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VERSION:2.0
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CALSCALE:GREGORIAN
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BEGIN:VEVENT
DTSTAMP:20260825T154026Z
LAST-MODIFIED:20180427T174508Z
DTSTART:20180430T163000Z
DTEND:20180430T173000Z
UID:event1918@bu.edu
URL:http://physics.bu.edu/internal/events/show/1918
SUMMARY:"THE BREAKDOWN OF NEURAL CIRCUIT FUNCTION UNDER VOLATILE ANESTHESIA
	: IN VIVO\, MULTINEURONAL IMAGING IN C. ELEGANS"
DESCRIPTION:Featuring Christopher Gabel\, Boston University School of Medic
	ine\n\nPart of the Biophysics Seminars.\n\nVolatile anesthetics produce all
	 stages of general anesthesia\, including unconsciousness\, amnesia\, analg
	esia\, and muscle relaxation. In this state\, the experience\, memory\, and
	 physical response to pain are all lost\, yet patients can be returned to c
	onsciousness\, making it an essential tool in modern medicine. However the 
	mechanism by which neuronal systems are disrupted to cause such effects rem
	ains a mystery. Medical methods of interrogation are limited by their resol
	ution\, with fMRI and EEG measurements reporting the mean activity of milli
	ons of neurons. Previous research has developed the nematode worm C. elegan
	s as an effective model for volatile anesthetics demonstrating that they di
	splay the same behavioral response to increasing levels of anesthesia as hu
	mans and identifying numerous genetic mutants that alter anesthetic suscept
	ibility. Taking advantage of C. elegans simple neuro-anatomy and its compre
	hensive capabilities in multi-neuron imaging\, we are defining the mechanis
	m of anesthesia on a circuit level with single neuron resolution. Employing
	 calcium based neuronal reporters (GCaMP)\, we can measure activity of neur
	ons within the well-defined command interneuron circuit that controls the a
	nimal’s forward and backward crawling with and without anesthetic. We fin
	d that under moderate anesthesia\, at which point C. elegans have become un
	responsive to external stimuli\, activity of individual neurons is not abol
	ished. Rather activity becomes randomized as measured through a loss in coo
	rdination between neurons and an increase in random high frequency dynamics
	. Under higher levels of anesthesia\, dysynchrony in the system is retained
	\, while individual neuronal activity is reduced mimicking the reduced acti
	vity observed in EEG measurements from humans at a similar level of anesthe
	sia. Our results indicate that the state of anesthesia stems from randomiza
	tion of individual neuron activity and dysynchrony between neurons thus dis
	rupting circuit signaling and function.
LOCATION:SCI 352\, 590 Commonwealth Avenue\, 02215
STATUS:CONFIRMED
CLASS:PUBLIC
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