Progress in Neurobiology最新文献

{"title":"Macaque monkeys and humans sample temporal regularities in the acoustic environment","authors":"Antonio Criscuolo ,&nbsp;Michael Schwartze ,&nbsp;Luis Prado ,&nbsp;Yaneri Ayala ,&nbsp;Hugo Merchant ,&nbsp;Sonja A. Kotz","doi":"10.1016/j.pneurobio.2023.102502","DOIUrl":"10.1016/j.pneurobio.2023.102502","url":null,"abstract":"<div><p>Many animal species show comparable abilities to detect basic rhythms and produce rhythmic behavior. Yet, the capacities to process complex rhythms and synchronize rhythmic behavior appear to be species-specific: vocal learning animals can, but some primates might not. This discrepancy is of high interest as there is a putative link between rhythm processing and the development of sophisticated sensorimotor behavior in humans. Do our closest ancestors show comparable endogenous dispositions to sample the acoustic environment in the absence of task instructions and training? We recorded EEG from macaque monkeys and humans while they passively listened to isochronous equitone sequences. Individual- and trial-level analyses showed that macaque monkeys’ and humans’ delta-band neural oscillations encoded and tracked the timing of auditory events. Further, mu- (8–15 Hz) and beta-band (12–20 Hz) oscillations revealed the superimposition of varied accentuation patterns on a subset of trials. These observations suggest convergence in the encoding and dynamic attending of temporal regularities in the acoustic environment, bridging a gap in the phylogenesis of rhythm cognition.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"229 ","pages":"Article 102502"},"PeriodicalIF":6.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10025226","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":"Ventrolateral prefrontal neurons of the monkey encode instructions in the ‘pragmatic’ format of the associated behavioral outcomes","authors":"Stefano Rozzi ,&nbsp;Alfonso Gravante ,&nbsp;Claudio Basile,&nbsp;Giorgio Cappellaro,&nbsp;Marzio Gerbella,&nbsp;Leonardo Fogassi","doi":"10.1016/j.pneurobio.2023.102499","DOIUrl":"10.1016/j.pneurobio.2023.102499","url":null,"abstract":"<div><p>The prefrontal cortex plays an important role in coding rules and producing context-appropriate behaviors. These processes necessarily require the generation of goals based on current context. Indeed, instructing stimuli are prospectively encoded in prefrontal cortex in relation to behavioral demands, but the coding format of this neural representation is, to date, largely unknown. In order to study how instructions and behaviors are encoded in prefrontal cortex, we recorded the activity of monkeys (<em>Macaca mulatta</em>) ventrolateral prefrontal neurons in a task requiring to perform (Action condition) or withhold (Inaction condition) grasping actions on real objects. Our data show that there are neurons responding in different task phases, and that the neuronal population discharge is stronger in the Inaction condition when the instructing cue is presented, and in the Action condition in the subsequent phases, from object presentation to action execution. Decoding analyses performed on neuronal populations showed that the neural activity recorded during the initial phases of the task shares the same type of format with that recorded during the final phases. We propose that this format has a pragmatic nature, that is instructions and goals are encoded by prefrontal neurons as predictions of the behavioral outcome.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"229 ","pages":"Article 102499"},"PeriodicalIF":6.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10399897","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":"A putative loop connection between VTA dopamine neurons and nucleus accumbens encodes positive valence to compensate for hunger","authors":"Xiao Cui ,&nbsp;Qiuping Tong ,&nbsp;Hao Xu,&nbsp;Chuantong Xie,&nbsp;Lei Xiao","doi":"10.1016/j.pneurobio.2023.102503","DOIUrl":"10.1016/j.pneurobio.2023.102503","url":null,"abstract":"<div><p><span>Dopamine (DA) signal play pivotal roles in regulating motivated behaviors, including feeding behavior, but the role of midbrain DA neurons in modulating food intake and neural circuitry mechanisms remain largely unknown. Here, we found that activating but not inhibiting </span>ventral tegmental area<span> (VTA) DA neurons reduces mouse food intake. Furthermore, DA neurons in ventral VTA, especially neurons projecting to the medial nucleus accumbens<span><span> (NAc), are activated by refeeding in the 24 h fasted mice. Combing neural circuitry tracing, optogenetic, chemogenetic, and pharmacological manipulations, we established that the VTA→medial NAc→VTA loop circuit is critical for the VTA DA neurons activation-induced food intake reduction. Moreover, activating either VTA DA neurons or </span>dopaminergic axons in medial NAc elevates positive valence, which will compensate for the hungry-induced food intake. Thus, our study identifies a subset of positive valence-encoded VTA DA neurons forming possible loop connections with medial NAc that are anorexigenic.</span></span></p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"229 ","pages":"Article 102503"},"PeriodicalIF":6.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10027344","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 role of N-methyl-D-aspartate glutamate receptors in Alzheimer’s disease: From pathophysiology to therapeutic approaches","authors":"Wenying Liu ,&nbsp;Yan Li ,&nbsp;Tan Zhao ,&nbsp;Min Gong ,&nbsp;Xuechu Wang ,&nbsp;Yue Zhang ,&nbsp;Lingzhi Xu ,&nbsp;Wenwen Li ,&nbsp;Yan Li ,&nbsp;Jianping Jia","doi":"10.1016/j.pneurobio.2023.102534","DOIUrl":"10.1016/j.pneurobio.2023.102534","url":null,"abstract":"<div><p>N-Methyl-<span>D</span><span>-aspartate glutamate receptors<span><span><span> (NMDARs) are involved in multiple physiopathological processes, including synaptic plasticity, neuronal network activities, excitotoxic events, and </span>cognitive impairment. Abnormalities in NMDARs can initiate a cascade of pathological events, notably in Alzheimer’s disease (AD) and even other neuropsychiatric disorders. The </span>subunit composition<span><span> of NMDARs is plastic, giving rise to a diverse array of receptor subtypes. While they are primarily found in neurons, NMDAR complexes, comprising both traditional and atypical subunits, are also present in non-neuronal cells, influencing the functions of various peripheral tissues. Furthermore, protein-protein interactions within NMDAR complexes has been linked with </span>Aβ accumulation, tau phosphorylation, neuroinflammation, and mitochondrial dysfunction, all of which potentially served as an obligatory relay of cognitive impairment. Nonetheless, the precise mechanistic link remains to be fully elucidated. In this review, we provided an in-depth analysis of the structure and function of NMDAR, investigated their interactions with various pathogenic proteins, discussed the current landscape of NMDAR-based therapeutics, and highlighted the remaining challenges during drug development.</span></span></span></p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"231 ","pages":"Article 102534"},"PeriodicalIF":6.7,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41128574","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":"Neuronal plasticity contributes to postictal death","authors":"Anastasia Brodovskaya ,&nbsp;Huayu Sun ,&nbsp;Nadia Adotevi ,&nbsp;Ian C. Wenker ,&nbsp;Keri E. Mitchell ,&nbsp;Rachel T. Clements ,&nbsp;Jaideep Kapur","doi":"10.1016/j.pneurobio.2023.102531","DOIUrl":"10.1016/j.pneurobio.2023.102531","url":null,"abstract":"<div><p><span><span><span>Repeated generalized tonic-clonic seizures (GTCSs) are the most critical risk factor for sudden unexpected death in epilepsy (SUDEP). GTCSs can cause fatal apnea. We investigated neuronal plasticity mechanisms that precipitate postictal apnea and seizure-induced death. Repeated seizures worsened </span>behavior, precipitated apnea, and enlarged active neuronal circuits, recruiting more neurons in such </span>brainstem<span><span> nuclei as periaqueductal gray (PAG) and dorsal raphe, indicative of brainstem plasticity. Seizure-activated neurons are more excitable and have enhanced AMPA-mediated excitatory transmission after a seizure. Global deletion of the GluA1 subunit of </span>AMPA receptors abolishes postictal apnea and seizure-induced death. Treatment with a drug that blocks Ca</span></span>²⁺<span>-permeable AMPA receptors also renders mice apnea-free with five-fold better survival than untreated mice. Repeated seizures traffic the GluA1 subunit-containing AMPA receptors to synapses, and blocking this mechanism decreases the probability of postictal apnea and seizure-induced death.</span></p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"231 ","pages":"Article 102531"},"PeriodicalIF":6.7,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41145879","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":"Photic sensitization is mediated by cortico-accumbens pathway in rats with trigeminal neuropathic pain","authors":"Jiahui Ma ,&nbsp;Xiaoling Huang ,&nbsp;Zhenxing Li ,&nbsp;Saiying Wang ,&nbsp;Xuebin Yan ,&nbsp;Dong Huang ,&nbsp;Haocheng Zhou","doi":"10.1016/j.pneurobio.2023.102533","DOIUrl":"10.1016/j.pneurobio.2023.102533","url":null,"abstract":"<div><p><span>Exposure to light stimuli may trigger or exacerbate perception of pain, also known as a common yet debilitating symptom of photophobia in patient with chronic orofacial pain. Mechanism underlying this phenomenon of photic sensitization in neuropathic condition remains elusive. Here, we found that rats developed hypersensitivity to normal light illumination after establishment of chronic constriction injury of infraorbital nerve<span> (ION-CCI) model, which can be attenuated by blocking the exposure of photic stimulation. Additionally, this behavioral phenotype of light-sensitivity impairment was associated with overexpression of anterior cingulate cortex (ACC) c-fos positive neurons, enhancement of neural excitability in the ACC neurons and its excitatory synaptic transmission between nucleus accumbens<span> (NAc). Optogenetic<span> and chemogenic silencing of ACC-NAc pathway improved trigeminal sensitization in responses to light stimuli by decreasing spontaneous pain-like episodes in ION-CCI animals. In contrast, selective activation of ACC-to-NAc circuits enhanced photic hypersensitivity in dark environment. Thus, our data provided novel role of ACC and its projection to NAc in bidirectional modulation of photic sensation, which may contribute to the understanding of photic allodynia in trigeminal </span></span></span></span>neuropathic pain status.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"231 ","pages":"Article 102533"},"PeriodicalIF":6.7,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41177970","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":"Carnosine synthase deficiency aggravates neuroinflammation in multiple sclerosis","authors":"Jan Spaas ,&nbsp;Thibaux Van der Stede ,&nbsp;Sarah de Jager ,&nbsp;Annet van de Waterweg Berends ,&nbsp;Assia Tiane ,&nbsp;Hans Baelde ,&nbsp;Shahid P. Baba ,&nbsp;Matthias Eckhardt ,&nbsp;Esther Wolfs ,&nbsp;Tim Vanmierlo ,&nbsp;Niels Hellings ,&nbsp;Bert O. Eijnde ,&nbsp;Wim Derave","doi":"10.1016/j.pneurobio.2023.102532","DOIUrl":"10.1016/j.pneurobio.2023.102532","url":null,"abstract":"<div><p><span><span>Multiple sclerosis<span> (MS) pathology features autoimmune-driven neuroinflammation, demyelination, and failed remyelination. </span></span>Carnosine<span> is a histidine-containing dipeptide<span> (HCD) with pluripotent homeostatic properties that is able to improve outcomes in an animal MS model (EAE) when supplied exogenously. To uncover if endogenous carnosine is involved in, and protects against, MS-related neuroinflammation, demyelination or remyelination failure, we here studied the HCD-synthesizing enzyme carnosine synthase (CARNS1) in human MS lesions and two preclinical mouse MS models (EAE, cuprizone). We demonstrate that due to its presence in oligodendrocytes, CARNS1 expression is diminished in demyelinated MS lesions and mouse models mimicking demyelination/inflammation, but returns upon remyelination. </span></span></span><em>Carns1</em><span>-KO mice that are devoid of endogenous HCDs display exaggerated neuroinflammation and clinical symptoms during EAE, which could be partially rescued by exogenous carnosine treatment. Worsening of the disease appears to be driven by a central, not peripheral immune-modulatory, mechanism possibly linked to impaired clearance of the reactive carbonyl acrolein in </span><em>Carns1</em><span>-KO mice. In contrast, CARNS1 is not required for normal oligodendrocyte precursor cell differentiation and (re)myelin to occur, and neither endogenous nor exogenous HCDs protect against cuprizone-induced demyelination. In conclusion, the loss of CARNS1 from demyelinated MS lesions can aggravate disease progression through weakening the endogenous protection against neuroinflammation.</span></p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"231 ","pages":"Article 102532"},"PeriodicalIF":6.7,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41164293","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":"Serine-129 Phosphorylated α-Synuclein Regulates Endoplasmic Reticulum-Mitochondria Calcium Homeostasis via Interaction with VAPB and PTPIP51 in an α-Synuclein-induced Parkinson Disease Model","authors":"Hui Yang, Ge Gao, Hui Yang, Jie Jiao, Tie Wang, Weijin Liu, Zihao Wang","doi":"10.60124/j.pneuro.2023.20.02","DOIUrl":"https://doi.org/10.60124/j.pneuro.2023.20.02","url":null,"abstract":"Serine-129 phosphorylated α-synuclein (p-α-syn), accounting for nearly 90% of α-synuclein (α-syn) found in Lewy bodies (LBs), is linked to the pathogenesis of Parkinson's disease (PD). The molecular targets for the cytotoxic effect of p-α-syn are not fully understood; however, so we sought to determine the role of p-α-syn in cell injury and describe the underlying molecular mechanism. Mitochondrial dysfunction was observed in primary neurons from Thy1-SNCA transgenic mice. Using co-immunoprecipitation coupled with mass spectrometry, we screened the p-α-syn interacting proteins in the midbrains of TG mice and validated the interaction with vesicle-associated membrane protein-associated protein (VAPB) and protein tyrosine phosphatase interacting protein 51 (PTPIP51), which are both located in the mitochondrion-associated endoplasmic reticulum (ER) membrane. VAPB binds to PTPIP51 tethering ER and mitochondria and has an important role in the transport of calcium. We showed that inhibition of α-syn phosphorylation at ser 129 increased the interaction between VAPB and PTPIP51. Moreover, we also demonstrated that inhibition of α-syn phosphorylation at ser 129 alleviated ER and mitochondrial calcium overload. These findings suggest that p-α-syn is involved in regulation of the ER and mitochondrial calcium, which provides new insight into the mechanism by which p-α-syn induces cellular toxicity and neurodegeneration.","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"31 15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135739835","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":"Association of Interoceptive Sensibility and Pain Psychophysics in Healthy Subjects and Chronic Pain Patients","authors":"Antonella Ciaramella, Giancarlo Carli, Melania Boni","doi":"10.60124/j.pneuro.2023.20.01","DOIUrl":"https://doi.org/10.60124/j.pneuro.2023.20.01","url":null,"abstract":"Objective: Interoception is the sense of the physiological condition of the body; it results from the integration of somatic information, including pain, with visceral information. The aim of the study was to assess whether interoceptive sensibility and awareness modulate the perception of experimental pain in healthy participants and recurrent/chronic pain patients. Methods: To assess whether interoceptive sensibility and awareness modulate the effects of experimental noxious stimuli, pain-free subjects (N=52) and patients with recurrent (N= 47) and chronic pain (N= 42) underwent the following psychophysical tests: von Frey filaments (punctate mechanical threshold), pressure pain threshold, heat and cold pain threshold and tolerance, and diffuse noxious inhibitory control (DNIC). They also completed the Body Perception Questionnaire Short Form (BPQ-SF), which discriminates between sub- and supradiaphragmatic interoception, and the Multidimensional Assessment of Interoceptive Awareness I (MAIA I), which measures multiple dimensions of interoceptive sensibility/awareness. Results: After controlling for age and psychopharmacological treatment, a significant difference in heat pain tolerance among groups (F=3.16; p=.047; η2=.06) was found cancelled however by all BPQ dimensions and noticing of MAIA I. Conclusion: Different mechanism of experimental pain perception can be suggested in subjects with and without pain, based on the role of interoceptive sensibility.","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"264 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2023-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79722324","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":"Early top-down control of internal selection induced by retrospective cues in visual working memory: advantage of peripheral over central cues","authors":"Sizhu Han ,&nbsp;Huihui Zhou ,&nbsp;Yonghong Tian ,&nbsp;Yixuan Ku","doi":"10.1016/j.pneurobio.2023.102521","DOIUrl":"10.1016/j.pneurobio.2023.102521","url":null,"abstract":"<div><p><span>Attention can be deployed among external sensory stimuli or internal working memory (WM) representations, and recent primate studies have revealed that these external and internal selections share a common neural basis in the prefrontal cortex (PFC). However, it remains to be elucidated how PFC implements these selections, especially in humans. The present study aimed to further investigate whether PFC responded differentially to the peripheral and central retrospective cues (retro-cues) that induced attention selection among WM representations. To achieve this, we combined magnetoencephalography<span> (MEG, Experiment 1) and transcranial magnetic stimulation (TMS, Experiment 2) with an orientation-recall paradigm. Experiment 1 found that a peripheral retro-cue with 100% reliability had a greater benefit on WM performance than a central retro-cue, while this advantage of peripheral over central cues vanished when the cue reliability dropped to 50% (non-informative). MEG source analysis indicated that the 100% peripheral retro-cue elicited earlier (∼125 ms) PFC responses than the central retro-cue (∼275 ms). Meanwhile, </span></span>Granger causality<span> analysis showed that PFC had earlier (0–200 ms) top-down signals projecting to the superior parietal lobule<span> (SPL) and the lateral occipital cortex<span> (LOC) after the onset of peripheral retro-cues, while these top-down signals appeared later (300–500 ms) after the onset of central retro-cues. Importantly, PFC activity within this period of 300–500 ms correlated with the peripheral advantage in behavior. Moreover, Experiment 2 applied TMS at different time points to test the causal influence of brain activity on behavior and found that stimulating PFC at 100 ms abolished the behavioral benefit of the peripheral retro-cue, as well as its advantage over the central retro-cue. Taken together, our results suggested that the advantage of peripheral over central retro-cues in the mnemonic domain is realized through faster top-down control from PFC, which challenged traditional opinions that the top-down control of attention on WM required at least 300 ms to appear. The present study highlighted that in addition to the causal role of PFC in attention selection of WM representations, timing was critical as well and faster was better.</span></span></span></p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"230 ","pages":"Article 102521"},"PeriodicalIF":6.7,"publicationDate":"2023-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10308576","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}