Therefore, we are using the recently developed model (see above) to block functional hyperemia while monitoring neuronal and astrocytic responses to sensory stimuli.
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Our lab is looking to hire. Interested post-docs and graduate students can contact poherron@augusta.edu. Post-doctoral applicants can apply here. (Job ID: 258134)
Johns Hopkins University, Neuroscience, PhD, 2009
George Mason University, Chemistry, BA, 2002
Christendom College, Philosophy, BA, 2000
2023 | Assistant Professor, Augusta University
2018 | Research Assistant Professor, Augusta University
2017-2018 | Research Assistant Professor, Medical University of South Carolina
My lab’s research focuses on questions of neurovascular coupling and visual processing. Our neurovascular coupling work seeks to determine how neural activity in the cortex drives hemodynamic responses (functional hyperemia) and, in turn, how important this increased blood flow is to healthy neuronal function.
We recently developed a mouse model to block functional hyperemia using optogenetics. This mouse expresses the red-shifted cation channel opsin ReaChR in vascular mural cells, allowing the vessels to be constricted with light. Using two-photon activation we are able to constrict individual vessels, and using widefield single-photon activation all the vessels in the cranial window can be constricted. We also established that sensory-stimulus-evoked vasodilation can be offset by optogenetic activation of the vessels.
Optogenetic vasoconstriction
All of the arteries constrict to a 100 ms flash of the LED light (seen as a brief dimming of the image) over the cranial window. Vessels in mouse visual cortex labeled with FITC dextranand simultaneously imaged with two photon microscopy during activation.
Visual stimuli activate neurons leading to dilation of vessels in the visual cortex (blue trace). When the visual stimuli are paired with pulses of light, the optogenetic evoked constriction blocks the usual functional hyperemia response (red trace).
We are currently investigating the role functional hyperemia plays in healthy neural function. It has been known for more than a century than brain activity causes increases in local blood flow, and the widely held assumption is that this is necessary for providing increases in oxygen and glucose to support the increase in neural activity. However, this hypothesis has never been directly tested and there are reasons to believe that this may not be the full explanation.
Therefore, we are using the recently developed model (see above) to block functional hyperemia while monitoring neuronal and astrocytic responses to sensory stimuli.
Another ongoing project in the lab involves a collaboration with Dr. Jessica Filosa here at Augusta University. We use this same optogenetic model to constrict vessels during spontaneous states (absence of visual stimulation) to study vasculo-glia-neuronal coupling - signalling from vessels back to astrocytes and neurons. This coupling was established previously in Dr. Filosa’s lab in brain slices (Kim et al. J Neuroscience 2016). We are now seeking to determine if vasoconstriction in vivo can directly alter astrocytic and neural activity patterns.
My introduction to neurovascular coupling came during my post-doctoral fellowship.
There I studied the correspondence between regions of active neural tissue and regions
of increased blood flow. We found that both neuronal spiking and synaptic activity
were more anatomically localized than the regional increase in blood flow. This work
will help to interpret hemodynamic imaging studies which use vascular signals as surrogates
for neural activity.
My PhD work was on visual processing in primate visual cortex. I studied figure-ground signals using electrophysiological recordings.
More recently, I have also studied how neuronal response properties vary with depth in the upper layers of mouse primary visual cortex
