Consciousness intuitions are illusory Philosophical discussions of the “hard problem” often invoke “problem intuitions”, as consciousness intuitions and consciousness are believed to be “closely connected” (Chalmers, 2018). Here, I challenge this assumption. In two experiments, I demonstrate that consciousness intuitions are illusory—they shift across different “problem intuitions”, akin to perceptual illusions. When presented with a duplication scenario, people do not view consciousness as physical (i.e., they believe that copying one’s physical body will not copy one’s conscious states). But when probed about a second scenario (that of Mary in the Black-and-White Room), consciousness now seems squarely physical, as people expect Mary’s novel experience of color to “show up” in a brain scan. I trace this shift to two psychological biases—intuitive Dualism and Essentialism. The shift in consciousness intuitions demonstrates that consciousness judgments are illusory, and as such, they cannot be trusted to reflect what consciousness is.
Differential locus coeruleus–hippocampus interactions during offline states Patterns of locus coeruleus (LC) activity and norepinephrine (NE) release during non-rapid-eye-movement (NREM) sleep suggest a critical role for the LC–NE system in offline modulation of forebrain circuits. NE transmission promotes synaptic plasticity and is required for memory consolidation, but the field has only begun to uncover how LC activity contributes to coordinated forebrain network dynamics. Hippocampal ripples, a hallmark of memory replay, are temporally coupled with thalamocortical oscillations; however, the circuit mechanisms underlying systems-level consolidation across larger brain networks remain incompletely understood. Here, using multi-site electrophysiology, we examined LC firing in relation to hippocampal ripples in freely behaving rats. LC activity and ripple occurrence were state-dependent and inversely related: heightened arousal was associated with increased LC firing and reduced ripple rates. At finer timescales, LC spiking decreased ∼1–2 seconds before ripple onset, with the strongest modulation during awake ripples but minimal change during ripple–spindle coupling. These findings reveal state-dependent dynamics of LC-hippocampal interactions, positioning the LC as a key component of a cortical–subcortical network supporting systems-level memory consolidation.
Neural and Navigational Features Influencing the Novelty Induced Benefits on Episodic Memory Studies in animals have robustly shown that exposure to novelty can promote memory for information presented in the temporal vicinity. In humans, however, evidence for such novelty-related memory benefits has been mixed. In this EEG study, we investigated the neurobiological mechanisms underlying effects of novelty on memory and whether individual differences in exploration patterns help explain these inconsistencies. We examined the role of theta oscillations in exploring a novel or familiar environment as well as whether spatial exploration behavior can modulate the beneficial effects of novelty on memory. Participants first explored one of two virtual environments and subsequently explored the same (familiar condition) or a new environment (novel condition). After exploring novel and familiar environments, participants performed a word learning task followed by a free recall and recognition memory test. Neurologically, exploration of the familiar rather than novel environment increased theta power, which may reflect environment-related memory processes. However, we did not observe any differences in theta power associated with successful encoding of words after exploring a novel versus familiar environment. Behaviorally, no main effect of novelty on free recall was observed. Crucially, when accounting for variance in spatial exploration patterns, words encoded after exploring a novel environment were recalled better than words encoded after exploring a familiar environment. Furthermore, an interaction effect between the condition and exploratory behavior revealed that increased exploration benefitted free recall specifically in the familiar condition. These findings emphasize the importance of considering the way in which individuals explore a virtual environment when examining novelty effects on memory.
Diencephalic integrity explains aspects of hippocampal amnesia Research on amnesia has been fundamental in establishing the role of the human hippocampus in memory. Even though other structures within the hippocampal-diencephalic-cingulate network also play a role in episodic memory, studies of hippocampal amnesia often ignore the importance of changes in this broader network. In a large cohort of patients (n = 38) with hippocampal damage due to autoimmune limbic encephalitis, we previously found that amnesia was predominantly explained by resting-state functional abnormalities across this network. Here, we examined the integrity of individual diencephalic nuclei and white matter pathways, and its relationship with memory function. We found atrophy in the mammillary bodies, and the anterior, laterodorsal, pulvinar, and dorsomedial thalamic nuclei. Atrophy was often as pronounced as that in the hippocampal formation. Diencephalic volumes predicted memory over and above any hippocampal/subicular subfield volume estimate. White matter was compromised within and beyond this network. Fornix integrity was linked to diencephalic and hippocampal volumes, but not to recollection/recall. We strongly advise caution in employing the term “focal hippocampal damage” in cognitive neuroscience, and highlight the need to study the significance of plausibly knock-on effects in specific diencephalic nuclei and white matter tracts within broader circuits.
Thalamic Activity Regulates Interneuron Density in the Developing Visual Thalamus Neural activity is a fundamental driver of early circuit assembly, yet how it shapes the distribution of inhibitory neurons across sensory networks remains poorly understood. Establishing an appropriate balance between excitation and inhibition is essential for effective sensory processing, but the contribution of activity-dependent mechanisms to interneuron allocation across subcortical and cortical stations is unclear. Here, we use region-specific transgenic mouse models of either sex to selectively manipulate activity at distinct loci and developmental stages of the visual pathway. We show that intrinsic thalamic activity is a key regulator of interneuron density in the dorsolateral geniculate nucleus during early postnatal development. Disruption of thalamic activity leads to persistent increases in interneuron proportion, independent of retinal axon targeting. Moreover, altered thalamic activity propagates to the cortex, producing layer-specific changes in parvalbumin- and somatostatin-expressing interneuron populations in primary visual cortex. Together, our findings identify intrinsic thalamic activity as a central organizer of inhibitory circuit assembly across the visual system, coordinating interneuron integration in both thalamus and cortex during critical developmental windows.
Young and old adult brains experience opposite effects of acute sleep restriction on the functional connectivity network Chronic, long-term sleep loss is detrimental to brain health and cognitive ability. However, older adults are affected differently by acute, short-term loss of sleep than young and middle-aged adults. Older adults are more resilient to the effects of acute sleep loss and, depending on the cognitive domain, may be completely unaffected while younger adults suffer. To elucidate the brain network responses to sleep loss underlying these cognitive differences between age groups, we investigated the static and dynamic functional connectivity effects of acute sleep restriction (sleep limited to 3 hours) and how these effects differ between younger adults (20–30 years) and older adults (65–75 years). We found a functional connectivity subnetwork that was primarily strengthened in younger adults after acute sleep restriction but weakened in older adults after acute sleep restriction. Similar crossover interactions were consistently observed in further analyses of functional connectivity degree, modularity, and dynamic functional connectivity state fractional occupancy. Our findings demonstrate that the effect of acute sleep restriction on older adults is fundamentally different from that on younger adults. These results most strongly support the compensation theory of ageing, which predicts a fundamental shift in the effects of acute sleep loss, rather than a mere dampening of the sleep benefits experienced by younger adults.
Attention modulates value normalization in human reinforcement learning by shaping reward encoding Contextual valuation is a well-documented phenomenon in reinforcement learning, typically manifesting as range normalization in outcome representation. However, recent findings have revealed systematic deviations from this model, particularly when three options with equally spaced values are presented. In this study, we hypothesize that these distortions in outcome normalization arise from attentional processes. To test this, we conduct three experiments with 105 participants in total while simultaneously tracking their gaze position with eye-tracking. Furthermore, we systematically manipulate attention using both top-down and bottom-up approaches. These manipulations significantly increase the subjective valuation of attended options, supporting a causal role of attention in shaping value representation. To account for these effects, we develop a reinforcement learning model that integrates attentional mechanisms, wherein gaze duration directly modulates the absolute value of options prior to range normalization. This attentional range model outperforms attention-free and choice-repetition alternatives, underscoring the critical influence of attention in value computation.
Endothelial KLF4 depletion drives age-related neurovascular dysfunction and neuropsychiatric impairment Deterioration of the blood–brain barrier (BBB), including impaired neurovascular uncoupling, contributes to cognitive decline in aging. The BBB is formed principally by brain microvascular endothelial cells (ECs), and ECs throughout the body are enriched for the transcription factor Krüppel-like factor 4 (KLF4). Because KLF4 levels in ECs decrease with age, we tested whether that decline contributes to aging-related BBB deterioration, neurovascular dysfunction, and cognitive impairment. Using EC-specific Klf4 knockout mice (EC-K4KO), we show that loss of EC KLF4 accelerates multiple age-related brain pathologies. Indeed, middle-aged EC-K4KO mice display pathological features that are not normally observed until advanced age, including marked BBB leakage, impaired neurovascular coupling, loss of microvessels, increased oxidative damage, neuroinflammation, neurodegeneration, anxiety-like behavior, and cognitive deficits. Single-cell RNA sequencing of brain vasculature reveals dysregulation of immune response and barrier-related genes in ECs lacking KLF4, indicating that KLF4 maintains brain endothelial homeostasis by constraining proinflammatory and senescence programs at the chromatin level. Together, these results identify loss of EC KLF4 as a key driver of neurovascular decline and age-associated cognitive dysfunction.