Progress in Neurobiology最新文献

{"title":"A molecularly defined orbitofrontal cortical neuron population controls compulsive-like behavior, but not inflexible choice or habit","authors":"Sophie T. Yount ,&nbsp;Silu Wang ,&nbsp;Aylet T. Allen ,&nbsp;Lauren P. Shapiro ,&nbsp;Laura M. Butkovich ,&nbsp;Shannon L. Gourley","doi":"10.1016/j.pneurobio.2024.102632","DOIUrl":"10.1016/j.pneurobio.2024.102632","url":null,"abstract":"<div><p>Habits are familiar behaviors triggered by cues, not outcome predictability, and are insensitive to changes in the environment. They are adaptive under many circumstances but can be considered antecedent to compulsions and intrusive thoughts that drive persistent, potentially maladaptive behavior. Whether compulsive-like and habit-like behaviors share neural substrates is still being determined. Here, we investigated mice bred to display inflexible reward-seeking behaviors that are insensitive to action consequences. We found that these mice demonstrate habitual response biases and compulsive-like grooming behavior that was reversible by fluoxetine and ketamine. They also suffer dendritic spine attrition on excitatory neurons in the orbitofrontal cortex (OFC). Nevertheless, synaptic melanocortin 4 receptor (MC4R), a factor implicated in compulsive behavior, is preserved, leading to the hypothesis that <em>Mc4r</em>+ OFC neurons may drive aberrant behaviors. Repeated chemogenetic stimulation of <em>Mc4r+</em> OFC neurons triggered compulsive and not inflexible or habitual response biases in otherwise typical mice. Thus, <em>Mc4r</em>+ neurons within the OFC appear to drive compulsive-like behavior that is dissociable from habitual behavior. Understanding which neuron populations trigger distinct behaviors may advance efforts to mitigate harmful compulsions.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"238 ","pages":"Article 102632"},"PeriodicalIF":6.7,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141184538","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}

{"title":"Control of goal-directed and inflexible actions by dorsal striatal melanocortin systems, in coordination with the central nucleus of the amygdala","authors":"Elizabeth C. Heaton ,&nbsp;Esther H. Seo ,&nbsp;Laura M. Butkovich ,&nbsp;Sophie T. Yount ,&nbsp;Shannon L. Gourley","doi":"10.1016/j.pneurobio.2024.102629","DOIUrl":"10.1016/j.pneurobio.2024.102629","url":null,"abstract":"<div><p>The dorsomedial striatum (DMS) is associated with flexible goal seeking, as opposed to routinized habits. Whether local mechanisms brake this function, for instance when habits may be adaptive, is incompletely understood. We find that a sub-population of dopamine D1 receptor-containing striatal neurons express the melanocortin-4 receptor (MC4R) for α-melanocyte stimulating hormone. These neurons within the DMS are necessary and sufficient for controlling the capacity of mice to flexibly adjust actions based on the likelihood that they will be rewarded. In investigating MC4R function, we found that it suppresses immediate-early gene levels in the DMS and concurrently, flexible goal seeking. MC4R+ neurons receive input from the central nucleus of the amygdala, and behavioral experiments indicate that they are functionally integrated into an amygdalo-striatal circuit that suppresses action flexibility in favor of routine. Publicly available spatial transcriptomics datasets were analyzed for gene transcript correlates of <em>Mc4r</em> expression across the striatal subregions, revealing considerable co-variation in dorsal structures. This insight led to the discovery that the function of MC4R in the dorsolateral striatum complements that in the DMS, in this case suppressing habit-like behavior. Altogether, our findings suggest that striatal MC4R controls the capacity for goal-directed and inflexible actions alike.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"238 ","pages":"Article 102629"},"PeriodicalIF":6.7,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141028527","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}

{"title":"Loss of glycine receptors in the nucleus accumbens and ethanol reward in an Alzheimer´s Disease mouse model","authors":"Lorena Armijo-Weingart ,&nbsp;Loreto San Martin ,&nbsp;Scarlet Gallegos ,&nbsp;Anibal Araya ,&nbsp;Macarena Konar-Nie ,&nbsp;Eduardo Fernandez-Pérez ,&nbsp;Luis G. Aguayo","doi":"10.1016/j.pneurobio.2024.102616","DOIUrl":"10.1016/j.pneurobio.2024.102616","url":null,"abstract":"<div><p>Alterations in cognitive and non-cognitive cerebral functions characterize Alzheimer's disease (AD). Cortical and hippocampal impairments related to extracellular accumulation of Aβ in AD animal models have been extensively investigated. However, recent reports have also implicated intracellular Aβ in limbic regions, such as the nucleus accumbens (nAc). Accumbal neurons express high levels of inhibitory glycine receptors (GlyRs) that are allosterically modulated by ethanol and have a role in controlling its intake. In the present study, we investigated how GlyRs in the 2xTg mice (AD model) affect nAc functions and ethanol intake behavior. Using transgenic and control aged-matched litter mates, we found that the GlyRα2 subunit was significantly decreased in AD mice (6-month-old). We also examined intracellular calcium dynamics using the fluorescent calcium protein reporter GCaMP in slice photometry. We also found that the calcium signal mediated by GlyRs, but not GABA_AR, was also reduced in AD neurons. Additionally, ethanol potentiation was significantly decreased in accumbal neurons in the AD mice. Finally, we performed drinking in the dark (DID) experiments and found that 2xTg mice consumed less ethanol on the last day of DID, in agreement with a lower blood ethanol concentration. 2xTg mice also showed lower sucrose consumption, indicating that overall food reward was altered. In conclusion, the data support the role of GlyRs in nAc neuron excitability and a decreased glycinergic activity in the 2xTg mice that might lead to impairment in reward processing at an early stage of the disease.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"237 ","pages":"Article 102616"},"PeriodicalIF":6.7,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899409","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}

{"title":"Persistent ∆FosB expression limits recurrent seizure activity and provides neuroprotection in the dentate gyrus of APP mice","authors":"Gabriel S. Stephens ,&nbsp;Jin Park ,&nbsp;Andrew Eagle ,&nbsp;Jason You ,&nbsp;Manuel Silva-Pérez ,&nbsp;Chia-Hsuan Fu ,&nbsp;Sumin Choi ,&nbsp;Corey P. St. Romain ,&nbsp;Chiho Sugimoto ,&nbsp;Shelly A. Buffington ,&nbsp;Yi Zheng ,&nbsp;Mauro Costa-Mattioli ,&nbsp;Yin Liu ,&nbsp;A.J. Robison ,&nbsp;Jeannie Chin","doi":"10.1016/j.pneurobio.2024.102612","DOIUrl":"10.1016/j.pneurobio.2024.102612","url":null,"abstract":"<div><p>Recurrent seizures lead to accumulation of the activity-dependent transcription factor ∆FosB in hippocampal dentate granule cells in both mouse models of epilepsy and mouse models of Alzheimer’s disease (AD), which is also associated with increased incidence of seizures. In patients with AD and related mouse models, the degree of ∆FosB accumulation corresponds with increasing severity of cognitive deficits. We previously found that ∆FosB impairs spatial memory in mice by epigenetically regulating expression of target genes such as calbindin that are involved in synaptic plasticity. However, the suppression of calbindin in conditions of neuronal hyperexcitability has been demonstrated to provide neuroprotection to dentate granule cells, indicating that ∆FosB may act over long timescales to coordinate neuroprotective pathways. To test this hypothesis, we used viral-mediated expression of ∆JunD to interfere with ∆FosB signaling over the course of several months in transgenic mice expressing mutant human amyloid precursor protein (APP), which exhibit spontaneous seizures and develop AD-related neuropathology and cognitive deficits. Our results demonstrate that persistent ∆FosB activity acts through discrete modes of hippocampal target gene regulation to modulate neuronal excitability, limit recurrent seizure activity, and provide neuroprotection to hippocampal dentate granule cells in APP mice.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"237 ","pages":"Article 102612"},"PeriodicalIF":6.7,"publicationDate":"2024-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140794335","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}

{"title":"Decoding the influence of central LEAP2 on food intake and its effect on accumbal dopamine release","authors":"Maximilian Tufvesson-Alm,&nbsp;Qian Zhang,&nbsp;Cajsa Aranäs,&nbsp;Sebastian Blid Sköldheden,&nbsp;Christian E. Edvardsson,&nbsp;Elisabet Jerlhag","doi":"10.1016/j.pneurobio.2024.102615","DOIUrl":"https://doi.org/10.1016/j.pneurobio.2024.102615","url":null,"abstract":"<div><p>The gut-brain peptide ghrelin and its receptor are established as a regulator of hunger and reward-processing. However, the recently recognized ghrelin receptor inverse agonist, liver-expressed antimicrobial peptide 2 (LEAP2), is less characterized. The present study aimed to elucidate LEAP2s central effect on reward-related behaviors through feeding and its mechanism. LEAP2 was administrated centrally in mice and effectively reduced feeding and intake of palatable foods. Strikingly, LEAP2s effect on feeding was correlated to the preference of the palatable food. Further, LEAP2 reduced the rewarding memory of high preference foods, and attenuated the accumbal dopamine release associated with palatable food exposure and eating. Interestingly, LEAP2 was widely expressed in the brain, and particularly in reward-related brain areas such as the laterodorsal tegmental area (LDTg). This expression was markedly altered when allowed free access to palatable foods. Accordingly, infusion of LEAP2 into LDTg was sufficient to transiently reduce acute palatable food intake. Taken together, the present results show that central LEAP2 has a profound effect on dopaminergic reward signaling associated with food and affects several aspects of feeding. The present study highlights LEAP2s effect on reward, which may have applications for obesity and other reward-related psychiatric and neurological disorders.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"236 ","pages":"Article 102615"},"PeriodicalIF":6.7,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0301008224000510/pdfft?md5=04123e9ab2abf3d1946dbb598f752cb2&pid=1-s2.0-S0301008224000510-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638311","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}

{"title":"C3aR in the medial prefrontal cortex modulates the susceptibility to LPS-induced depressive-like behaviors through glutamatergic neuronal excitability","authors":"Rui Sun ,&nbsp;Meng-Yu Tang ,&nbsp;Dan Yang ,&nbsp;Yan-Yi Zhang ,&nbsp;Yi-Heng Xu ,&nbsp;Yong Qiao ,&nbsp;Bin Yu ,&nbsp;Shu-Xia Cao ,&nbsp;Hao Wang ,&nbsp;Hui-Qian Huang ,&nbsp;Hong Zhang ,&nbsp;Xiao-Ming Li ,&nbsp;Hong Lian","doi":"10.1016/j.pneurobio.2024.102614","DOIUrl":"https://doi.org/10.1016/j.pneurobio.2024.102614","url":null,"abstract":"<div><p>Complement activation and prefrontal cortical dysfunction both contribute to the pathogenesis of major depressive disorder (MDD), but their interplay in MDD is unclear. We here studied the role of complement C3a receptor (C3aR) in the medial prefrontal cortex (mPFC) and its influence on depressive-like behaviors induced by systematic lipopolysaccharides (LPS) administration. C3aR knockout (KO) or intra-mPFC C3aR antagonism confers resilience, whereas C3aR expression in mPFC neurons makes KO mice susceptible to LPS-induced depressive-like behaviors. Importantly, the excitation and inhibition of mPFC neurons have opposing effects on depressive-like behaviors, aligning with increased and decreased excitability by C3aR deletion and activation in cortical neurons. In particular, inhibiting mPFC glutamatergic (mPFC^Glu) neurons, the main neuronal subpopulation expresses C3aR, induces depressive-like behaviors in saline-treated WT and KO mice, but not in LPS-treated KO mice. Compared to hypoexcitable mPFC^Glu neurons in LPS-treated WT mice, C3aR-null mPFC^Glu neurons display hyperexcitability upon LPS treatment, and enhanced excitation of mPFC^Glu neurons is anti-depressant, suggesting a protective role of C3aR deficiency in these circumstances. In conclusion, C3aR modulates susceptibility to LPS-induced depressive-like behaviors through mPFC^Glu neuronal excitability. This study identifies C3aR as a pivotal intersection of complement activation, mPFC dysfunction, and depression and a promising therapeutic target for MDD.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"236 ","pages":"Article 102614"},"PeriodicalIF":6.7,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140645196","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}

{"title":"Prefrontal-subthalamic theta signaling mediates delayed responses during conflict processing","authors":"Jeong Woo Choi ,&nbsp;Mahsa Malekmohammadi ,&nbsp;Soroush Niketeghad ,&nbsp;Katy A. Cross ,&nbsp;Hamasa Ebadi ,&nbsp;Amirreza Alijanpourotaghsara ,&nbsp;Adam Aron ,&nbsp;Ueli Rutishauser ,&nbsp;Nader Pouratian","doi":"10.1016/j.pneurobio.2024.102613","DOIUrl":"https://doi.org/10.1016/j.pneurobio.2024.102613","url":null,"abstract":"<div><p>While medial frontal cortex (MFC) and subthalamic nucleus (STN) have been implicated in conflict monitoring and action inhibition, respectively, an integrated understanding of the spatiotemporal and spectral interaction of these nodes and how they interact with motor cortex (M1) to definitively modify motor behavior during conflict is lacking. We recorded neural signals intracranially across presupplementary motor area (preSMA), M1, STN, and globus pallidus internus (GPi), during a flanker task in 20 patients undergoing deep brain stimulation implantation surgery for Parkinson disease or dystonia. Conflict is associated with sequential and causal increases in local theta power from preSMA to STN to M1 with movement delays directly correlated with increased STN theta power, indicating preSMA is the MFC locus that monitors conflict and signals STN to implement a ‘break.’ Transmission of theta from STN-to-M1 subsequently results in a transient increase in M1-to-GPi beta flow immediately prior to movement, modulating the motor network to actuate the conflict-related action inhibition (i.e., delayed response). Action regulation during conflict relies on two distinct circuits, the conflict-related theta and movement-related beta networks, that are separated spatially, spectrally, and temporally, but which interact dynamically to mediate motor performance, highlighting complex parallel yet interacting networks regulating movement.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"236 ","pages":"Article 102613"},"PeriodicalIF":6.7,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140619210","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}

{"title":"Atypical connectome topography and signal flow in temporal lobe epilepsy","authors":"Ke Xie ,&nbsp;Jessica Royer ,&nbsp;Sara Larivière ,&nbsp;Raul Rodriguez-Cruces ,&nbsp;Stefan Frässle ,&nbsp;Donna Gift Cabalo ,&nbsp;Alexander Ngo ,&nbsp;Jordan DeKraker ,&nbsp;Hans Auer ,&nbsp;Shahin Tavakol ,&nbsp;Yifei Weng ,&nbsp;Chifaou Abdallah ,&nbsp;Thaera Arafat ,&nbsp;Linda Horwood ,&nbsp;Birgit Frauscher ,&nbsp;Lorenzo Caciagli ,&nbsp;Andrea Bernasconi ,&nbsp;Neda Bernasconi ,&nbsp;Zhiqiang Zhang ,&nbsp;Luis Concha ,&nbsp;Boris C. Bernhardt","doi":"10.1016/j.pneurobio.2024.102604","DOIUrl":"https://doi.org/10.1016/j.pneurobio.2024.102604","url":null,"abstract":"<div><p>Temporal lobe epilepsy (TLE) is the most common pharmaco-resistant epilepsy in adults. While primarily associated with mesiotemporal pathology, recent evidence suggests that brain alterations in TLE extend beyond the paralimbic epicenter and impact macroscale function and cognitive functions, particularly memory. Using connectome-wide manifold learning and generative models of effective connectivity, we examined functional topography and directional signal flow patterns between large-scale neural circuits in TLE at rest. Studying a multisite cohort of 95 patients with TLE and 95 healthy controls, we observed atypical functional topographies in the former group, characterized by reduced differentiation between sensory and transmodal association cortices, with most marked effects in bilateral temporo-limbic and ventromedial prefrontal cortices. These findings were consistent across all study sites, present in left and right lateralized patients, and validated in a subgroup of patients with histopathological validation of mesiotemporal sclerosis and post-surgical seizure freedom. Moreover, they were replicated in an independent cohort of 30 TLE patients and 40 healthy controls. Further analyses demonstrated that reduced differentiation related to decreased functional signal flow into and out of temporolimbic cortical systems and other brain networks. Parallel analyses of structural and diffusion-weighted MRI data revealed that topographic alterations were independent of TLE-related cortical thinning but partially mediated by white matter microstructural changes that radiated away from paralimbic circuits. Finally, we found a strong association between the degree of functional alterations and behavioral markers of memory dysfunction. Our work illustrates the complex landscape of macroscale functional imbalances in TLE, which can serve as intermediate markers bridging microstructural changes and cognitive impairment.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"236 ","pages":"Article 102604"},"PeriodicalIF":6.7,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140622261","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}

{"title":"The STRAT-PARK cohort: A personalized initiative to stratify Parkinson’s disease","authors":"Kjersti Eline Stige ,&nbsp;Simon Ulvenes Kverneng ,&nbsp;Soumya Sharma ,&nbsp;Geir-Olve Skeie ,&nbsp;Erika Sheard ,&nbsp;Mona Søgnen ,&nbsp;Solveig Af Geijerstam ,&nbsp;Therese Vetås ,&nbsp;Anne Grete Wahlvåg ,&nbsp;Haakon Berven ,&nbsp;Sagar Buch ,&nbsp;David Reese ,&nbsp;Dina Babiker ,&nbsp;Yekta Mahdi ,&nbsp;Trevor Wade ,&nbsp;Gala Prado Miranda ,&nbsp;Jacky Ganguly ,&nbsp;Yokhesh Krishnasamy Tamilselvam ,&nbsp;Jia Ren Chai ,&nbsp;Saurabh Bansal ,&nbsp;Charalampos Tzoulis","doi":"10.1016/j.pneurobio.2024.102603","DOIUrl":"https://doi.org/10.1016/j.pneurobio.2024.102603","url":null,"abstract":"<div><p>The STRAT-PARK initiative aims to provide a platform for stratifying Parkinson’s disease (PD) into biological subtypes, using a bottom-up, multidisciplinary biomarker-based and data-driven approach. PD is a heterogeneous entity, exhibiting high interindividual clinicopathological variability. This diversity suggests that PD may encompass multiple distinct biological entities, each driven by different molecular mechanisms. Molecular stratification and identification of disease subtypes is therefore a key priority for understanding and treating PD. STRAT-PARK is a multi-center longitudinal cohort aiming to recruit a total of 2000 individuals with PD and neurologically healthy controls from Norway and Canada, for the purpose of identifying molecular disease subtypes. Clinical assessment is performed annually, whereas biosampling, imaging, and digital and neurophysiological phenotyping occur every second year. The unique feature of STRAT-PARK is the diversity of collected biological material, including muscle biopsies and platelets, tissues particularly useful for mitochondrial biomarker research. Recruitment rate is ∼150 participants per year. By March 2023, 252 participants were included, comprising 204 cases and 48 controls. STRAT-PARK is a powerful stratification initiative anticipated to become a global research resource, contributing to personalized care in PD.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"236 ","pages":"Article 102603"},"PeriodicalIF":6.7,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S030100822400039X/pdfft?md5=630f3f1dd52d384d33d0134b2a4afa3b&pid=1-s2.0-S030100822400039X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140638313","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}

{"title":"Mixed selectivity in monkey anterior intraparietal area during visual and motor processes","authors":"Monica Maranesi,&nbsp;Marco Lanzilotto,&nbsp;Edoardo Arcuri,&nbsp;Luca Bonini","doi":"10.1016/j.pneurobio.2024.102611","DOIUrl":"https://doi.org/10.1016/j.pneurobio.2024.102611","url":null,"abstract":"<div><p>Classical studies suggest that the anterior intraparietal area (AIP) contributes to the encoding of specific information such as objects and actions of self and others, through a variety of neuronal classes, such as canonical, motor and mirror neurons. However, these studies typically focused on a single variable, leaving it unclear whether distinct sets of AIP neurons encode a single or multiple sources of information and how multimodal coding emerges. Here, we chronically recorded monkey AIP neurons in a variety of tasks and conditions classically employed in separate experiments. Most cells exhibited mixed selectivity for observed objects, executed actions, and observed actions, enhanced when this information came from the monkey’s peripersonal working space. In contrast with the classical view, our findings indicate that multimodal coding emerges in AIP from partially-mixed selectivity of individual neurons for a variety of information relevant for planning actions directed to both physical objects and other subjects.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"236 ","pages":"Article 102611"},"PeriodicalIF":6.7,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0301008224000479/pdfft?md5=595c2691d9c5fbf031e55a7f08f39ced&pid=1-s2.0-S0301008224000479-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140650146","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}