Neural Basis of Arousal Signaling for Non-Photic Resetting of the Circadian Clock

dc.contributor.advisorAntle, Michael Christopher
dc.contributor.authorMoshirpour, Mahtab
dc.contributor.committeememberDyck, Richard
dc.contributor.committeememberSpanswick, Simon
dc.contributor.committeememberBorgland, Stephanie
dc.contributor.committeememberMintz, Eric M.
dc.date2023-11
dc.date.accessioned2023-09-28T21:19:30Z
dc.date.available2023-09-28T21:19:30Z
dc.date.issued2023-09-21
dc.description.abstractInput 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.
dc.identifier.citationMoshirpour, M. (2023). Neural basis of arousal signaling for non-photic resetting of the circadian clock (Doctoral thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca.
dc.identifier.urihttps://hdl.handle.net/1880/117274
dc.language.isoen
dc.publisher.facultyGraduate Studies
dc.publisher.institutionUniversity of Calgary
dc.rightsUniversity of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.
dc.subjectCircadian Rhythms
dc.subjectCircadian Clock
dc.subjectNeuroscience
dc.subjectOrexin
dc.subjectGlutamate
dc.subjectAcetylcholine
dc.subjectAdenosine
dc.subject.classificationNeuroscience
dc.subject.classificationPsychology--Experimental
dc.titleNeural Basis of Arousal Signaling for Non-Photic Resetting of the Circadian Clock
dc.typedoctoral thesis
thesis.degree.disciplinePsychology
thesis.degree.grantorUniversity of Calgary
thesis.degree.nameDoctor of Philosophy (PhD)
ucalgary.thesis.accesssetbystudentI do not require a thesis withhold – my thesis will have open access and can be viewed and downloaded publicly as soon as possible.
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