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Frank D. Nelli, Michael F. Wesner; Diurnal variation of glucocorticoids appears to modulate V1-specific perceptual learning. Journal of Vision 2011;11(11):999. doi: 10.1167/11.11.999.
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Research has shown that learning deficits may occur due to excessive glucocorticoid exposure. Furthermore, human striate cortex (V1) has been found to contain a significant concentration of glucocorticoid receptors (Perlman et al., 2007). We examined whether V1 perceptual learning was affected by diurnal glucocorticoid variation. Learning was assessed using a classic texture discrimination task (Karni & Sagi, 1991). Research suggests that TDT learning is V1 specific (Schwartz et al., 2002), and that visual-cortical plasticity is likely NMDA-receptor mediated (e.g., Bear, 1996). Learning deficits in the presence of heightened glucocorticoid exposure suggests that these steroids may modify V1 functionality. For training, participants were grouped according to endogenous glucocorticoid phase: (1) during AM, before 11:30 (high levels), (2) during PM, between 12:30–7:00 (low levels), and (3) an exploratory PM group concurrently using antidepressant (serotonin-selective reuptake inhibitor/SSRI) medications. Percent correct was measured as a function of seven SOA (stimulus-onset asynchrony) levels. Results were fitted with Weibull functions, and threshold was interpolated at 75% correct. No effect of learning was observed for those trained during AM hours, however, increases in task efficiency were noted (i.e., fitted slope change). Those trained during PM hours showed significant overall sensitivity increases (i.e., shift in psychometric function). The AM group showed significantly higher cortisol levels versus the PM group, as determined by enzyme-linked immunosorbent assay. The SSRI group showed no effect of learning between sessions. Performance differences between AM and PM groups were expected, as heightened glucocorticoid levels are known to impair hippocampus-dependent memory (e.g., Domes et al., 2005). Therefore, we reasoned a similar mechanism may be present in V1. The lack of performance improvement within the SSRI group was unexpected. Previous research has suggested that NMDA-receptor functionality may be modified by SSRIs (Raabe & Gentile, 2008), and thus comparable plasticity changes may be occurring in V1.
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