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Optical probing of hemodynamic responses in vivo with channelrhodopsin-2

University of British Columbia

Maintenance of neuronal function depends on the timely delivery of oxygen and glucose through changes in blood flow that are linked to the level of ongoing neuronal and glial activity, yet the mechanisms underlying this stimulus-dependent control of blood flow remain unclear. Here, using transgenic mice expressing channelrhodopsin-2 in a subset of layer 5b pyramidal neurons, we report that changes in intrinsic optical signals and blood flow can be evoked by activation of channelrhodopsin-2 neurons without direct involvement of other cell types. We have used a combination of imaging and pharmacology to examine the importance of glutamatergic synaptic signaling in neurovascular coupling. In contrast to sensory-evoked responses, we observed that glutamate-dependent neuronal signalling is not essential for the production of channelrhodopsin-evoked hemodynamic responses. Our results rather suggest that ChR2-activated neurons are coupled to the surrounding vasculature through a glutamate-dependent astrocytic pathway mediated by the Group I metabotropic glutamate receptor mGluR5.

Text

2011-08-02

Attribution-ShareAlike 3.0 Unported

http://hdl.handle.net/2429/36449

Neuroscience

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-sa/3.0/