Browsing by Author "Antle, Michael Christopher"

Now showing 1 - 2 of 2
  • Thumbnail Image
    ItemOpen Access
    Neural Basis of Arousal Signaling for Non-Photic Resetting of the Circadian Clock
    (2023-09-21) Moshirpour, Mahtab; Antle, Michael Christopher; Dyck, Richard; Spanswick, Simon; Borgland, Stephanie; Mintz, Eric M.
    Input to the suprachiasmatic nucleus (SCN) from the intergeniculate leaflet (IGL) is necessary for non-photic entrainment. However, the underlying mechanisms of IGL activation remain unknown. There are several arousal centers in the brain that could be involved in bringing about non-photic entrainment. These include the lateral hypothalamus (LH) which contains clock-projecting orexin cells, and the cholinergic basal forebrain that directly communicates with the SCN. Even though arousal is the key component of non-photic entrainment, the relationship between the IGL and these arousal areas is unclear. We investigated the neural basis of arousal signaling by first studying the potential inputs to the IGL from the LH and the basal forebrain of Syrian hamsters. Projections to the IGL, from both the LH and the basal forebrain cholinergic cells were found. Next, we examined whether orexin is necessary and sufficient for non-photic phase shifting by both blocking orexin prior to an arousal-inducing protocol such as sleep deprivation and administering orexin in the IGL. It was found that orexin alone is not necessary or sufficient to cause shifts. Instead, it was found that dual administration of a glutamate receptor agonist with orexin is sufficient to cause significant shifts, suggesting an additive effect at the IGL. We next examined whether acetylcholine is necessary for non-photic entrainment. No attenuation of the arousal-induced response was observed by blocking acetylcholine at the IGL, suggesting that it is not necessary for non-photic entrainment, though it has been reported to be critical at the SCN level. Finally, accumulation of the sleep factor adenosine in the basal forebrain was mimicked as a potential signal for activating the basal forebrain. No significant phase shifts or cellular activation of the basal forebrain was observed after blocking adenosine at the basal forebrain. Taken together, the results present the first report of a dual role for orexin and glutamate in potentially gating the IGL’s non-photic inputs to the SCN.
  • Thumbnail Image
    ItemOpen Access
    The effects of sleep deprivation and poor sleep quality on Emotional Empathy: the behavioral and neural mechanisms in healthy controls
    (2017) Guadagni, Veronica; Iaria, Giuseppe; Protzner, Andrea; Antle, Michael Christopher; Longman, Richard Stewart; Carrier, Julie
    This dissertation describes a series of experiments exploring the intricate relationship between sleep and Emotional Empathy, i.e., the ability to understand someone else’s emotions through vicarious sharing. First, I used a sleep deprivation protocol, in which sleep quality was experimentally manipulated, to test the hypothesis that sleep deprivation negatively affects the Emotional Empathy of healthy individuals (Chapter 3). The findings of this study revealed a blunting of Emotional Empathy responses across all valences for participants in the sleep deprivation group compared to participants in the control groups. I then tested the hypothesis that sleep quality accounts for variability in individuals’ empathic responses by looking at effects of natural occurring changes in sleep quality on Emotional Empathy (Chapter 4). In this study, I collected subjective (questionnaires) and objective (actigraphy) measures of sleep and used a sophisticated statistical analysis to reduce the number of collected sleep variables and generate independent factors that were then entered into a series of stepwise regressions. The results of this study showed that the subjective sleep quality factor best explained participants’ Emotional Empathy responses to negative images compared to neutral, while the total sleep duration factor best explained overall Empathy scores. Finally, to test the hypothesis of a modulatory role of sleep quality on the neural activity of areas identified as components of the Emotional Empathy network, I conducted a Region of Interest (ROI) analysis, and measured Blood Oxygen Level Dependent (BOLD) signal change while participants performed an Emotional Empathy task. In addition, I tested the effects of sleep quality on the task based functional connectivity between the selected ROIs. The data revealed decreased BOLD signal change in a selective region within the left anterior insula for individuals with poor subjective sleep quality together with increased functional connectivity between subcomponents of the anterior insula, indicating lower functional specialization. Overall, these studies suggest a detrimental effect of poor sleep quality on Emotional Empathy and its underlying neural mechanisms. These findings could benefit individuals affected by sleep disorders but also bring insight on the importance of considering sleep loss in daily life as a detrimental factor when planning work schedules.