bioRxiv Science⌕ Search

bioRxiv · 10.1101/186411

Expect to neglect: Cross-modal resource allocation in anticipation of visual load

Abstract

Human information processing is limited in capacity. To prevent sensory overload, expectation of upcoming events has been suggested to allocate processing resources to task-relevant regions (e.g., visual system), at the expense of processing in task-irrelevant regions (e.g., auditory system). In support of this, for tasks involving a high visual perceptual load (e.g. visual target search within physically similar distractors), auditory evoked responses were found to be attenuated1. This EEG study aimed to further elucidate the neural mechanisms by which the brain prepares for sensory overload. We investigated how expectancy about visual load modulated neural activity, prior to the onset of visual stimuli. Visual load in a letter search task was manipulated by varying the target letters similarity to the remaining letters and the letter set size from which flankers were randomly drawn. Importantly, audio-visual cues signaled the likely visual load of the upcoming stimulus-array, manipulating expectancy about visual task load. Cues signaling high visual load elicited attenuated auditory-evoked responses and increased alpha activity over task-irrelevant (auditory) regions, suggesting a functional inhibition of those regions already prior to the arrival of the visual array to suppress auditory cue processing. We also observed a sustained posterior positivity in the ERPs after high perceptual load cues, whose amplitude correlated with reaction times, suggestive of resource allocation for the upcoming visual targets. Expectation about visual load may thus prepare the attentional system both by facilitating target processing and task execution and inhibiting irrelevant sensory processing, thus providing efficient means to overcome attentional limits in situations with complex visual input.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Bangel, K. A., Slagter, H. A., Mazaheri, A.. 2017-09-10. Expect to neglect: Cross-modal resource allocation in anticipation of visual load. https://doi.org/10.1101/186411

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Sex differences in fear extinction are conditional, not categorical

Threat memories are dynamic, and their behavioral expression can change with subsequent experience and the passage of time. Extinction training can reduce conditioned fear responses, yet these responses may re-emerge over time through spontaneous recovery. Although biological sex has been implicated as modulatory factor in fear and extinction memory processes, studies have reported inconsistent findings. Here, we investigated how differences in extinction training and the timing of memory assessment influence extinction memory in male and female mice. Using contextual fear conditioning, we assessed fear acquisition and threat retention, characterized within-session and across-session extinction during repeated training, and compared shorter (3-minute) and longer (6-minute) daily extinction sessions. We subsequently evaluated extinction memory retention and spontaneous recovery at a later time point. Estrous-cycle stage in females was monitored daily throughout the experimental protocol to examine its potential association with fear and extinction behavior. We found that males and females demonstrated comparable fear acquisition and threat memory, as well as similar extinction progression across days. During longer extinction sessions, but not shorter, males showed greater within-session reductions in freezing, whereas females exhibited modestly higher overall freezing. We found no significant sex difference in the magnitude of spontaneous recovery. There was no significant association between estrous-cycle stage and freezing behavior. Together, our findings suggest that sex-dependent differences in contextual fear extinction are not uniformly expressed, but rather depend on the experimental conditions under which extinction is assessed

neuroscience↗

LAMA2-related muscular dystrophy alters Schwann cell calcium homeostasis and increases peripheral nerve inflammation

LAMA2-related muscular dystrophy (LAMA2-RD) affects skeletal muscle and peripheral nerves, yet the consequences of LAMA2 deficiency on peripheral nerve integrity beyond early postnatal development remain incompletely understood. We investigated sciatic nerve architecture and molecular alterations across postnatal life in hypomorphic Lama2dy2J/dy2J mice. LAMA2 localizes around the abaxonal surface of myelinating Schwann cells in control nerves. LAMA2-deficient nerves exhibited patchy regions lacking myelinated axons from early postnatal stages into adulthood, including expanded Remak bundles along with axons completely lacking normal Schwann cell ensheathment. In adult nerves, myelin infolding and reduced myelin circularity revealed abnormalities in the architecture of myelin that had formed. Bulk sciatic nerve RNA sequencing identified altered calcium-signaling and immune-related transcriptional signatures. Complementary Fura Red measurements in primary nerve-derived Schwann cell cultures demonstrated decreased intracellular calcium in LAMA2-deficient samples, while ATP-evoked responses were preserved. Older LAMA2-deficient nerves also exhibited increased CD45+CD11b+ myeloid-cell infiltration. Together, these observations extend the characterization of LAMA2-associated neuropathy into adulthood and identify calcium homeostasis and neuroimmune responses as candidate processes relevant to persistent peripheral nerve pathology.

neuroscience↗

Endothelin-1 from Tongue Glands Gates 1 Sodium Taste and Intake

Sodium is an essential nutrient. To survive sodium deficiency, animals dramatically increase their appetite for salt. However, whether and how sodium depletion impacts the taste of salt to drive sodium intake is unknown. Here we show that tongue gland-derived endothelin-1 (EDN1) regulates the amiloride-sensitive, sodium-selective salt taste. Edn1 is specifically expressed in the glands embedded within the tongue. Under normal conditions, EDN1 suppresses salt taste by acting on its receptor EDNRB on the projections of salt-sensing taste neurons innervating taste buds. When internal sodium levels drop, EDN1 expression decreases, lifting this inhibition and enhancing responses to salt. Applying EDN1 directly to the tongue, using a nonionic eutectic-based organogel (Neogel) delivery technology that we establish here, dampens the activity of the salt-sensing taste neurons and reduces salt intake and preference. Conversely, genetic deletion of Ednrb in taste neurons mimics the effects of sodium deficiency, enhancing salt-sensing neuron activity and increasing salt consumption. These findings reveal a peripheral mechanism that regulates salt taste and intake in response to internal sodium levels, highlighting a direct role of the taste pathway in maintaining nutrient homeostasis.

neuroscience↗