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Effects of a circadian mutation on adult neurogenesis

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dc.contributor.advisorEric Bittman
dc.contributor.advisorJoseph Bergan
dc.contributor.advisorRolf Karlstrom
dc.contributor.authorBahiru, Michael
dc.contributor.departmentUniversity of Massachusetts Amherst
dc.contributor.departmentNeuroscience & Behavior
dc.date2024-03-28T20:43:33.000
dc.date.accessioned2024-04-26T18:06:26Z
dc.date.available2024-04-26T18:06:26Z
dc.date.issued2021-02-01
dc.date.submittedFebruary
dc.date.submitted2021
dc.description.abstractRotating shift work, irregular sleep patterns and jetlag disrupt circadian rhythms, induce or aggravate disease, and produce deficits in cognitive function. Internal misalignment, a state in which abnormal phase relationships prevail between and within organs, is widely proposed to account for these adverse effects of circadian disruption. This hypothesis has been difficult to test because phase shifts of the entraining environmental cycle lead to transient desynchrony. Thus, it remains possible that phase shifts, regardless of internal desynchrony, account for adverse effects of circadian disruption. I have used the duper mutant hamster, whose locomotor activity rhythms re-entrain 5-fold faster than wild types after a phase shift of 8 hours, to test whether internal desynchrony can account for adverse effects of jet lag on adult neurogenesis. I subjected wild type and duper female hamsters to alternating 8h phase advances and delays of the LD cycle at 16-day intervals. I injected 5-Bromo-2’-deoxyuridine (BrdU, a thymidine analogue) after the 4th shift and collected brains after the 8th shift. As expected, mutants re-entrained activity rhythms more rapidly than did wild types. On the other hand, estrous cycles, as assessed by vaginal smears, were rarely disrupted by repeated phase shifts in either genotype. I next compared cell proliferation and neurogenesis in the subgranular zone of the hippocampus between Duper mutants and wild type siblings using the S-phase marker BrdU and the neuronal marker NeuN. I assessed the total number of BrdU cells in the subgranular zone of the hippocampus, as the proportion that expressed NeuN. Duper mutants had more BrdU-ir cells, and more BrdU+/NeuN+ cells than did wild types, whether or not they experienced phase shifts, revealing an unexpected increase in neurogenesis. Surprisingly, repeated phase shifts increased neurogenesis in WT but not duper hamsters. Despite the increase in neurogenesis, phase shifts reduced the number of adult-born non-neuronal (BrdU+/NeuN-) cells in WT hamsters but had no such effect on duper mutants. In addition, the duper mutation increases hippocampal neurogenesis regardless of circadian. Our results suggest that adult-born non-neuronal cells are most vulnerable to circadian disruption, and that internal desynchrony promotes their demise. disruption.
dc.description.degreeMaster of Science (M.S.)
dc.identifier.doihttps://doi.org/10.7275/21093232
dc.identifier.orcidhttps://orcid.org/0000-0003-1371-2552
dc.identifier.urihttps://hdl.handle.net/20.500.14394/32658
dc.relation.urlhttps://scholarworks.umass.edu/cgi/viewcontent.cgi?article=2075&context=masters_theses_2&unstamped=1
dc.source.statuspublished
dc.subjectCircadian Neurogenesis Desynchronization Duper Shifting
dc.subjectBehavioral Neurobiology
dc.subjectDevelopmental Neuroscience
dc.subjectMolecular and Cellular Neuroscience
dc.titleEffects of a circadian mutation on adult neurogenesis
dc.typeopenaccess
dc.typearticle
dc.typethesis
digcom.contributor.authorisAuthorOfPublication|email:mbahiru@umass.edu|institution:University of Massachusetts Amherst|Bahiru, Michael
digcom.identifiermasters_theses_2/1003
digcom.identifier.contextkey21093232
digcom.identifier.submissionpathmasters_theses_2/1003
dspace.entity.typePublication
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