Noradrenergic activity selectively modulates conscious (but not unconscious) neural processing, making it 'a key target for pharmacological manipulations of consciousness.'
Key Findings
Results
Dexmedetomidine selectively altered brain activity during conscious visuospatial processing without affecting unconscious processing.
fMRI BOLD signal changes were observed selectively during conscious processing conditions under Dexmedetomidine.
This selective effect contrasts with Propofol, which the authors previously demonstrated influences both conscious and unconscious neural processing.
The finding suggests noradrenergic mechanisms specifically contribute to conscious rather than unconscious processing.
Results
Sleep deprivation also selectively altered brain activity during conscious processing, mirroring Dexmedetomidine's selectivity but not its direction of effect.
Sleep deprivation was used as a natural state of altered arousal with partially overlapping effects on noradrenaline levels compared to Dexmedetomidine.
Like Dexmedetomidine, sleep deprivation produced selective fMRI BOLD signal changes during conscious processing only.
Sleep deprivation did not alter unconscious neural processing, consistent with the pattern seen with Dexmedetomidine.
Both manipulations converged on selectivity for conscious processing despite being pharmacologically and physiologically distinct interventions.
Results
Dexmedetomidine and sleep deprivation produced opposite effects on visuospatial bias, with Dexmedetomidine reducing leftward bias and sleep deprivation increasing leftward bias.
Visuospatial bias (leftward bias) is a measure of asymmetric spatial attention processing.
Dexmedetomidine reduced leftward visuospatial bias during low arousal conditions.
Sleep deprivation increased leftward visuospatial bias during low arousal conditions.
These divergent directional effects on the same behavioral measure occurred despite both conditions involving reduced arousal.
Results
Sleep deprivation produced an unexpected increase in sympathetic drive, indicating increased rather than decreased noradrenaline levels during task performance.
Increased activity was observed in the central autonomic network under sleep deprivation.
Heart rate was also increased under sleep deprivation, serving as a peripheral index of sympathetic activation.
This increased sympathetic drive was described as 'unexpected,' as sleep deprivation is generally associated with reduced arousal.
The differential sympathetic response explained the opposite direction of visuospatial bias effects between sleep deprivation and Dexmedetomidine.
The authors interpret this as indicating that noradrenaline levels were actually elevated during task performance in the sleep-deprived state.
Background
Propofol, unlike Dexmedetomidine and sleep deprivation, influences both conscious and unconscious neural processing, limiting its specificity as a tool for studying consciousness.
The authors cite their own prior work demonstrating Propofol affects both conscious and unconscious processing.
This non-selectivity means Propofol-induced effects cannot be assumed a priori to reflect specifically conscious neural processes.
The contrast with Dexmedetomidine and sleep deprivation underscores the importance of mechanism-specific interventions when investigating consciousness.
The authors argue that 'effects on both conscious and unconscious processes need to be considered' when using pharmacological tools.
Conclusions
Noradrenergic activity is identified as a key target for pharmacological manipulation of consciousness and a window into its neurophysiological underpinnings.
Both Study 1 (Dexmedetomidine) and Study 2 (sleep deprivation) converge on noradrenergic modulation as specifically relevant to conscious processing.
The authors conclude that noradrenergic activity could 'open a window to its neurophysiological underpinnings' of consciousness.
The α2A noradrenergic receptor subtype targeted by Dexmedetomidine is highlighted as a specific pharmacological target.
The study used fMRI BOLD signal change as the primary neuroimaging measure across both studies.
What This Means
This research suggests that a specific brain chemical system — the noradrenergic system, which uses the neurotransmitter noradrenaline (also called norepinephrine) — plays a special role in generating conscious experiences. The researchers used two different ways to alter noradrenaline levels in the brain: a sedative drug called Dexmedetomidine (which specifically targets noradrenaline receptors) and sleep deprivation (a natural way to affect noradrenaline). Brain scans showed that both approaches changed brain activity only during tasks that required conscious awareness, leaving unconscious brain processing untouched. This contrasts with another common sedative, Propofol, which the same team had previously shown affects both conscious and unconscious processing — making it a less precise tool for studying what makes us conscious.
Interestingly, while both Dexmedetomidine and sleep deprivation reduced arousal, they had opposite effects on a spatial attention task: Dexmedetomidine made participants less biased toward the left side of space, while sleep deprivation made them more biased toward the left. The researchers traced this surprising difference to the fact that sleep-deprived participants actually showed signs of increased noradrenaline activity during the task — their hearts beat faster and brain regions involved in controlling the body's stress response became more active — suggesting the body was compensating for fatigue by ramping up its alerting system.
This research matters because understanding which brain systems are specifically involved in conscious (versus unconscious) processing is a fundamental step toward explaining how the brain produces awareness. The findings point to the noradrenergic system as a promising, precise target for future studies and potentially for clinical situations where consciousness is compromised, such as in disorders of consciousness or during anesthesia.
Karampela O, Fontan A, Lindgren L, Pedale T, Brorsson C, Bergström F, et al.. (2026). Noradrenergic activity as a key target in modulating consciousness.. Scientific reports. https://doi.org/10.1038/s41598-026-41819-2