Progress in Neurobiology最新文献_第3页

Population coding for figure-ground texture segregation in macaque V1 and V4 猕猴 V1 和 V4 中图形-地面纹理分离的群体编码。

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-07-04 DOI: 10.1016/j.pneurobio.2024.102655

Xing-Nan Zhao , Xing-Si Dong , Dan-Qing Jiang , Si Wu , Shi-Ming Tang , Cong Yu

{"title":"Population coding for figure-ground texture segregation in macaque V1 and V4","authors":"Xing-Nan Zhao , Xing-Si Dong , Dan-Qing Jiang , Si Wu , Shi-Ming Tang , Cong Yu","doi":"10.1016/j.pneurobio.2024.102655","DOIUrl":"10.1016/j.pneurobio.2024.102655","url":null,"abstract":"<div><p>Object recognition often involves the brain segregating objects from their surroundings. Neurophysiological studies of figure-ground texture segregation have yielded inconsistent results, particularly on whether V1 neurons can perform figure-ground texture segregation or just detect texture borders. To address this issue from a population perspective, we utilized two-photon calcium imaging to simultaneously record the responses of large samples of V1 and V4 neurons to figure-ground texture stimuli in awake, fixating macaques. The average response changes indicate that V1 neurons mainly detect texture borders, while V4 neurons are involved in figure-ground segregation. However, population analysis (SVM decoding of PCA-transformed neuronal responses) reveal that V1 neurons not only detect figure-ground borders, but also contribute to figure-ground texture segregation, although requiring substantially more principal components than V4 neurons to reach a 75 % decoding accuracy. Individually, V1/V4 neurons showing larger (negative/positive) figure-ground response differences contribute more to figure-ground segregation. But for V1 neurons, the contribution becomes significant only when many principal components are considered. We conclude that V1 neurons participate in figure-ground segregation primarily by defining the figure borders, and the poorly structured figure-ground information V1 neurons carry could be further utilized by V4 neurons to accomplish figure-ground segregation.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"240 ","pages":"Article 102655"},"PeriodicalIF":6.7,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141538570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The homogenous hippocampus: How hippocampal cells process available and potential goals 同质海马：海马细胞如何处理可用目标和潜在目标。

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-07-02 DOI: 10.1016/j.pneurobio.2024.102653

Neil McNaughton , David Bannerman

引用次数: 0

Adolescent cannabinoid exposure rescues phencyclidine-induced social deficits through modulation of CA2 transmission 青春期大麻素暴露可通过调节 CA2 传输来挽救苯环利定诱发的社交障碍。

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-06-30 DOI: 10.1016/j.pneurobio.2024.102652

Marta Barrera-Conde , Carla Ramon-Duaso , Jose Antonio González-Parra , Emma Veza-Estevez , Vivien Chevaleyre , Rebecca A. Piskorowski , Rafael de la Torre , Arnau Busquets-García , Patricia Robledo

{"title":"Adolescent cannabinoid exposure rescues phencyclidine-induced social deficits through modulation of CA2 transmission","authors":"Marta Barrera-Conde , Carla Ramon-Duaso , Jose Antonio González-Parra , Emma Veza-Estevez , Vivien Chevaleyre , Rebecca A. Piskorowski , Rafael de la Torre , Arnau Busquets-García , Patricia Robledo","doi":"10.1016/j.pneurobio.2024.102652","DOIUrl":"10.1016/j.pneurobio.2024.102652","url":null,"abstract":"<div><p>Psychotic disorders entail intricate conditions marked by disruptions in cognition, perception, emotions, and social behavior. Notably, psychotic patients who use cannabis tend to show less severe deficits in social behaviors, such as the misinterpretation of social cues and the inability to interact with others. However, the biological underpinnings of this epidemiological interaction remain unclear. Here, we used the NMDA receptor blocker phencyclidine (PCP) to induce psychotic-like states and to study the impact of adolescent cannabinoid exposure on social behavior deficits and synaptic transmission changes in hippocampal area CA2, a region known to be active during social interactions. In particular, adolescent mice underwent 7 days of subchronic treatment with the synthetic cannabinoid, WIN 55, 212–2 (WIN) followed by one injection of PCP. Using behavioral, biochemical, and electrophysiological approaches, we showed that PCP persistently reduced sociability, decreased GAD67 expression in the hippocampus, and induced GABAergic deficits in proximal inputs from CA3 and distal inputs from the entorhinal cortex (EC) to CA2. Notably, WIN exposure during adolescence specifically restores adult sociability deficits, the expression changes in GAD67, and the GABAergic impairments in the EC-CA2 circuit, but not in the CA3-CA2 circuit. Using a chemogenetic approach to target EC-CA2 projections, we demonstrated the involvement of this specific circuit on sociability deficits. Indeed, enhancing EC-CA2 transmission was sufficient to induce sociability deficits in vehicle-treated mice, but not in animals treated with WIN during adolescence, suggesting a mechanism by which adolescent cannabinoid exposure rescues sociability deficits caused by enhanced EC-CA2 activity in adult mice.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"240 ","pages":"Article 102652"},"PeriodicalIF":6.7,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141493202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Astrocyte-secreted C3 signaling impairs neuronal development and cognition in autoimmune diseases 星形胶质细胞分泌的C3信号损害自身免疫性疾病的神经元发育和认知能力

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-06-28 DOI: 10.1016/j.pneurobio.2024.102654

Fan Zhu , Pengyan He , Wei Jiang , Shabbir Khan Afridi , Huiming Xu , Maali Alahmad , Yu-Wen Alvin Huang , Wei Qiu , Guangyou Wang , Changyong Tang

{"title":"Astrocyte-secreted C3 signaling impairs neuronal development and cognition in autoimmune diseases","authors":"Fan Zhu , Pengyan He , Wei Jiang , Shabbir Khan Afridi , Huiming Xu , Maali Alahmad , Yu-Wen Alvin Huang , Wei Qiu , Guangyou Wang , Changyong Tang","doi":"10.1016/j.pneurobio.2024.102654","DOIUrl":"10.1016/j.pneurobio.2024.102654","url":null,"abstract":"<div><p>Neuromyelitis optica (NMO) arises from primary astrocytopathy induced by autoantibodies targeting the astroglial protein aquaporin 4 (AQP4), leading to severe neurological sequelae such as vision loss, motor deficits, and cognitive decline. Mounting evidence has shown that dysregulated activation of complement components contributes to NMO pathogenesis. Complement C3 deficiency has been shown to protect against hippocampal neurodegeneration and cognitive decline in neurodegenerative disorders (e.g., Alzheimer's disease, AD) and autoimmune diseases (e.g., multiple sclerosis, MS). However, whether inhibiting the C3 signaling can ameliorate cognitive dysfunctions in NMO remains unclear. In this study, we found that the levels of C3a, a split product of C3, significantly correlate with cognitive impairment in our patient cohort. In response to the stimulation of AQP4 autoantibodies, astrocytes were activated to secrete complement C3, which inhibited the development of cultured neuronal dendritic arborization. NMO mouse models exhibited reduced adult hippocampal newborn neuronal dendritic and spine development, as well as impaired learning and memory functions, which could be rescued by decreasing C3 levels in astrocytes. Mechanistically, we found that C3a engaged with C3aR to impair neuronal development by dampening β-catenin signalling. Additionally, inhibition of the C3-C3aR-GSK3β/β-catenin cascade restored neuronal development and ameliorated cognitive impairments. Collectively, our results suggest a pivotal role of the activation of the C3-C3aR network in neuronal development and cognition through mediating astrocyte and adult-born neuron communication, which represents a potential therapeutic target for autoimmune-related cognitive impairment diseases.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"240 ","pages":"Article 102654"},"PeriodicalIF":6.7,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141470452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-06-13 DOI: 10.1016/j.pneurobio.2024.102637

Ying Huang , Michael Brosch

引用次数: 0

TRPV1 channel in the pathophysiology of epilepsy and its potential as a molecular target for the development of new antiseizure drug candidates 癫痫病理生理学中的 TRPV1 通道及其作为候选抗癫痫新药开发分子靶点的潜力

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-06-02 DOI: 10.1016/j.pneurobio.2024.102634

Katarzyna Socała , Marcin Jakubiec , Michał Abram , Jakub Mlost , Katarzyna Starowicz , Rafał M. Kamiński , Katarzyna Ciepiela , Marta Andres-Mach , Mirosław Zagaja , Cameron S. Metcalf , Przemysław Zawadzki , Piotr Wlaź , Krzysztof Kamiński

{"title":"TRPV1 channel in the pathophysiology of epilepsy and its potential as a molecular target for the development of new antiseizure drug candidates","authors":"Katarzyna Socała , Marcin Jakubiec , Michał Abram , Jakub Mlost , Katarzyna Starowicz , Rafał M. Kamiński , Katarzyna Ciepiela , Marta Andres-Mach , Mirosław Zagaja , Cameron S. Metcalf , Przemysław Zawadzki , Piotr Wlaź , Krzysztof Kamiński","doi":"10.1016/j.pneurobio.2024.102634","DOIUrl":"10.1016/j.pneurobio.2024.102634","url":null,"abstract":"<div><p>Identification of transient receptor potential cation channel, subfamily V member 1 (TRPV1), also known as capsaicin receptor, in 1997 was a milestone achievement in the research on temperature sensation and pain signalling. Very soon after it became evident that TRPV1 is implicated in a wide array of physiological processes in different peripheral tissues, as well as in the central nervous system, and thereby could be involved in the pathophysiology of numerous diseases. Increasing evidence suggests that modulation of TRPV1 may also affect seizure susceptibility and epilepsy. This channel is localized in brain regions associated with seizures and epilepsy, and its overexpression was found both in animal models of seizures and in brain samples from epileptic patients. Moreover, modulation of TRPV1 on non-neuronal cells (microglia, astrocytes, and/or peripheral immune cells) may have an impact on the neuroinflammatory processes that play a role in epilepsy and epileptogenesis. In this paper, we provide a comprehensive and critical overview of currently available data on TRPV1 as a possible molecular target for epilepsy management, trying to identify research gaps and future directions. Overall, several converging lines of evidence implicate TRPV1 channel as a potentially attractive target in epilepsy research but more studies are needed to exploit the possible role of TRPV1 in seizures/epilepsy and to evaluate the value of TRPV1 ligands as candidates for new antiseizure drugs.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"240 ","pages":"Article 102634"},"PeriodicalIF":6.7,"publicationDate":"2024-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141228952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Experience-dependent regulation of dopaminergic signaling in the somatosensory cortex 体感皮层多巴胺能信号传导的经验依赖性调节

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-06-02 DOI: 10.1016/j.pneurobio.2024.102630

Tousif Jamal , Xuan Yan , Angelica da Silva Lantyer , Judith G. ter Horst , Tansu Celikel

{"title":"Experience-dependent regulation of dopaminergic signaling in the somatosensory cortex","authors":"Tousif Jamal , Xuan Yan , Angelica da Silva Lantyer , Judith G. ter Horst , Tansu Celikel","doi":"10.1016/j.pneurobio.2024.102630","DOIUrl":"10.1016/j.pneurobio.2024.102630","url":null,"abstract":"<div><p>Dopamine critically influences reward processing, sensory perception, and motor control. Yet, the modulation of dopaminergic signaling by sensory experiences is not fully delineated. Here, by manipulating sensory experience using bilateral single-row whisker deprivation, we demonstrated that gene transcription in the dopaminergic signaling pathway (<em>DSP</em>) undergoes experience-dependent plasticity in both granular and supragranular layers of the primary somatosensory (barrel) cortex (<em>S</em>1). Sensory experience and deprivation compete for the regulation of <em>DSP</em> transcription across neighboring cortical columns, and sensory deprivation-induced changes in <em>DSP</em> are topographically constrained. These changes in <em>DSP</em> extend beyond cortical map plasticity and influence neuronal information processing. Pharmacological regulation of D2 receptors, a key component of <em>DSP</em>, revealed that D2 receptor activation suppresses excitatory neuronal excitability, hyperpolarizes the action potential threshold, and reduces the instantaneous firing rate. These findings suggest that the dopaminergic drive originating from midbrain dopaminergic neurons, targeting the sensory cortex, is subject to experience-dependent regulation and might create a regulatory feedback loop for modulating sensory processing. Finally, using topological gene network analysis and mutual information, we identify the molecular hubs of experience-dependent plasticity of <em>DSP</em>. These findings provide new insights into the mechanisms by which sensory experience shapes dopaminergic signaling in the brain and might help unravel the sensory deficits observed after dopamine depletion.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"239 ","pages":"Article 102630"},"PeriodicalIF":6.7,"publicationDate":"2024-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141228839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A theory of hippocampal function: New developments 海马功能理论：新进展

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-06-02 DOI: 10.1016/j.pneurobio.2024.102636

Edmund T. Rolls , Alessandro Treves

{"title":"A theory of hippocampal function: New developments","authors":"Edmund T. Rolls , Alessandro Treves","doi":"10.1016/j.pneurobio.2024.102636","DOIUrl":"10.1016/j.pneurobio.2024.102636","url":null,"abstract":"<div><p>We develop further here the only quantitative theory of the storage of information in the hippocampal episodic memory system and its recall back to the neocortex. The theory is upgraded to account for a revolution in understanding of spatial representations in the primate, including human, hippocampus, that go beyond the place where the individual is located, to the location being viewed in a scene. This is fundamental to much primate episodic memory and navigation: functions supported in humans by pathways that build ‘where’ spatial view representations by feature combinations in a ventromedial visual cortical stream, separate from those for ‘what’ object and face information to the inferior temporal visual cortex, and for reward information from the orbitofrontal cortex. Key new computational developments include the capacity of the CA3 attractor network for storing whole charts of space; how the correlations inherent in self-organizing continuous spatial representations impact the storage capacity; how the CA3 network can combine continuous spatial and discrete object and reward representations; the roles of the rewards that reach the hippocampus in the later consolidation into long-term memory in part via cholinergic pathways from the orbitofrontal cortex; and new ways of analysing neocortical information storage using Potts networks.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"238 ","pages":"Article 102636"},"PeriodicalIF":6.7,"publicationDate":"2024-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0301008224000728/pdfft?md5=e792602997e8ebff53c4e95af5dbc3e9&pid=1-s2.0-S0301008224000728-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141228908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Multimodal mapping of macaque monkey somatosensory cortex 猕猴躯体感觉皮层的多模式绘图

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-06-01 DOI: 10.1016/j.pneurobio.2024.102633

Meiqi Niu , Lucija Rapan , Seán Froudist-Walsh , Ling Zhao , Thomas Funck , Katrin Amunts , Nicola Palomero-Gallagher

{"title":"Multimodal mapping of macaque monkey somatosensory cortex","authors":"Meiqi Niu , Lucija Rapan , Seán Froudist-Walsh , Ling Zhao , Thomas Funck , Katrin Amunts , Nicola Palomero-Gallagher","doi":"10.1016/j.pneurobio.2024.102633","DOIUrl":"10.1016/j.pneurobio.2024.102633","url":null,"abstract":"<div><p>The somatosensory cortex is a brain region responsible for receiving and processing sensory information from across the body and is structurally and functionally heterogeneous. Since the chemoarchitectonic segregation of the cerebral cortex can be revealed by transmitter receptor distribution patterns, by using a quantitative multireceptor architectonical analysis, we determined the number and extent of distinct areas of the macaque somatosensory cortex. We identified three architectonically distinct cortical entities within the primary somatosensory cortex (i.e., 3bm, 3bli, 3ble), four within the anterior parietal cortex (i.e., 3am, 3al, 1 and 2) and six subdivisions (i.e., S2l, S2m, PVl, PVm, PRl and PRm) within the lateral fissure. We provide an ultra-high resolution 3D atlas of macaque somatosensory areas in stereotaxic space, which integrates cyto- and receptor architectonic features of identified areas. Multivariate analyses of the receptor fingerprints revealed four clusters of identified areas based on the degree of (dis)similarity of their receptor architecture. Each of these clusters can be associated with distinct levels of somatosensory processing, further demonstrating that the functional segregation of cortical areas is underpinned by differences in their molecular organization.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"239 ","pages":"Article 102633"},"PeriodicalIF":6.7,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0301008224000698/pdfft?md5=520ea428ca44bd90fb9aa8023a2674e4&pid=1-s2.0-S0301008224000698-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141233268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Calcium plays an essential role in early-stage dendrite injury detection and regeneration 钙在早期树突损伤检测和再生中发挥着至关重要的作用。

IF 6.7 2区医学

Progress in Neurobiology Pub Date : 2024-05-31 DOI: 10.1016/j.pneurobio.2024.102635

Vinicius N. Duarte , Vicky T. Lam , Dario S. Rimicci , Katherine L. Thompson-Peer

{"title":"Calcium plays an essential role in early-stage dendrite injury detection and regeneration","authors":"Vinicius N. Duarte , Vicky T. Lam , Dario S. Rimicci , Katherine L. Thompson-Peer","doi":"10.1016/j.pneurobio.2024.102635","DOIUrl":"10.1016/j.pneurobio.2024.102635","url":null,"abstract":"<div><p>Dendrites are injured in a variety of clinical conditions such as traumatic brain and spinal cord injuries and stroke. How neurons detect injury directly to their dendrites to initiate a pro-regenerative response has not yet been thoroughly investigated. Calcium plays a critical role in the early stages of axonal injury detection and is also indispensable for regeneration of the severed axon. Here, we report cell and neurite type-specific differences in laser injury-induced elevations of intracellular calcium levels. Using a human KCNJ2 transgene, we demonstrate that hyperpolarizing neurons only at the time of injury dampens dendrite regeneration, suggesting that inhibition of injury-induced membrane depolarization (and thus early calcium influx) plays a role in detecting and responding to dendrite injury. In exploring potential downstream calcium-regulated effectors, we identify L-type voltage-gated calcium channels, inositol triphosphate signaling, and protein kinase D activity as drivers of dendrite regeneration. In conclusion, we demonstrate that dendrite injury-induced calcium elevations play a key role in the regenerative response of dendrites and begin to delineate the molecular mechanisms governing dendrite repair.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"239 ","pages":"Article 102635"},"PeriodicalIF":6.7,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0301008224000716/pdfft?md5=a0adc6d1c7949f6dab645403af92ebc7&pid=1-s2.0-S0301008224000716-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0