Pubertal Testosterone Tracks the Developmental Trajectory of Neural Oscillatory Activity Serving Visuospatial Processing
Abstract Puberty is a period of substantial hormonal fluctuations that induce dramatic physical, neurological, and behavioral changes. Previous research has demonstrated that pubertal hormones modulate cortical development, as well as sex- and age-specific patterns of cognitive development during ch...
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Veröffentlicht in: | Cerebral cortex (New York, N.Y. 1991) N.Y. 1991), 2020-10, Vol.30 (11), p.5960-5971 |
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Sprache: | eng |
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Zusammenfassung: | Abstract
Puberty is a period of substantial hormonal fluctuations that induce dramatic physical, neurological, and behavioral changes. Previous research has demonstrated that pubertal hormones modulate cortical development, as well as sex- and age-specific patterns of cognitive development during childhood and adolescence. However, the influence of pubertal hormones on the brain’s functional development, specifically neural oscillatory dynamics, has yet to be fully examined. Thus, in the current study, we used magnetoencephalography to investigate the oscillatory dynamics serving visuospatial perception and attention, and testosterone levels and chronological age as measures of development. Within a sample of typically developing youth, age was associated with changes in alpha, theta, and gamma oscillatory activity. Novel testosterone-by-sex interactions in the gamma range were identified in critical areas of the visual and attention networks. Females had increased gamma activity with increasing testosterone in the right temporal-parietal junction and occipital cortices, while males showed increased gamma activity in the right insula with increasing testosterone. These findings reveal robust developmental alterations in the oscillatory dynamics serving visuospatial processing during childhood and adolescence and provide novel insight into the hormonal basis of sexually dimorphic patterns of functional brain development during the pubertal transition that is at least partially mediated by endogenous testosterone. |
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ISSN: | 1047-3211 1460-2199 |
DOI: | 10.1093/cercor/bhaa169 |