highly and mildly positive than for neutral stimuli, an effect positively related to the feminine score and localized to the precuneus, posterior cingulate, and superior temporal gyrus. Machine learning analyses verified that single-trial N2 and P3 amplitudes of feminine subjects reliably discriminated the intensity of negative and positive stimuli, respectively. For ecological considerations, in Study 2 we used an observational approach (n = 300) and confirmed that feminine gender role, rather than biological sex, predicted individual differences in daily experience of emotion-related psychopathological symptoms. These findings provide solid evidence for the critical impact of gender role rather than sex on emotional susceptibility.
ABSTRACT
<p><b>BACKGROUND</b>The neurogenesis in retina of adult mammals is generally abolished, and this renders the retina lack of regenerative capacity. Despite this, there is a small population of nestin-positive cells in the ciliary epithelium which retains neurogenic potential. The present study aimed at investigating the effect of two drugs, corticosterone and paroxetine, on the cell proliferation of the ciliary body.</p><p><b>METHODS</b>Adult Sprague-Dawley rats were given vehicle, corticosterone, paroxetine, or both corticosterone and paroxetine treatment for 14 days. Cell proliferation in the ciliary body was quantified using 5-bromo-2-deoxyuridine (BrdU) immunohistochemistry. Co-labelling of BrdU and stem cell marker was used to phenotype the BrdU immunoreactive cells.</p><p><b>RESULTS</b>Corticosterone treatment suppressed while paroxetine treatment increased the cell proliferation of the ciliary body. Co-labelling with cell markers revealed that the BrdU positive cells also showed nestin expression but not glial fibrillary acidic protein (GFAP).</p><p><b>CONCLUSIONS</b>The results illustrate that proliferation of retinal progenitor cells situated in ciliary body are subjected to regulation by selective serotonin reuptake inhibitors (SSRI) and corticosteroid, which is similar to our previous findings in neurogenic regions in central nervous system (CNS). Paroxetine treatment could reverse the suppressive effect of corticosterone on ciliary body cell proliferation. This provides information for future investigation of retinal stem cell biology and potential treatment of retinal degenerative diseases.</p>
Subject(s)
Animals , Male , Rats , Adrenal Glands , Pathology , Body Weight , Cell Proliferation , Ciliary Body , Cell Biology , Corticosterone , Pharmacology , Immunohistochemistry , In Vitro Techniques , Organ Size , Paroxetine , Pharmacology , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>The literature has shown that cognitive and emotional changes may occur after chronic treatment with glucocorticoids. This might be caused by the suppressive effect of glucocorticoids on hippocampal neurogenesis and cell proliferation. Paroxetine, a selective serotonin reuptake transporter, is a commonly used antidepressant for alleviation of signs and symptoms of clinical depression. It was discovered to promote hippocampal neurogenesis in the past few years and we wanted to investigate its interaction with glucocorticoid in this study.</p><p><b>METHODS</b>Adult rats were given vehicle, corticosterone, paroxetine, or both corticosterone and paroxetine for 14 d. Cell proliferation in the dentate gyrus was quantified using 5-bromo-2-deoxyuridine (BrdU) immunohistochemistry.</p><p><b>RESULTS</b>The corticosterone treatment suppressed while paroxetine treatment increased hippocampal cell proliferation. More importantly, paroxetine treatment could reverse the suppressive effect of corticosterone on hippocampal cell proliferation.</p><p><b>CONCLUSION</b>This may have clinic application in preventing hippocampal damage after glucocorticoid treatment.</p>