Noninvasive Ultrasound Stimulation of Ventral Tegmental Area Induces Reanimation from General Anaesthesia in Mice

Evidence in animals suggests that deep brain stimulation or optogenetics can be used for recovery from disorders of consciousness (DOC). However, these treatments require invasive procedures. This report presents a noninvasive strategy to stimulate central nervous system neurons selectively for recovery from DOC in mice. Through the delivery of ultrasound energy to the ventral tegmental area, mice were aroused from an unconscious, anaesthetized state in this study, and this process was controlled by adjusting the ultrasound parameters. The mice in the sham group under isoflurane-induced, continuous, steady-state general anaesthesia did not regain their righting reflex. On insonation, the emergence time from inhaled isoflurane anaesthesia decreased (sham: 13.63±0.53 min, ultrasound: 1.5±0.19 min, p<0.001). Further, the induction time (sham: 12.0±0.6 min, ultrasound: 17.88±0.64 min, p<0.001) and the concentration for 50% of the maximal effect (EC50) of isoflurane (sham: 0.6%, ultrasound: 0.7%) increased. In addition, ultrasound stimulation reduced the recovery time in mice with traumatic brain injury (sham: 30.38±1.9 min, ultrasound: 7.38±1.02 min, p<0.01). This noninvasive strategy could be used on demand to promote emergence from DOC and may be a potential treatment for such disorders.

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Increased number of TH-immunoreactive cells in the ventral tegmental area after deep brain stimulation of the anterior nucleus of the thalamus

Brain Structure and Function ◽

10.1007/s00429-014-0832-7 ◽

2014 ◽

Vol 220 (5) ◽

pp. 3061-3066 ◽

Cited By ~ 4

Author(s):

J. A. D. Dela Cruz ◽

S. Hescham ◽

B. Adriaanse ◽

F. L. Campos ◽

H. W. M. Steinbusch ◽

...

Keyword(s):

Deep Brain Stimulation ◽

Ventral Tegmental Area ◽

Brain Stimulation ◽

Anterior Nucleus ◽

Ventral Tegmental ◽

Deep Brain ◽

Stimulation Of

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Ventral tegmental area dopaminergic lesion-induced depressive phenotype in the rat is reversed by deep brain stimulation of the medial forebrain bundle

Behavioural Brain Research ◽

10.1016/j.bbr.2015.11.036 ◽

2016 ◽

Vol 299 ◽

pp. 132-140 ◽

Cited By ~ 16

Author(s):

L.L. Furlanetti ◽

V.A. Coenen ◽

M.D. Döbrössy

Keyword(s):

Deep Brain Stimulation ◽

Ventral Tegmental Area ◽

Brain Stimulation ◽

Medial Forebrain Bundle ◽

Ventral Tegmental ◽

Deep Brain ◽

Stimulation Of

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Faculty Opinions recommendation of Electrical stimulation of the ventral tegmental area induces reanimation from general anesthesia.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718230967.793498856 ◽

2014 ◽

Author(s):

Stan Leung ◽

Tao Luo

Keyword(s):

Electrical Stimulation ◽

General Anesthesia ◽

Ventral Tegmental Area ◽

Ventral Tegmental ◽

Stimulation Of

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Acute withdrawal from chronic escalating-dose binge cocaine administration alters kappa opioid receptor stimulation of [35S] guanosine 5′-O-[gamma-thio]triphosphate acid binding in the rat ventral tegmental area

Neuroscience ◽

10.1016/j.neuroscience.2010.04.060 ◽

2010 ◽

Vol 169 (2) ◽

pp. 751-757 ◽

Cited By ~ 14

Author(s):

A.P. Piras ◽

Y. Zhou ◽

S.D. Schlussman ◽

A. Ho ◽

M.J. Kreek

Keyword(s):

Ventral Tegmental Area ◽

Opioid Receptor ◽

Kappa Opioid Receptor ◽

Kappa Opioid ◽

Receptor Stimulation ◽

Cocaine Administration ◽

Acute Withdrawal ◽

Ventral Tegmental ◽

Stimulation Of

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Cardiovascular depressor responses to stimulation of substantia nigra and ventral tegmental area

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.273.6.h2549 ◽

1997 ◽

Vol 273 (6) ◽

pp. H2549-H2557 ◽

Cited By ~ 13

Author(s):

Gilbert J. Kirouac ◽

John Ciriello

Keyword(s):

Substantia Nigra ◽

Ventral Tegmental Area ◽

Intravenous Administration ◽

Dopaminergic Neurons ◽

Cardiovascular Responses ◽

Receptor Blocker ◽

Transitional Region ◽

Pars Lateralis ◽

Ventral Tegmental ◽

Stimulation Of

Experiments were done in α-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect ofl-glutamate (Glu) stimulation of the substantia nigra (SN) and ventral tegmental area (VTA) on arterial pressure (AP) and heart rate (HR). Glu stimulation of the SN pars compacta (SNC) elicited decreases in both mean AP (MAP; −18.9 ± 1.3 mmHg; n = 52) and HR (−26.1 ± 1.6 beats/min; n = 46) at 81% of the sites stimulated. On the other hand, stimulation of the SN pars lateralis or pars reticulata did not elicit cardiovascular responses. Stimulation of the adjacent VTA region elicited similar decreases in MAP (−18.0 ± 2.6 mmHg; n = 20) and HR (−25.4 ± 3.8 beats/min; n = 17) at ∼74% of the sites stimulated. Intravenous administration of the dopamine D2-receptor antagonist raclopride significantly attenuated both the MAP (70%) and the HR (54%) responses elicited by stimulation of the transitional region where the SNC merges with the lateral VTA (SNC-VTA region). Intravenous administration of the muscarinic receptor blocker atropine methyl bromide had no effect on the magnitude of the MAP and HR responses to stimulation of the SNC-VTA region, whereas administration of the nicotinic receptor blocker hexamethonium bromide significantly attenuated both the depressor and the bradycardic responses. These data suggest that dopaminergic neurons in the SNC-VTA region activate a central pathway that exerts cardiovascular depressor effects that are mediated by the inhibition of sympathetic vasoconstrictor fibers to the vasculature and cardioacceleratory fibers to the heart.

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