Thalamus Modulates Consciousness Via Layer-Specific Control of Cortex

Redinbaugh, Michelle J.; Phillips, Jessica M.; Kambi, Niranjan A.; Mohanta, Sounak; Andryk, Samantha; Dooley, Gaven L.; Afrasiabi, Mohsen; Raz, Aeyal; Saalmann, Yuri B.

doi:10.2139/ssrn.3493781

Cited by 55 publications

(88 citation statements)

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“…Our results are generally in agreement with a recent study that used similar techniques in NHPs (Redinbaugh et al, 2020). Redinbaugh et al (2020) reported that the unconscious state was not characterized by increased slow-frequency synchronization between cortex and thalamus. We found that increased slow-frequency power and coherence is an important feature of the propofol-induced unconscious state in all areas.…”

Section: Discussionsupporting

confidence: 93%

“…Thalamic stimulation has improved behavioral performance of a minimally conscious patient (Schiff et al, 2007). Correspondingly, we found that stimulation of the central thalamus caused monkeys to regain arousal, similar to a recent report (Redinbaugh et al, 2020). The stimulation increased cortical spike rates, diminished slow-frequency power, and re-instated higher-frequency power.…”

Section: Discussionsupporting

confidence: 91%

“…We found that increased slow-frequency power and coherence is an important feature of the propofol-induced unconscious state in all areas. Redinbaugh et al (2020) only found decreases in spike rate in deep cortical layers. We found a stronger decrease in superficial layers.…”

Section: Discussionmentioning

confidence: 89%

“…Details of propofol-induced unconsciousness remain to be clarified because its dynamics have been investigated mostly using extracranial measures such as electroencephalography (EEG) with limited spatial specificity and fMRI with limited temporal specificity (but see Redinbaugh et al, 2020). Microelectrode recordings in patients have highly precise temporal resolution but limited spatial coverage.…”

Section: Introductionmentioning

confidence: 99%

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Neural effects of propofol-induced unconsciousness and its reversal using thalamic stimulation

Bastos

Donoghue

Brincat

et al. 2020

Preprint

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AbstractThe specific circuit mechanisms through which anesthetics induce unconsciousness have not been completely characterized. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with the anesthetic propofol. Unconsciousness was marked by slow frequency (~1 Hz) oscillations in local field potentials, entrainment of local spiking to Up states alternating with Down states of little spiking, and decreased coherence in frequencies above 4 Hz. Thalamic stimulation “awakened” anesthetized NHPs and reversed the electrophysiologic features of unconsciousness. Unconsciousness is linked to cortical and thalamic slow frequency synchrony coupled with decreased spiking, and loss of higher-frequency dynamics. This may disrupt cortical communication/integration.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Neural effects of propofol-induced unconsciousness and its reversal using thalamic stimulation

Bastos

Donoghue

Brincat

et al. 2020

Preprint

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“…Like pair-wise neuronal correlations, coherence analysis is entangled. Some showed enhanced coherence during anesthesia (Michelson and Kozai, 2018;Sellers et al, 2015) while others showed reduced coherence at alpha and frequencies (alpha 8-15 Hz; Redinbaugh et al, 2020) which dominates the VSD signal (Gilad et al, 2012). It has to be noted that coherence studies are strongly affected by the frequency band studied and thus the results may vary depending on the analysis.…”

Section: Reduced Local and Inter-areal Synchronization Under Differenmentioning

confidence: 99%

Spatio-temporal patterns of population responses in the visual cortex under Isoflurane: from wakefulness to loss of consciousness

Margalit

Golomb

Tsur

et al. 2020

Preprint

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Anesthetic drugs are widely used in medicine and research to mediate loss of consciousness (LOC). Despite the vast use of anesthesia, how LOC affects cortical sensory processing and the underlying neural circuitry, is not well understood. We measured neuronal population activity in the visual cortices of awake and isoflurane anesthetized mice and compared the visually evoked responses under different levels of consciousness. We used voltage-sensitive dye imaging (VSDI) to characterize the temporal and spatial properties of cortical responses to visual stimuli over a range of states from wakefulness to deep anesthesia. VSDI enabled measuring the neuronal population responses at high spatial (meso-scale) and temporal resolution from several visual regions (V1, extrastiate-lateral (ESL) and extrastiate-medial (ESM)) simultaneously. We found that isoflurane has multiple effects on the population evoked response that augmented with anesthetic depth, where the largest changes occurred at LOC. Isoflurane reduced the response amplitude and prolonged the latency of response in all areas. In addition, the intra-areal spatial spread of the visually evoked activity decreased. During visual stimulation, intra-areal and inter-areal correlation between neuronal populations decreased with increasing doses of isoflurane. Finally, while in V1 the majority of changes occurred at higher doses of isoflurane, higher visual areas showed marked changes at lower doses of isoflurane. In conclusion, our results demonstrate a reverse hierarchy shutdown of the visual cortices regions: low-dose isoflurane diminishes the visually evoked activity in higher visual areas before lower order areas and cause a reduction in inter-areal connectivity leading to a disconnected network.

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Brain‐wide mapping of inputs to the mouse lateral posterior (LP/Pulvinar) thalamus–anterior cingulate cortex network

Leow

Zhou

Sullivan

et al. 2022

J of Comparative Neurology

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The rodent homolog of the primate pulvinar, the lateral posterior (LP) thalamus, is extensively interconnected with multiple cortical areas. While these cortical interactions can span the entire LP, subdivisions of the LP are characterized by differential connections with specific cortical regions. In particular, the medial LP has reciprocal connections with frontoparietal cortical areas, including the anterior cingulate cortex (ACC). The ACC plays an integral role in top-down sensory processing and attentional regulation, likely exerting some of these functions via the LP. However, little is known about how ACC and LP interact, and about the information potentially integrated in this reciprocal network. Here, we address this gap by employing a projectionspecific monosynaptic rabies tracing strategy to delineate brain-wide inputs to bottomup LP→ACC and top-down ACC→LP neurons. We find that LP→ACC neurons receive inputs from widespread cortical regions, including primary and higher order sensory and motor cortical areas. LP→ACC neurons also receive extensive subcortical inputs, particularly from the intermediate and deep layers of the superior colliculus (SC).Sensory inputs to ACC→LP neurons largely arise from visual cortical areas. In addition, ACC→LP neurons integrate cross-hemispheric prefrontal cortex inputs as well as inputs from higher order medial cortex. Our brain-wide anatomical mapping of inputs to the reciprocal LP-ACC pathways provides a roadmap for understanding how LP and ACC communicate different sources of information to mediate attentional control and visuomotor functions.

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Thalamus Modulates Consciousness Via Layer-Specific Control of Cortex

Cited by 55 publications

References 0 publications

Neural effects of propofol-induced unconsciousness and its reversal using thalamic stimulation

Neural effects of propofol-induced unconsciousness and its reversal using thalamic stimulation

Spatio-temporal patterns of population responses in the visual cortex under Isoflurane: from wakefulness to loss of consciousness

Brain‐wide mapping of inputs to the mouse lateral posterior (LP/Pulvinar) thalamus–anterior cingulate cortex network

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