Thesis (M. S.)--Psychology, Georgia Institute of Technology, 2010. / Committee Chair: Dr. Phillip L. Ackerman; Committee Member: Dr. Paul Corballis; Committee Member: Dr. Ruth Kanfer. Part of the SMARTech Electronic Thesis and Dissertation Collection.

Mood and cognition, along with numerous other physiological processes, are under circadian regulation. The synthesis and secretion rhythm of the pineal hormone melatonin is under the direct regulation of the central circadian pacemaker and the secretion rhythm of melatonin can be used to assess circadian alterations. In this thesis, it was demonstrated that low levels of endogenous nocturnal melatonin was associated with subsyndromal depression and alterations in sleep architecture. Studies in individuals with endogenous circadian rhythm disorder, with and without comorbid depressive symptoms, revealed that individuals with depressive symptoms had a greater phase delay in melatonin profiles as compared to individuals without depressive symptoms. Furthermore, in the same study, exogenous melatonin administered to induce phase advances significantly improved depression scores and sleep initiation. In addition to endogenous circadian disruption, circadian rhythms can also be disrupted by repeated atypical alterations in environmental time cues. In mammals, light is the strongest environmental cue that can modulate circadian rhythms. Recent studies suggest that circadian response to photic stimuli is preferentially sensitive to short wavelengths in the range of 450-480 nm. Using an animal model it was demonstrated that filtering a 10 nm bandwidth between 470-480 nm from polychromatic white light prevents nocturnal light exposure induced disruptions in melatonin and corticosterone secretion as well as central and peripheral clock gene expression. These findings were further investigated in humans and revealed that filtering short wavelengths below 480 nm attenuates 12 h nocturnal light exposure induced suppression of melatonin secretion, increased cortisol secretion and disrupted peripheral clock gene expression. Furthermore, attenuation of these changes was associated with improvements in mood, alertness and vigilance at a time close to the endogenous circadian wake drive. However, filtering short wavelengths below 460 nm or reducing the optical transmission by up to 30% below 480 nm did not attenuate the disruptive effects of nocturnal light exposure on physiological and behavioural variables. Overall, the results presented in this thesis support the role of circadian dysfunction in neuropsychometric impairment and presents evidence supporting spectral modulation as a promising approach to attenuate light-mediated chronodisruption.

Mood and cognition, along with numerous other physiological processes, are under circadian regulation. The synthesis and secretion rhythm of the pineal hormone melatonin is under the direct regulation of the central circadian pacemaker and the secretion rhythm of melatonin can be used to assess circadian alterations. In this thesis, it was demonstrated that low levels of endogenous nocturnal melatonin was associated with subsyndromal depression and alterations in sleep architecture. Studies in individuals with endogenous circadian rhythm disorder, with and without comorbid depressive symptoms, revealed that individuals with depressive symptoms had a greater phase delay in melatonin profiles as compared to individuals without depressive symptoms. Furthermore, in the same study, exogenous melatonin administered to induce phase advances significantly improved depression scores and sleep initiation. In addition to endogenous circadian disruption, circadian rhythms can also be disrupted by repeated atypical alterations in environmental time cues. In mammals, light is the strongest environmental cue that can modulate circadian rhythms. Recent studies suggest that circadian response to photic stimuli is preferentially sensitive to short wavelengths in the range of 450-480 nm. Using an animal model it was demonstrated that filtering a 10 nm bandwidth between 470-480 nm from polychromatic white light prevents nocturnal light exposure induced disruptions in melatonin and corticosterone secretion as well as central and peripheral clock gene expression. These findings were further investigated in humans and revealed that filtering short wavelengths below 480 nm attenuates 12 h nocturnal light exposure induced suppression of melatonin secretion, increased cortisol secretion and disrupted peripheral clock gene expression. Furthermore, attenuation of these changes was associated with improvements in mood, alertness and vigilance at a time close to the endogenous circadian wake drive. However, filtering short wavelengths below 460 nm or reducing the optical transmission by up to 30% below 480 nm did not attenuate the disruptive effects of nocturnal light exposure on physiological and behavioural variables. Overall, the results presented in this thesis support the role of circadian dysfunction in neuropsychometric impairment and presents evidence supporting spectral modulation as a promising approach to attenuate light-mediated chronodisruption.

To investigate the effects of emotional arousal on information processing strategy, three different moods (sadness, anger, and happiness) were hypnotically induced at three different levels of intensity (high, medium, and low) in 29 male and female undergraduate students, while engaging them in a visual information processing task. Subjects were screened for hypnotic susceptibility and assigned to either a high susceptibility group or low susceptibility group to account for the attentional bias associated with this trait. All subjects were trained to access the three emotions at the three levels of intensity. During separate experimental sessions, subjects were hypnotized, and asked to access a mood and experience each level of intensity while being administered the Navon Design Discrimination Task, a measure of global and analytic visual information processing. Scores were derived for global processing, analytic processing, and a percentage of global to analytic processing for each level of mood and intensity. Two (hypnotic susceptibility) x 3 (emotion) x 3 (intensity level) repeated measures ANOVAs were computed on the global, analytic, and percentage scores. In addition, two separate ANCOVAs were computed on each dependent measure to account for the effects of handedness, and cognitive style. None of these analyses revealed significant main effects or interactions. The analysis of the percentage scores revealed a trend toward differences between the emotions, but in a direction opposite to that hypothesized. Hypnotic susceptibility does not appear to mediate global and analytic responses to the Navon visual information processing task when emotions are being experienced. Results regarding emotions and emotional intensity were discussed in terms of the problems with adequate control and manipulation of mood and intensity level. Difficulties with the Navon measure were also explored with regard to the exposure duration in the Navon task, and its adequacy in measuring shifts in information processing associated with transient mood states. Implications for future research were discussed.

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