The nervous system is exquisitely tuned to mount the appropriate behavioral response to sensory stimuli ranging from a gentle caress to a harsh mechanical insult. How our nervous systems encode this information, from the level of sensory neuron activation in peripheral tissues up towards the central nervous system, in both normal and diseased states, remains enigmatic. Taking advantage of mouse molecular and genetic tools, the Abdus-Saboor lab is addressing important questions about sensory system perception – from the level of the gene to the level of organismal behavior. Using an integrative approach spanning molecular optogenetics and chemogenetics, automated tracking of behavior coupled with high-speed videography, viral circuit tracing, calcium imaging in dissociated neurons and intact animals, and whole-cell and slice patch clamp physiology, our overall goal is to increase our basic understanding of the mechanisms governing encoding of somatosensory stimuli.

We frequently use mouse genetics to target effector proteins to specific subsets of peripheral sensory neurons that allow us to ablate, activate, or silence dorsal root or trigeminal ganglion neurons in behaving mice. For example, we routinely target the light-sensitive ion channel, ChR2, to different populations of neurons that respond to noxious mechanical, noxious thermal, light touch, or itch sensations (shown in green in the confocal microscope images below). Using novel behavioral paradigms, we can turn on these sensations trans-dermally through the skin with light in freely behaving animals. At the very bottom of the page are examples of activation of mechanical-sensitive neurons in vivo. 

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ChR2 is targeted to mechanical-sensing neurons via Mrgprd-Cre.


ChR2 is targeted to cold-sensing neurons via TrpM8-Cre.

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ChR2 is targeted to touch neurons via Split-Cre.

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ChR2 is targeted to touch neurons via Split-Cre. Shown here is the neuron-schwann cell sensory organ - the pacinian corpuscle.

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ChR2 is targeted to itch-sensing neurons via MrgprA3-Cre.