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Michael E. Dailey, Ph.D.
Dept. of Biological Sciences
Neuroscience Program
University of Iowa

Focusing on...

Glial Cell Structure and Function as it relates to Development and Pathology of the Mammalian Brain.



News from the Dailey Lab!

Journal Cover Highlight

  • Image from the Dailey Lab adorns the cover of the December 2013 issue of Cold Spring Harbor Protocols. Confocal image stack showing GFP-expressing microglia (green) and YFP-expressing neurons (yellow) in area CA3 of a hippocampal tissue slice from postnatal day 12 mouse (CX3CR1GFP/+:Thy1-YFP).

    See the article: "Imaging Microglia in Brain Slices and Slice Cultures." by M.E. Dailey, U. Eyo, L. Fuller, J. Hass, and D. Kurpius.


Protocols cover


Public lecture by Dailey Lab graduate student

  • Kate Ahlers, a graduate student in the Dailey Lab, gave a public lecture summarizing her research on microglial responses to neural injury in a mouse model of Fetal Alcohol Spectrum Disorders (FASD).

Kate flyer

Publication highlight:

  • A review article entitled, "Microglia: Key Elements in Neural Development, Plasticity, and Pathology" was published with cover photo in the Journal of Neuroimmune Pharmacology 8:494-509, 2013.

    Abstract: A century after Cajal identified a “third element” of the nervous system, many issues have been clarified about the identity and function of one of its major components, the microglia.  Here, we review recent findings by microgliologists, highlighting results from imaging studies that are helping provide new views of microglial behavior and function. In vivo imaging in the intact adult rodent CNS has revolutionized our understanding of microglial behaviors in situ and has raised speculation about their function in the uninjured adult brain. Imaging studies in ex vivo mammalian tissue preparations and in intact model organisms including zebrafish are providing insights into microglial behaviors during brain development. These data suggest that microglia play important developmental roles in synapse remodeling, developmental apoptosis, phagocytic clearance, and angiogenesis. Because microglia also contribute to pathology, including neurodevelopmental and neurobehavioral disorders, ischemic injury, and neuropathic pain, promising new results raise the possibility of leveraging microglia for therapeutic roles. Finally, exciting recent work is addressing unanswered questions regarding the nature of microglial-neuronal communication.  While it is now apparent that microglia play diverse roles in neural development, behavior, and pathology, future research using neuroimaging techniques will be essential to more fully exploit these intriguing cellular targets for effective therapeutic intervention applied to a variety of conditions.

JNIP cover


Publication highlight:

  • Dailey Lab graduate student Ukpong Eyo published a research article entitled, "Effects of Oxygen-Glucose Deprivation on Microglial Mobility and Viability in Developing Mouse Hippocampal Tissues," along with cover photo, in the journal Glia 60:1747-1760, 2012.

    Abstract: As brain-resident immune cells, microglia (MG) survey the brain parenchyma to maintain homeostasis during development and following injury.  Recent work in perinatal stroke, a leading cause of lifelong disability, has implicated MG as targets for therapeutic intervention during stroke progression. Although MG responses are complex, work in developing rodents suggests that MG limit brain damage and promote recovery after stroke. However, little is known about how energy-limiting conditions affect MG survival and mobility in developing brain tissues. Here, we used confocal time-lapse imaging to monitor MG viability and motility during hypoxia or oxygen-glucose deprivation (OGD) in neonatal hippocampal tissue slices derived from GFP-reporter mice (CX3CR1GFP/+). We found that MG in P5-P7 neonatal tissues remain viable for at least 6 hr of hypoxia but begin to die after 2 hr of OGD.  Both hypoxia and OGD reduced MG motility. Unexpectedly, some MG retain or recover motility during OGD, and these active MG can contact and engulf dead cells.  MG from younger neonates (P2-P3) are more resistant to OGD than those from older ones, indicating increasing vulnerability with developmental age. Finally, we show that transient (2 hr) OGD reduces MG motility, migration, and viability.  Although MG motility is rapidly restored after transient OGD, it remains below control levels for many hours. Together, these results show that MG in neonatal mouse brain tissues are vulnerable to both transient and sustained OGD, and many MG die within hours after onset of OGD.  Preventing MG death may, therefore, provide a strategy for promoting tissue restoration after stroke.


Glia cover 2012


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