Pub Date : 2026-06-01Epub Date: 2026-01-30DOI: 10.1016/j.crneur.2026.100155
Kwangjun Lee , Lorenzo Baracco , Cyriel M.A. Pennartz , Mototaka Suzuki , Jorge F. Mejias
Artificial neural networks commonly have deep hierarchical structures that were originally inspired by the neuroanatomical evidence of cortico-cortical connectivity pattern found in the mammalian brain. Largely under-represented in those models are non-hierarchical aspects of brain architecture, namely the subcortical pathways and the interactions between cortical and subcortical areas regardless of their hierarchical locations. Inspired by this principle, we present a computational model combining cortical hierarchical processing with subcortical pathways based on neuroanatomical evidence. We show the versatility of our model by implementing the cortical hierarchy in two alternative ways—a convolutional feedforward network and a predictive coding network. Both model variants can replicate behavioral observations in humans and monkeys on a perceptual context-dependent decision-making task. The model also reveals that subcortical structures lead decisions for easy trials while the more complex hierarchical network is necessary for the harder trials. Our results suggest that the parallel cortico-subcortical processing explored in the model represents a fundamental property that cannot be neglected in understanding the computational principles used by the brain.
{"title":"A computational architecture incorporating shallow brain networks: integrating parallel cortical and subcortical processing","authors":"Kwangjun Lee , Lorenzo Baracco , Cyriel M.A. Pennartz , Mototaka Suzuki , Jorge F. Mejias","doi":"10.1016/j.crneur.2026.100155","DOIUrl":"10.1016/j.crneur.2026.100155","url":null,"abstract":"<div><div>Artificial neural networks commonly have deep hierarchical structures that were originally inspired by the neuroanatomical evidence of cortico-cortical connectivity pattern found in the mammalian brain. Largely under-represented in those models are non-hierarchical aspects of brain architecture, namely the subcortical pathways and the interactions between cortical and subcortical areas regardless of their hierarchical locations. Inspired by this principle, we present a computational model combining cortical hierarchical processing with subcortical pathways based on neuroanatomical evidence. We show the versatility of our model by implementing the cortical hierarchy in two alternative ways—a convolutional feedforward network and a predictive coding network. Both model variants can replicate behavioral observations in humans and monkeys on a perceptual context-dependent decision-making task. The model also reveals that subcortical structures lead decisions for easy trials while the more complex hierarchical network is necessary for the harder trials. Our results suggest that the parallel cortico-subcortical processing explored in the model represents a fundamental property that cannot be neglected in understanding the computational principles used by the brain.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"10 ","pages":"Article 100155"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146192564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-06-01Epub Date: 2026-01-30DOI: 10.1016/j.crneur.2026.100156
Grant S. Mannino , Andrea Lugo , Sean M. Murphy , Mark R. Opp , Rachel K. Rowe
Quantifying sleep quality in rodent models is critical for understanding its impact on neurological health and disease. Piezoelectric cage systems enable rapid, noninvasive measurement of multiple sleep metrics for large sample sizes of rodents. Although sleep duration is commonly reported, sleep fragmentation, which is a key feature of sleep architecture implicated in neurodegenerative disease, circadian rhythm disruption, and injury models, is not directly measured. We developed a standardized Microsoft Excel™-based tool for quantifying sleep-wake transitions, a scalable proxy for sleep fragmentation, in data from rodents recorded using a piezoelectric cage system. The tool extracts transitions from 2-s binned activity data, which are output by the system's software. Our pipeline, which incorporates this tool, enables high-throughput analysis of sleep fragmentation across large datasets with minimal user intervention. We demonstrate the applicability of this tool and the associated pipeline by analyzing 24-h sleep-wake behavior in wild-type male and female mice. The approach facilitated identification of biologically meaningful sex differences in sleep fragmentation patterns. Female mice exhibited more frequent transitions between sleep and wake states, particularly during the light period, consistent with increased sleep fragmentation. This is the first method developed for quantifying sleep fragmentation from activity data recorded by noninvasive piezoelectric cage systems, and represents a standardized, reproducible, and publicly accessible approach with wide application in rodent models. It enhances the utility of piezoelectric cage systems and supports noninvasive phenotyping of sleep architecture in neuroscience research, particularly where high-throughput or minimally invasive methods are required.
{"title":"A tool for high-throughput quantification of sleep-wake transitions in data from noninvasive piezoelectric cage systems","authors":"Grant S. Mannino , Andrea Lugo , Sean M. Murphy , Mark R. Opp , Rachel K. Rowe","doi":"10.1016/j.crneur.2026.100156","DOIUrl":"10.1016/j.crneur.2026.100156","url":null,"abstract":"<div><div>Quantifying sleep quality in rodent models is critical for understanding its impact on neurological health and disease. Piezoelectric cage systems enable rapid, noninvasive measurement of multiple sleep metrics for large sample sizes of rodents. Although sleep duration is commonly reported, sleep fragmentation, which is a key feature of sleep architecture implicated in neurodegenerative disease, circadian rhythm disruption, and injury models, is not directly measured. We developed a standardized Microsoft Excel™-based tool for quantifying sleep-wake transitions, a scalable proxy for sleep fragmentation, in data from rodents recorded using a piezoelectric cage system. The tool extracts transitions from 2-s binned activity data, which are output by the system's software. Our pipeline, which incorporates this tool, enables high-throughput analysis of sleep fragmentation across large datasets with minimal user intervention. We demonstrate the applicability of this tool and the associated pipeline by analyzing 24-h sleep-wake behavior in wild-type male and female mice. The approach facilitated identification of biologically meaningful sex differences in sleep fragmentation patterns. Female mice exhibited more frequent transitions between sleep and wake states, particularly during the light period, consistent with increased sleep fragmentation. This is the first method developed for quantifying sleep fragmentation from activity data recorded by noninvasive piezoelectric cage systems, and represents a standardized, reproducible, and publicly accessible approach with wide application in rodent models. It enhances the utility of piezoelectric cage systems and supports noninvasive phenotyping of sleep architecture in neuroscience research, particularly where high-throughput or minimally invasive methods are required.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"10 ","pages":"Article 100156"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146192565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-06-28DOI: 10.1016/j.crneur.2025.100154
Estelle Maret , Tatjana Sajic , Kim Wiskott , Sylvain Le Gludic , Federica Gilardi , Youssef Daali , Tony Fracasso , Aurélien Thomas
Abusive head trauma (AHT) is a severe form of traumatic brain injury (TBI) and causes significant brain lesions by vigorous shaking. It is the leading cause of mortality and morbidity in children under 2 years of age. If not fatal, AHT can result in severe disabilities, often requiring long-term care. Clinical diagnosis of AHT is challenging, because symptoms are often non-specific, overlap with those of other diseases and relies on screening for intracranial, spinal, and ocular lesions. To date, no screening test has been developed to preselect children suspected to be victims of AHT for further clinical investigations. However, as recently demonstrated via analysis of serum proteomes of infant victims of AHT, large-scale omic analysis of blood serum samples could help identify molecules with high potential for early detection of human pathologies. Here, we investigated the circulating serum metabolome of infants with severe head trauma with a Glasgow Coma Scale (GCS) score of 3–4 and compared it to infants with no signs of head trauma during medico-legal examinations. Using liquid chromatography coupled to high resolution mass spectrometry (LC-HRMS), we identified 53 metabolites with the most significant differences between the groups. Six metabolites were already known to be implicated in different gross pathologies associated with neurological diseases. In addition, our analysis revealed several lipids and lipid-like molecules, all with an increased profile in the peripheral blood circulation of infant victims of AHT. As we speculated some of the identified metabolites to come from specific brain regions affected by the shaking mechanism, we further performed a multi-omic integration by integrating metabolites showing evidence of their presence in the brain and publicly available proteomic data. As results, we found significant metabolite-protein correlations which could be closely associated with AHT, thus, providing evidence of tensions and supporting strong dynamic changes occurring within the brain during assault.
{"title":"Exploration of circulating metabolites in infants with abusive head trauma","authors":"Estelle Maret , Tatjana Sajic , Kim Wiskott , Sylvain Le Gludic , Federica Gilardi , Youssef Daali , Tony Fracasso , Aurélien Thomas","doi":"10.1016/j.crneur.2025.100154","DOIUrl":"10.1016/j.crneur.2025.100154","url":null,"abstract":"<div><div>Abusive head trauma (AHT) is a severe form of traumatic brain injury (TBI) and causes significant brain lesions by vigorous shaking. It is the leading cause of mortality and morbidity in children under 2 years of age. If not fatal, AHT can result in severe disabilities, often requiring long-term care. Clinical diagnosis of AHT is challenging, because symptoms are often non-specific, overlap with those of other diseases and relies on screening for intracranial, spinal, and ocular lesions. To date, no screening test has been developed to preselect children suspected to be victims of AHT for further clinical investigations. However, as recently demonstrated via analysis of serum proteomes of infant victims of AHT, large-scale omic analysis of blood serum samples could help identify molecules with high potential for early detection of human pathologies. Here, we investigated the circulating serum metabolome of infants with severe head trauma with a Glasgow Coma Scale (GCS) score of 3–4 and compared it to infants with no signs of head trauma during medico-legal examinations. Using liquid chromatography coupled to high resolution mass spectrometry (LC-HRMS), we identified 53 metabolites with the most significant differences between the groups. Six metabolites were already known to be implicated in different gross pathologies associated with neurological diseases. In addition, our analysis revealed several lipids and lipid-like molecules, all with an increased profile in the peripheral blood circulation of infant victims of AHT. As we speculated some of the identified metabolites to come from specific brain regions affected by the shaking mechanism, we further performed a multi-omic integration by integrating metabolites showing evidence of their presence in the brain and publicly available proteomic data. As results, we found significant metabolite-protein correlations which could be closely associated with AHT, thus, providing evidence of tensions and supporting strong dynamic changes occurring within the brain during assault.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"9 ","pages":"Article 100154"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144604681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-04-17DOI: 10.1016/j.crneur.2025.100149
Lauren Shute , Mark Fry
The subfornical organ (SFO) is a sensory circumventricular organ, lacking a blood-brain barrier. It is well-recognized as a key center for detection and integration of osmotic, ionic and hormonal signals for maintenance of hydromineral balance and cardiovascular regulation. Recently, the SFO has also been recognized as a center for the detection and integration of circulating satiety signals for regulation of energy balance. Neuropeptide Y (NPY) is a multifunctional neuropeptide, with effects on energy balance, cardiovascular tone and other aspects of homeostasis. Interestingly, despite the overlap of function between SFO and NPY, and observations that SFO expresses several subtypes of Y receptors, NPY regulation of SFO neurons has never been investigated. In this study, we examined the effects of NPY on dissociated rat SFO neurons using patch clamp electrophysiology. We observed that 300 nM NPY caused depolarization of 16 % of SFO neurons tested, and hyperpolarization of 26 %, while the remaining neurons were insensitive to NPY (n = 31). These effects were dose-dependent with an apparent EC50 of 3.9 nM for depolarizing neurons and 3.5 nM for hyperpolarizing neurons. Activation of Y5 receptors alone led to predominately hyperpolarizing effects, while activation of Y1 or Y2 receptors alone led to mixed responses. Voltage-clamp experiments demonstrated that NPY caused increases in voltage-gated K+ current amplitude as well as hyperpolarizing shifts in persistent Na+ current, mediating the hyperpolarizing and depolarizing effects, respectively. These findings indicate that NPY elicits direct electrophysiological effects on SFO neurons, suggesting that NPY acts via the SFO to regulate energy homeostatic function.
{"title":"Neuropeptide Y modulates the electrical activity of subfornical organ neurons","authors":"Lauren Shute , Mark Fry","doi":"10.1016/j.crneur.2025.100149","DOIUrl":"10.1016/j.crneur.2025.100149","url":null,"abstract":"<div><div>The subfornical organ (SFO) is a sensory circumventricular organ, lacking a blood-brain barrier. It is well-recognized as a key center for detection and integration of osmotic, ionic and hormonal signals for maintenance of hydromineral balance and cardiovascular regulation. Recently, the SFO has also been recognized as a center for the detection and integration of circulating satiety signals for regulation of energy balance. Neuropeptide Y (NPY) is a multifunctional neuropeptide, with effects on energy balance, cardiovascular tone and other aspects of homeostasis. Interestingly, despite the overlap of function between SFO and NPY, and observations that SFO expresses several subtypes of Y receptors, NPY regulation of SFO neurons has never been investigated. In this study, we examined the effects of NPY on dissociated rat SFO neurons using patch clamp electrophysiology. We observed that 300 nM NPY caused depolarization of 16 % of SFO neurons tested, and hyperpolarization of 26 %, while the remaining neurons were insensitive to NPY (n = 31). These effects were dose-dependent with an apparent EC<sub>50</sub> of 3.9 nM for depolarizing neurons and 3.5 nM for hyperpolarizing neurons. Activation of Y5 receptors alone led to predominately hyperpolarizing effects, while activation of Y1 or Y2 receptors alone led to mixed responses. Voltage-clamp experiments demonstrated that NPY caused increases in voltage-gated K<sup>+</sup> current amplitude as well as hyperpolarizing shifts in persistent Na<sup>+</sup> current, mediating the hyperpolarizing and depolarizing effects, respectively. These findings indicate that NPY elicits direct electrophysiological effects on SFO neurons, suggesting that NPY acts via the SFO to regulate energy homeostatic function.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"8 ","pages":"Article 100149"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143863746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-04-08DOI: 10.1016/j.crneur.2025.100150
Erik N. Oldre, Barrett D. Webb, Justin E. Sperringer, Patricia F. Maness
The perisomatic region of cortical pyramidal neurons (PNs) integrates local and long-range inputs and regulates firing. This domain receives GABAergic inputs from cholecystokinin (CCK)- and Parvalbumin (PV)-expressing basket cells (BCs) but how synaptic contacts are established is unclear. Neuron-glial related cell adhesion molecule (NrCAM) is a homophilic transmembrane protein that binds the scaffold protein Ankyrin B. Here we show that NrCAM and Ankyrin B mediate perisomatic synaptic contact between CCK-BCs and PNs in mouse medial prefrontal cortex (mPFC). Immunolabeling of CCK-BC terminals for vesicular glutamate transporter-3 (VGLUT3) or vesicular GABA transporter (VGAT) revealed a significant decrease in CCK-BC synaptic puncta on PN soma in NrCAM-null mice, however no decrease in PV-BC puncta or cell loss. VGLUT3+ CCK-BC puncta were also decreased by Ankyrin B deletion from PNs in Nex1Cre-ERT2:Ank2flox/flox:EGFP mice. A novel CCK-BC reporter mouse expressing tdTomato (tdT) at the Synuclein-γ (Sncg) locus showed NrCAM localized to Sncg + CCK-BCs, and to postsynaptic PN soma in Nex1Cre-ERT2:Ank2+/+:EGFP mice. Results suggest that NrCAM and Ankyrin B contribute to the establishment of connectivity between CCK-BCs and excitatory neurons of the mPFC.
{"title":"Regulation of perisomatic synapses from cholecystokinin basket interneurons through NrCAM and Ankyrin B","authors":"Erik N. Oldre, Barrett D. Webb, Justin E. Sperringer, Patricia F. Maness","doi":"10.1016/j.crneur.2025.100150","DOIUrl":"10.1016/j.crneur.2025.100150","url":null,"abstract":"<div><div>The perisomatic region of cortical pyramidal neurons (PNs) integrates local and long-range inputs and regulates firing. This domain receives GABAergic inputs from cholecystokinin (CCK)- and Parvalbumin (PV)-expressing basket cells (BCs) but how synaptic contacts are established is unclear. Neuron-glial related cell adhesion molecule (NrCAM) is a homophilic transmembrane protein that binds the scaffold protein Ankyrin B. Here we show that NrCAM and Ankyrin B mediate perisomatic synaptic contact between CCK-BCs and PNs in mouse medial prefrontal cortex (mPFC). Immunolabeling of CCK-BC terminals for vesicular glutamate transporter-3 (VGLUT3) or vesicular GABA transporter (VGAT) revealed a significant decrease in CCK-BC synaptic puncta on PN soma in NrCAM-null mice, however no decrease in PV-BC puncta or cell loss. VGLUT3+ CCK-BC puncta were also decreased by Ankyrin B deletion from PNs in Nex1Cre-ERT2:Ank2<sup>flox/flox</sup>:EGFP mice. A novel CCK-BC reporter mouse expressing tdTomato (tdT) at the Synuclein-γ (<em>Sncg</em>) locus showed NrCAM localized to Sncg + CCK-BCs, and to postsynaptic PN soma in Nex1Cre-ERT2:Ank2<sup>+/+</sup>:EGFP mice. Results suggest that NrCAM and Ankyrin B contribute to the establishment of connectivity between CCK-BCs and excitatory neurons of the mPFC.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"8 ","pages":"Article 100150"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143820382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2024-11-28DOI: 10.1016/j.crneur.2024.100141
Gaoyuan Ma, Jonathan M. Chan, Katrina H. Worthy, Marcello G.P. Rosa, Nafiseh Atapour
Lesions of the primary visual cortex (V1) cause retrograde neuronal degeneration, volume loss and neurochemical changes in the lateral geniculate nucleus (LGN). Here we characterised the timeline of these processes in adult marmoset monkeys, after various recovery times following unilateral V1 lesions. Observations in NeuN-stained sections obtained from animals with short recovery times (2, 3 or 14 days) showed that the volume and neuronal density in the LGN ipsilateral to the lesions were similar to those in the contralateral hemispheres. However, neuronal density in the lesion projection zone of LGN dropped rapidly thereafter, with approximately 50% of the population lost within a month post-lesion. This level of neuronal loss remained stable for over three years post-lesion. In comparison, shrinkage of the LGN volume progressed more gradually, not reaching a stable value until 6 months post lesion. We also determined the time course of the expression of the calcium-binding protein calbindin (CB) in magnocellular (M) and parvocellular (P) layer neurons, a form of neurochemical plasticity previously reported to be triggered by V1 lesions. We found that CB expression could be detected in surviving M and P neurons as early as two weeks after lesion, with the percentage of neurons showing this neurochemical phenotype gradually increasing over 6 months. Thus, neurochemical change precedes neuronal degeneration, suggesting it may be linked to a protective mechanism. This study highlights the limited time window for any possible interventions aimed at reducing secondary neuronal loss in the visual afferent pathways following damage to V1.
{"title":"Rapid degeneration and neurochemical plasticity of the lateral geniculate nucleus following lesions of the primary visual cortex in marmoset monkeys","authors":"Gaoyuan Ma, Jonathan M. Chan, Katrina H. Worthy, Marcello G.P. Rosa, Nafiseh Atapour","doi":"10.1016/j.crneur.2024.100141","DOIUrl":"10.1016/j.crneur.2024.100141","url":null,"abstract":"<div><div>Lesions of the primary visual cortex (V1) cause retrograde neuronal degeneration, volume loss and neurochemical changes in the lateral geniculate nucleus (LGN). Here we characterised the timeline of these processes in adult marmoset monkeys, after various recovery times following unilateral V1 lesions. Observations in NeuN-stained sections obtained from animals with short recovery times (2, 3 or 14 days) showed that the volume and neuronal density in the LGN ipsilateral to the lesions were similar to those in the contralateral hemispheres. However, neuronal density in the lesion projection zone of LGN dropped rapidly thereafter, with approximately 50% of the population lost within a month post-lesion. This level of neuronal loss remained stable for over three years post-lesion. In comparison, shrinkage of the LGN volume progressed more gradually, not reaching a stable value until 6 months post lesion. We also determined the time course of the expression of the calcium-binding protein calbindin (CB) in magnocellular (M) and parvocellular (P) layer neurons, a form of neurochemical plasticity previously reported to be triggered by V1 lesions. We found that CB expression could be detected in surviving M and P neurons as early as two weeks after lesion, with the percentage of neurons showing this neurochemical phenotype gradually increasing over 6 months. Thus, neurochemical change precedes neuronal degeneration, suggesting it may be linked to a protective mechanism. This study highlights the limited time window for any possible interventions aimed at reducing secondary neuronal loss in the visual afferent pathways following damage to V1.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"8 ","pages":"Article 100141"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2024-11-23DOI: 10.1016/j.crneur.2024.100143
Matthew A. Bennett , Lucy S. Petro , Clement Abbatecola , Lars F. Muckli
Identifying the objects embedded in natural scenes relies on recurrent processing between lower and higher visual areas. How is cortical feedback information related to objects and scenes organised in lower visual areas? The spatial organisation of cortical feedback converging in early visual cortex during object and scene processing could be retinotopically specific as it is coded in V1, or object centred as coded in higher areas, or both. Here, we characterise object and scene-related feedback information to V1. Participants identified foreground objects or background scenes in images with occluded central and peripheral subsections, allowing us to isolate feedback activity to foveal and peripheral regions of V1. Using fMRI and multivoxel pattern classification, we found that background scene information is projected to both foveal and peripheral V1 but can be disrupted in the fovea by a sufficiently demanding object discrimination task, during which we found evidence of foveal object decoding when using naturalistic stimuli. We suggest that the feedback connections during scene perception project back to earlier visual areas an automatic sketch of occluded information to the predicted retinotopic location. In the case of a cognitive task however, feedback pathways project content to foveal retinotopic space, potentially for introspection, functioning as a cognitive active blackboard and not necessarily predicting the object's location. This feedback architecture could reflect the internal mapping in V1 of the brain's endogenous models of the visual environment that are used to predict perceptual inputs.
{"title":"Retinotopic biases in contextual feedback signals to V1 for object and scene processing","authors":"Matthew A. Bennett , Lucy S. Petro , Clement Abbatecola , Lars F. Muckli","doi":"10.1016/j.crneur.2024.100143","DOIUrl":"10.1016/j.crneur.2024.100143","url":null,"abstract":"<div><div>Identifying the objects embedded in natural scenes relies on recurrent processing between lower and higher visual areas. How is cortical feedback information related to objects and scenes organised in lower visual areas? The spatial organisation of cortical feedback converging in early visual cortex during object and scene processing could be retinotopically specific as it is coded in V1, or object centred as coded in higher areas, or both. Here, we characterise object and scene-related feedback information to V1. Participants identified foreground objects or background scenes in images with occluded central and peripheral subsections, allowing us to isolate feedback activity to foveal and peripheral regions of V1. Using fMRI and multivoxel pattern classification, we found that background scene information is projected to both foveal and peripheral V1 but can be disrupted in the fovea by a sufficiently demanding object discrimination task, during which we found evidence of foveal object decoding when using naturalistic stimuli. We suggest that the feedback connections during scene perception project back to earlier visual areas an automatic sketch of occluded information to the predicted retinotopic location. In the case of a cognitive task however, feedback pathways project content to foveal retinotopic space, potentially for introspection, functioning as a cognitive active blackboard and not necessarily predicting the object's location. This feedback architecture could reflect the internal mapping in V1 of the brain's endogenous models of the visual environment that are used to predict perceptual inputs.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"8 ","pages":"Article 100143"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142984135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-03-06DOI: 10.1016/j.crneur.2025.100148
Cyril Atkinson-Clement , David Howett , Mohammad Alkhawashki , James Ross , Ben Slater , Marilyn Gatica , Fabien Balezeau , Chencheng Zhang , Jerome Sallet , Chris Petkov , Marcus Kaiser
Transcranial ultrasound stimulation (TUS) is a promising non-invasive neuromodulation modality, characterized by deep-brain accuracy and the capability to induce longer-lasting effects. However, most TUS datasets are underpowered, hampering efforts to identify TUS longevity and temporal dynamics. This primate case was studied awake with over 50 fMRI datasets, with and without left anterior hippocampus TUS. We therefore amassed the highest-powered TUS dataset to date required to reveal TUS longevity and dynamics. Most of the effects were found in the TUS region itself and alongside the default mode and sensorimotor networks. Seed-based functional connectivity exhibited a time-constrained alteration which dissipated ∼60 min post-TUS. Intrinsic activity measure and regional homogeneity displayed extended diffusivity and longer durations. This high-powered dataset allowed predicting TUS using pre-stimulation features that can now extend to modeling of individuals scanned less extensively. This case report reveals the diversity of TUS temporal dynamics to help to advance long-lasting human applications.
{"title":"Temporal dynamics of offline transcranial ultrasound stimulation","authors":"Cyril Atkinson-Clement , David Howett , Mohammad Alkhawashki , James Ross , Ben Slater , Marilyn Gatica , Fabien Balezeau , Chencheng Zhang , Jerome Sallet , Chris Petkov , Marcus Kaiser","doi":"10.1016/j.crneur.2025.100148","DOIUrl":"10.1016/j.crneur.2025.100148","url":null,"abstract":"<div><div>Transcranial ultrasound stimulation (TUS) is a promising non-invasive neuromodulation modality, characterized by deep-brain accuracy and the capability to induce longer-lasting effects. However, most TUS datasets are underpowered, hampering efforts to identify TUS longevity and temporal dynamics. This primate case was studied awake with over 50 fMRI datasets, with and without left anterior hippocampus TUS. We therefore amassed the highest-powered TUS dataset to date required to reveal TUS longevity and dynamics. Most of the effects were found in the TUS region itself and alongside the default mode and sensorimotor networks. Seed-based functional connectivity exhibited a time-constrained alteration which dissipated ∼60 min post-TUS. Intrinsic activity measure and regional homogeneity displayed extended diffusivity and longer durations. This high-powered dataset allowed predicting TUS using pre-stimulation features that can now extend to modeling of individuals scanned less extensively. This case report reveals the diversity of TUS temporal dynamics to help to advance long-lasting human applications.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"8 ","pages":"Article 100148"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143580540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-03-08DOI: 10.1016/j.crneur.2025.100147
Ana Maria Orellana , Natacha Medeiros S. Port's , Larissa de Sá Lima , Jacqueline Alves Leite , Diana Zukas Andreotti , Paula Fernanda Kinoshita , Arthur B. Cantanzaro , João Agostinho M. Neto , Cristoforo Scavone , Elisa M. Kawamoto
{"title":"Ouabain increases neuronal differentiation of hippocampal neural precursor cells","authors":"Ana Maria Orellana , Natacha Medeiros S. Port's , Larissa de Sá Lima , Jacqueline Alves Leite , Diana Zukas Andreotti , Paula Fernanda Kinoshita , Arthur B. Cantanzaro , João Agostinho M. Neto , Cristoforo Scavone , Elisa M. Kawamoto","doi":"10.1016/j.crneur.2025.100147","DOIUrl":"10.1016/j.crneur.2025.100147","url":null,"abstract":"","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"8 ","pages":"Article 100147"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143631870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2024-11-23DOI: 10.1016/j.crneur.2024.100142
Silke Kreitz , Bruno Pradier , Daniel Segelcke , Saeedeh Amirmohseni , Andreas Hess , Cornelius Faber , Esther M. Pogatzki-Zahn
Although the pathophysiology of pain has been investigated tremendously, there are still many open questions with regard to specific pain entities and their pain-related symptoms. To increase the translational impact of (preclinical) animal neuroimaging pain studies, the use of disease-specific pain models, as well as relevant stimulus modalities, are critical. We developed a comprehensive framework for brain network analysis combining functional magnetic resonance imaging (MRI) with graph-theory (GT) and data classification by linear discriminant analysis. This enabled us to expand our knowledge of stimulus modalities processing under incisional (INC) and pathogen-induced inflammatory (CFA) pain entities compared to acute pain conditions. GT-analysis has uncovered specific features in pain modality processing that align well with those previously identified in humans. These include areas such as S1, M1, CPu, HC, piriform, and cingulate cortex. Additionally, we have identified unique Network Signatures of Pain Hypersensitivity (NSPH) for INC and CFA. This leads to a diminished ability to differentiate between stimulus modalities in both pain models compared to control conditions, while also enhancing aversion processing and descending pain modulation. Our findings further show that different pain entities modulate sensory input through distinct NSPHs. These neuroimaging signatures are an important step toward identifying novel cerebral pain biomarkers for certain diseases and relevant outcomes to evaluate target engagement of novel therapeutic and diagnostic options, which ultimately can be translated to the clinic.
{"title":"Distinct functional cerebral hypersensitivity networks during incisional and inflammatory pain in rats","authors":"Silke Kreitz , Bruno Pradier , Daniel Segelcke , Saeedeh Amirmohseni , Andreas Hess , Cornelius Faber , Esther M. Pogatzki-Zahn","doi":"10.1016/j.crneur.2024.100142","DOIUrl":"10.1016/j.crneur.2024.100142","url":null,"abstract":"<div><div>Although the pathophysiology of pain has been investigated tremendously, there are still many open questions with regard to specific pain entities and their pain-related symptoms. To increase the translational impact of (preclinical) animal neuroimaging pain studies, the use of disease-specific pain models, as well as relevant stimulus modalities, are critical. We developed a comprehensive framework for brain network analysis combining functional magnetic resonance imaging (MRI) with graph-theory (GT) and data classification by linear discriminant analysis. This enabled us to expand our knowledge of stimulus modalities processing under incisional (INC) and pathogen-induced inflammatory (CFA) pain entities compared to acute pain conditions. GT-analysis has uncovered specific features in pain modality processing that align well with those previously identified in humans. These include areas such as S1, M1, CPu, HC, piriform, and cingulate cortex. Additionally, we have identified unique Network Signatures of Pain Hypersensitivity (NSPH) for INC and CFA. This leads to a diminished ability to differentiate between stimulus modalities in both pain models compared to control conditions, while also enhancing aversion processing and descending pain modulation. Our findings further show that different pain entities modulate sensory input through distinct NSPHs. These neuroimaging signatures are an important step toward identifying novel cerebral pain biomarkers for certain diseases and relevant outcomes to evaluate target engagement of novel therapeutic and diagnostic options, which ultimately can be translated to the clinic.</div></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"8 ","pages":"Article 100142"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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