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        <title>Frontiers in Neural Circuits | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/neural-circuits</link>
        <description>RSS Feed for Frontiers in Neural Circuits | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-09T21:18:04.285+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1834765</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1834765</link>
        <title><![CDATA[Cellular mechanisms underlying social regulation of the posterior tubercular nucleus in zebrafish (Danio rerio)]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Carrie L. Adams</author><author>Emily M. Scott</author><author>Fadi A. Issa</author>
        <description><![CDATA[Social status profoundly influences animal behavior through neural plasticity, yet the cellular mechanisms that mediate reconfiguration of neuromodulatory systems remain poorly understood. Here, we investigated status-dependent structural changes in the posterior tubercular nucleus (PTN) of adult zebrafish. Animals were assigned to four social conditions: communal, isolated, dominant, or subordinate. Using markers for cell proliferation (PCNA) and birth-dating (BrdU), we demonstrate that social dominance significantly enhances cell proliferation, leading to an increased population of PTN dopaminergic neurons. In contrast, subordinate and isolated fish exhibited suppressed proliferation and elevated expression of superoxide dismutase 1 (SOD1), suggesting that chronic social stress induces an oxidative burden that may lead to neuronal loss. Furthermore, we identified evidence of neurotransmitter phenotypic plasticity; subordinate fish displayed a significantly higher ratio of glutamatergic (vglut2a) to dopaminergic (dat) expression in PTN neurons compared to dominants, suggesting a status-dependent shift in neuromodulatory identity. Multivariate principal component analysis showed distinct neurobiological profiles that separate social ranks, suggesting that status-dependent plasticity is a coordinated multi-modal response whereby increased BrdU and PCNA expression clustered with the dominant profile while increased expression of cellular stress and shift to glutamate cellular identity clustered with social subordinate and isolate profiles. Collectively, our results improve our understanding of how social experience reshapes the zebrafish brain through integrated changes in cell proliferation, cellular shift in neurotransmitter identity and regulation of cellular viability; thus, providing a potential mechanism for the maintenance of stable behavioral phenotypes in competitive social environments.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1863549</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1863549</link>
        <title><![CDATA[Correction: Post-ischemic modification of neurogenesis and oligodendrogenesis in rodent models]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Yoshihide Sehara</author><author>Shinya Mochizuki</author><author>Reiji Yamazaki</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1809125</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1809125</link>
        <title><![CDATA[Motor imagery affects both cortical and spinal circuitry: a transcranial and trans-spinal magnetic stimulation study]]></title>
        <pubdate>2026-04-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Asma Benachour</author><author>Nikolay Syrov</author><author>Mikhail Lebedev</author>
        <description><![CDATA[IntroductionMotor imagery (MI), the mental rehearsal of movement without physical execution, is a key technique in brain-computer interfaces (BCIs), known for eliciting cortical modulations similar to those exhibited during real movement. Beyond cortical effects, MI could also modulate spinal cord processing, which offers additional potential for neurorehabilitation in conditions like spinal cord injury (SCI) and stroke, where BCIs are used for therapy.Material and methodsTo investigate the interactions of MI with both the cortex and the spinal cord, we employed both transcranial magnetic stimulation (TMS) and trans-spinal magnetic stimulation (TSMS) while recording brain and muscle activities.Results and conclusionWith proper coil orientation, TSMS elicited lateralized MEPs in ipsilateral forearm muscles at significantly shorter latencies than M1-evoked MEPs, confirming direct spinal cord activation. Importantly, right-hand kinesthetic MI selectively facilitated TSMS-evoked MEPs in the stimulated ipsilateral side only, providing direct evidence that MI modulates spinal cord excitability. Moreover, TSMS-evoked cortical responses were modulated by imagery, demonstrating that MI increases cortical processing of the ascending spinal volley. This within-group demonstration of MI affecting both cortical and spinal circuitry underscores its potential as a powerful strategy for BCI-driven neurorehabilitation, including pairing MI with spinal magnetic stimulation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1818927</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1818927</link>
        <title><![CDATA[The choroid plexus- cerebrospinal fluid axis as a lifespan regulator of neural stem cells and circuit plasticity]]></title>
        <pubdate>2026-04-22T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Kelren S. Rodrigues</author><author>Rie Yamashita</author><author>Sayako Katada</author>
        <description><![CDATA[The choroid plexus-cerebrospinal fluid axis (ChP-CSF) functions as a dynamic signaling system that coordinates neural stem cell (NSC) behavior and neural circuit plasticity across the lifespan. Beyond its classical roles in cushioning the brain, CSF serves as a regulated conduit for growth factors, ions, extracellular vesicles, and other bioactive molecules. Emerging evidence suggests that the ChP contributes to shaping CSF composition through energy-dependent transport and state-responsive secretion. Ventricular-contacting NSCs sense CSF cues via apical endfeet and primary cilia, integrating signals to regulate their behavior. Lifespan-dependent remodeling of CSF composition and niche architecture reshapes NSC function from embryonic expansion to adult homeostasis and age-associated decline. Beyond the ventricular niche, ChP-derived factors influence circuit maturation and vulnerability to neurodegeneration. Orthodenticle homeobox 2 regulates critical period timing and neuroblast integration, whereas apolipoprotein E couples lipid metabolisms and amyloid-β homeostasis to neurogenesis with Alzheimer’s disease risk. Additional ChP-secreted proteins, including transthyretin and clusterin, further shape the extracellular proteostatic and lipid environment. Together, these findings support the view of the ChP-CSF axis as an adaptive regulator across the lifespan that integrates stem cell dynamics, circuit plasticity, and neurodegenerative susceptibility.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1803118</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1803118</link>
        <title><![CDATA[Post-ischemic modification of neurogenesis and oligodendrogenesis in rodent models]]></title>
        <pubdate>2026-04-16T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Yoshihide Sehara</author><author>Shinya Mochizuki</author><author>Reiji Yamazaki</author>
        <description><![CDATA[Neurogenesis and oligodendrogenesis occur throughout life under both physiological and pathophysiological conditions. Brain insults such as ischemia, trauma, epilepsy, or Alzheimer disease result in the promotion of neurogenesis and oligodendrogenesis; however, the mechanisms and the roles of this promotion are not well elucidated. Neurogenesis occurs in two distinct regions in the brain, namely, the subventricular zone (SVZ) of the lateral ventricle and the subgranular zone (SGZ) of the dentate gyrus. Neural stem cells (NSCs) have the potential to self-renew, proliferate, and differentiate into various cell types. NSCs in the SVZ migrate toward the site of injury, and those in the SGZ migrate toward the granule cell layer after ischemic insult. Numerous animal experiments have shown that inhibition of post-ischemic neurogenesis both in the SVZ and the dentate gyrus impairs functional recovery. Oligodendrogenesis regenerates myelin around demyelinated axons after white matter injury, thus promoting functional recovery after ischemia. Oligodendrocyte progenitor cells derived from NSCs and progenitor cells of the SVZ and from intrinsic cells from other brain regions proliferate at the demyelinated lesions. However, deposition of extracellular matrices, including chondroitin sulfate proteoglycans, hyaluronan, fibronectin, and fibrinogen, have been reported to inhibit remyelination. Furthermore, our data showed that type I collagen was deposited in the white matter lesions of stroke patients, and that it may inhibit oligodendrocyte differentiation in these lesions. In this review, we focus on the mechanisms and the roles of post-ischemic neurogenesis and oligodendrogenesis based on recently published data of mainly rodent models.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1741762</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1741762</link>
        <title><![CDATA[Task-dependent increases and decreases of BOLD signal in theory of mind brain regions during strategic social interaction]]></title>
        <pubdate>2026-04-08T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Maya Zheltyakova</author><author>Maxim Kireev</author><author>Irina Knyazeva</author><author>Artem Myznikov</author><author>Vladimir Kiselev</author><author>Mikhail Didur</author><author>Denis Cherednichenko</author><author>Alexander Korotkov</author>
        <description><![CDATA[Theory of Mind (ToM) is known as the capacity to infer others’ thoughts, intentions, and emotions, supported by a distributed neural brain network, including the medial prefrontal cortex (mPFC), temporoparietal junction (TPJ), inferior frontal gyrus (IFG), and precuneus. Although the Rock-Paper-Scissors (RPS) game is used to study the cognitive ToM domain, previous fMRI studies had methodological limitations, including lack of appropriate control conditions and the absence of analyses addressing the directionality of BOLD signal changes. The present fMRI study employed a modified RPS paradigm designed to overcome these limitations. Forty-six healthy adults performed the RPS game and a control task. Whole-brain analyses contrasted neural activity and task-modulated functional connectivity (TMFC) between these conditions and examined BOLD signal changes relative to baseline. In contrast to prior findings of BOLD signal suppression below baseline in affective ToM tasks, RPS elicited increased BOLD responses in canonical ToM regions, including the mPFC, bilateral TPJ, IFG, and precuneus, as well as additional frontal, cingulate and visual regions. TMFC analyses converged with these findings, demonstrating increased RPS-related functional interactions between the bilateral TPJ and precuneus with the left IFG, and between the mPFC and the right TPJ with the right IFG. Additionally, greater deactivation (negative BOLD deflection) below baseline during RPS was observed in the midcingulate cortex and opercular regions bilaterally. These findings extend current understanding of ToM network functioning by demonstrating that the engagement of its affective and cognitive domains manifest through TMFC changes and directionally distinct neural responses.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1777115</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1777115</link>
        <title><![CDATA[Disruption of afferent neural circuits leads to arrhythmia in the animal model of hereditary sensory and autonomic neuropathy 6]]></title>
        <pubdate>2026-04-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nozomu Yoshioka</author><author>Masayuki Kurose</author><author>Kazuki Tainaka</author><author>Takako Ichiki</author><author>Yousuke Tsuneoka</author><author>Hiromasa Funato</author><author>Masaki Ueno</author><author>Hayato Ohshima</author><author>Ikuo Kageyama</author><author>Hirohide Takebayashi</author>
        <description><![CDATA[Hereditary sensory and autonomic neuropathies (HSANs) are a group of recessive genetic disorders affecting the sensory and autonomic components of the peripheral nervous system (PNS). Compared with somatosensory dysfunctions, the pathogenesis of visceral dysfunction in HSANs remains understudied. This study investigated the neural circuit mechanisms underlying the arrhythmias observed in conditional Dystonin (Dst) gene-trap mice, an animal model of HSAN type VI (HSAN-VI) in which Cre recombinase inactivates Dst expression in selective neural circuits. Inactivation of the Dst gene in PNS neurons using Advillin-Cre caused the degeneration of sensory and sympathetic ganglionic neurons. This was accompanied by arrhythmia, characterized by increased heart rate variability and irregular pulse frequency, which was prominent under isoflurane anesthesia and occurred in the absence of protein aggregate cardiomyopathy. Furthermore, selective inactivation of the Dst gene in PNS sensory neurons using Vglut2-Cre resulted in similar dysregulation of cardiac rhythm. These findings suggest that arrhythmias caused by Dst mutations arise from the disruption of visceral afferent circuits, and that these neural circuits could be potential therapeutic targets for visceral dysfunction in HSAN-VI.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1791625</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1791625</link>
        <title><![CDATA[Oxytocin modulation of the insular cortex: implications for social cognition and neurodevelopmental disorders]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Shuhei Fujima</author><author>Masaaki Sato</author>
        <description><![CDATA[Social cognition relies on the integration of sensory information, emotional cues, and internal bodily signals to guide behavior toward others. The insular cortex (IC) is anatomically and functionally well positioned to support this integration, as it receives interoceptive input and connects sensory, limbic, and autonomic systems. Accumulating evidence across species suggests that the IC contributes to social behavior through at least two complementary modes of processing: emotional mirroring, which links observed social cues to internal affective states, and contextual modulation, which adjusts social behavior according to familiarity, prior experience, and internal state. In this Mini Review, we discuss how neuromodulatory systems shape these modes of IC processing, with a particular focus on oxytocin (OXT). In rodents, OXT signaling within the IC influences social affective behaviors under specific social conditions, whereas human studies report heterogeneous and context-dependent effects of OXT on IC activity. Altered IC function and OXT signaling have also been implicated in neurodevelopmental disorders characterized by social deficits, including autism spectrum disorder. We propose that OXT modulates IC function in a context- and state-dependent manner, shaping social cognition by influencing how interoceptive, emotional, and contextual information is integrated.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1783133</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1783133</link>
        <title><![CDATA[Clarifying the neural circuit mechanisms of spontaneous social behavior in macaques]]></title>
        <pubdate>2026-03-25T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Taihei Ninomiya</author><author>Takaaki Kaneko</author><author>Yuzuha Ono</author><author>Kenta Kobayashi</author><author>Masaki Isoda</author>
        <description><![CDATA[Research using nonhuman primates has investigated how the brain processes and represents a wide range of socially relevant information, such as others’ faces, actions and rewards. While our understanding has expanded considerably in recent years, much of the research has been conducted under highly controlled task conditions, leaving the neural underpinnings of naturally occurring social behaviors largely unexplored. In this Perspective, we first highlight recent efforts utilizing freely behaving primates to overcome these challenges. We then detail our own experiments, demonstrating how the combined use of behavioral analysis and neural manipulation techniques in freely moving macaques enabled us to identify a specific neural circuit critical for the spontaneous expression of mounting behavior. These strategies offer novel opportunities to validate and extend established knowledge concerning the neural basis of social behavior in experimental settings that more closely resemble those occurring in a real world.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1738731</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1738731</link>
        <title><![CDATA[Ascending propriospinal modulation of thoracic sympathetic preganglionic neurons during lumbar locomotor activity]]></title>
        <pubdate>2026-03-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lucia E. Dominguez-Rodriguez</author><author>Chioma V. Nwachukwu</author><author>Narjes Shahsavani</author><author>Juanita Garcia</author><author>Jeremy W. Chopek</author><author>Kristine C. Cowley</author>
        <description><![CDATA[Although the autonomic sympathetic system is activated in parallel with locomotion, the underlying neural mechanisms mediating this coordination are not completely understood. Descending exercise or “central command” signals from hypothalamic and brainstem regions are thought to activate thoracic spinal sympathetic neurons in parallel with descending locomotor commands. In turn, subsets of thoracic sympathetic preganglionic neurons (SPNs) increase activity in a constellation of tissues and organs that provide homeostatic and metabolic support during movement and exercise. It is known that ascending drive from lumbar locomotor networks is mediated in part via propriospinal neurons that can also activate and coordinate autonomic systems. However, the extent to which this ascending drive is distributed to SPNs within thoracic regions is unknown. To investigate this, we applied neurochemicals to elicit whole-cord or lumbar-evoked locomotor activity in an in vitro spinal cord preparation, simultaneously recording lumbar ventral root (VR) activity and changes in normalized calcium fluorescence (Ca-RI) of pre-labelled SPNs in thoracic segments. Using whole-bath drug application SPN responses appeared unimodal, such that SPN Ca-RI was increased in rostral (T4-FT7) compared to caudal (T8-T11) segments during tonic activity. During rhythmic activity in either whole or split-bath configuration, and during tonic activity in split-bath configuration, SPN responses appeared trimodal, such that SPN Ca-RI was increased in mid-thoracic segments (T6-7) and reduced at more rostral (T4-5) and caudal (T8-9) levels. In both approaches, the greatest increases in SPNs Ca-RI during rhythmic activity were at T6-7, and most decreased at caudal segments (T8-T11). Together, these findings reveal a strong ascending lumbar to thoracic integrating communication pathway, which may represent a key feature of spinal neural network function normally. Such communication pathways should be further investigated for targeted autonomic function(s) activation and therapeutic benefit after spinal cord injury.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1782975</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1782975</link>
        <title><![CDATA[Editorial: Chemical senses in health and disease]]></title>
        <pubdate>2026-03-17T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Carla Mucignat-Caretta</author><author>Sachiko Koyama</author><author>Vera V. Voznessenskaya</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1789080</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1789080</link>
        <title><![CDATA[The circuitry regulation of associative learning: dissociated and integrated function of the perirhinal cortex and hippocampus]]></title>
        <pubdate>2026-03-17T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jingyi Zhang</author><author>Xiaohui Zhang</author>
        <description><![CDATA[The formation of associations, which involves binding disparate pieces of information, is fundamental to constructing episodic memory. This process primarily relies on the neural circuitry within the medial temporal lobe, specifically the hippocampal-parahippocampal network. Within this network, the perirhinal cortex (PER) and the hippocampus (HPC) are recognized as essential components for associative processing. While the traditional dual-pathway model depicts a hierarchically organized, sequential transmission of information along the medial temporal lobe, recent anatomical and functional studies reveal that the PER and HPC are embedded within a far more extensive and complex multi-pathway connectivity architecture. These connections enable parallel and dynamic interactions between PER, HPC, and other medial temporal lobe structures, supporting flexible modes of information processing and integration essential for associative learning. This review systematically re-evaluates the roles of the PER and HPC in associative learning. We begin by advancing the view that the PER acts not as a passive sensory gateway, but as an associative hub for multimodal association formation, whose special local inhibition provides the computational foundation for integrating complex information of both object features, and spatiotemporal context or affective valence. Building on this perspective, we then synthesize evidence on the dynamic interactions between the PER and HPC, encompassing findings from extensive anatomical and electrophysiological studies. Finally, we focus on the HPC, elucidating how it precisely coordinates information from the PER and other regions, with a particular emphasis on the critical regulatory roles played by inhibitory neurons in this integrative process. The reciprocal neuronal connections, coherent neuronal oscillatory activities and shared neuromodulation in the PER-HPC circuit facilitate the integration of associative learning.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1731513</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1731513</link>
        <title><![CDATA[From small brains to smart machines: translating Caenorhabditis elegans neural circuits into artificial intelligence]]></title>
        <pubdate>2026-03-09T00:00:00Z</pubdate>
        <category>Review</category>
        <author>He Liu</author><author>Panpan Zheng</author><author>Xuebin Wang</author>
        <description><![CDATA[The hermaphroditic Caenorhabditis elegans, with its fully mapped connectome of 302 neurons, offers a paradigmatic example of how a minimal nervous system governs biotic, adaptive, and context-dependent behaviors. In contrast, modern artificial intelligence systems achieve intelligence through scale rather than efficiency, relying instead on massive datasets and artificially engineered architectures. This mini-review explores how Caenorhabditis elegans neural circuits can inform the development of more efficient and flexible artificial neural networks. We highlight recent studies that translate the principles inherent to Caenorhabditis elegans neural circuits into artificial neural network architectures, with applications in machine control and image classification, resulting in enhanced robustness and improved performance. By distilling neural principles from the simplest known nervous system, this mini-review outlines a pathway toward compact, adaptive, and biologically inspired artificial intelligence systems.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1781653</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1781653</link>
        <title><![CDATA[Brain mechanisms underlying self-other distinction for bodily self-recognition]]></title>
        <pubdate>2026-03-04T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Yuuki G. Oka</author><author>Masaki Isoda</author>
        <description><![CDATA[Accumulating evidence indicates that single neurons in the primate brain specifically encode sensorimotor experience about the self or others. Although the self-other distinction has been a major focus of social neuroscience research, little is known about the underlying mechanisms that enable the recognition of bodily self. Here, we review the literature demonstrating that pre-reflective bodily self-recognition can be achieved through the spatiotemporally contingent integration of visual, somatosensory, and motor signals arising from sensorimotor experience. We propose a self-other inference model as a neural computation for self-other distinction, in which the likelihood of being oneself is updated constantly based on Bayesian causal inference using appearance, contingency, and perspective cues. The results of simulation incorporating a state-space point-process model revealed that our self-other inference model successfully captures the latent state representation about the self-other distinction from synthetic neural activity. We hypothesize that the self-other inference model is implemented by distinct brain areas that process individual cues and their integrative hubs. This hypothesis is experimentally testable using cutting-edge technologies such as area-specific or pathway-selective silencing.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1782196</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1782196</link>
        <title><![CDATA[Absence of local retinotopy in the mouse optic tract]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Matteo Tripodi</author><author>Hiroki Asari</author>
        <description><![CDATA[Retinotopy is a fundamental organizational principle of the visual system, where neighboring neurons represent adjacent points in visual space. This spatial relationship is established by precise anatomical wiring across successive areas, e.g., from the retina to the lateral geniculate nucleus (LGN) to the visual cortex. To examine the precision of this topographic arrangement within the long-range projection axons themselves, we recorded retinal ganglion cell (RGC) axons in the mouse optic tract (OT) and mapped their receptive fields (RFs). As expected for a retinotopically organized area, we found that nearby LGN cell pairs had significantly smaller RF distances than distant pairs. In contrast, no such relationship was observed among RGC axons in the OT. Modelling analyses further confirmed that the observed RF distances in the OT were incompatible with any locally retinotopic arrangement. Instead, the OT retained only coarse topography, with ~18° RF deviations or ~40 μm axonal displacements from an ideal retinotopic organization. These results demonstrate that the mouse OT lacks fine-scale retinotopy and maintains only broad topographic structure.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1781811</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1781811</link>
        <title><![CDATA[Social learning and exploration–exploitation dilemma in decision-making]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Gota Morishita</author><author>Shinsuke Suzuki</author>
        <description><![CDATA[This mini review examines the neurocomputational principles of social learning through the lens of the exploration–exploitation dilemma. While the neural mechanisms of learning from others—mediated by distinct signals in the ventromedial and lateral prefrontal cortices—are well established, less is known about how these mechanisms interact with the fundamental trade-off between gathering information (“exploration”) and maximizing rewards (“exploitation”). We discuss how social environments shape this trade-off, leading to strategic behaviors such as informational free-riding or conformity. A central focus of this review is the issue of source selection: how agents decide whom to observe. We present recent evidence suggesting that, contrary to the predictions of optimal information-seeking theories, humans often exhibit a “reliability-seeking” bias, preferring to learn from consistent, exploitation-oriented partners rather than highly exploratory ones. We conclude by discussing the limitations of current paradigms, specifically the inherent confounding of social cues such as competence and predictability, and outline a computational framework for isolating the specific drivers of adaptive social decision-making.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2025.1545031</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2025.1545031</link>
        <title><![CDATA[A concise mathematical description of signal transformations across the hippocampal apical CA3 to CA1 dendritic response]]></title>
        <pubdate>2026-02-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sandra Gattas</author><author>Aliza A. Le</author><author>Javad Karimi Abadchi</author><author>Ben Pruess</author><author>Rohit Amba</author><author>Yanning Shen</author><author>A. Swindlehurst</author><author>Michael A. Yassa</author><author>Gary Lynch</author>
        <description><![CDATA[The synapse is the fundamental unit of communication in the nervous system. Determining how information is transferred across the synaptic interface is one of the most complex endeavors in neuroscience, owing to the large number of contributing factors and events. An approach to solving this problem involves collapsing across these complexities to derive concise mathematical formulas that fully capture the governing dynamics of synaptic transmission. We investigated the feasibility of deriving such a formula – an input-output transformation function for the CA3 to CA1 node of the hippocampus – using the Volterra expansion technique for non-linear system identification. The timecourse of the fEPSP in the apical dendrites of mouse brain slices was described with >94% accuracy by a 2nd order equation that captured the linear and non-linear influence of past inputs on current outputs. This function generalized to cases not included in its derivation and uncovered previously undetected timing rules. The basal dendrites expressed a substantially different transfer function and evidence was obtained that, unlike the apical system, a 3rd order system or higher will be needed for complete characterization. At scale, the approach will also provide information needed for the construction of biologically realistic models of brain networks.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2025.1706704</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2025.1706704</link>
        <title><![CDATA[The cerebellum engages multiple pre-motor pathways through a divergent-convergent architecture to shape whisker dynamics]]></title>
        <pubdate>2026-01-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Staf Bauer</author><author>Peipei Zhai</author><author>Nathalie van Wingerden</author><author>Hehe Zhao</author><author>Vincenzo Romano</author>
        <description><![CDATA[The cerebellar output can trigger whisker movement through indirect projections that pass via several brainstem pre-motor nuclei before reaching the facial nucleus, which directly controls whisker movements in rodents. Although the central pattern generator function of the intermediate reticular formation has been recently clarified, the roles of the other whisker pre-motor nuclei remain unclear. Here, we set out to compare the whisker movement kinematics of the main pre-motor whisker nuclei connecting the cerebellum and the facial nucleus. We optogenetically stimulated neurons located in the cerebellar cortex: Purkinje cells (PCs), the cerebellar nuclei (CN), the red nucleus (RN), the superior colliculus (SC), the spinal trigeminal nucleus (SV), and the reticular formation (RF); in head-fixed awake mice while monitoring the bilateral whisker movement. We show that optogenetic stimulation of the RN, SC, and SV resulted in a predominant midpoint change, whereas optogenetic stimulation of the PCs, CN, and RF resulted in faster whisker movements. In addition, the excitation of PCs, the RN, and SC resulted in symmetric bilateral whisking. In contrast, the excitation of the RF, and SV resulted in initial asymmetric movement, followed by a more dominantly symmetrical bilateral whisking. Importantly, PC excitation generated a robust rhythmic whisking pattern that could not be reproduced by direct CN stimulation, indicating that the cerebellar cortex sculpts CN population output rather than simply gating it. Our results suggest that cerebellar output engages multiple, specialized pre-motor pathways through a divergent-convergent architecture. This system allows different pre-motor nuclei to modulate distinct aspects of whisking kinematics, ultimately shaping whisker motor dynamics.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1776224</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1776224</link>
        <title><![CDATA[Editorial: Bridging computation, biophysics, medicine, and engineering in neural circuits]]></title>
        <pubdate>2026-01-21T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Haruyuki Kamiya</author><author>Hideaki Yamamoto</author><author>Jordi Soriano</author><author>Shigeo Sato</author><author>Toshiaki Omori</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fncir.2026.1725431</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fncir.2026.1725431</link>
        <title><![CDATA[Morphological and transcriptomic change of brain pericytes by lipopolysaccharide treatment]]></title>
        <pubdate>2026-01-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Taiki Asai</author><author>Yoshino Yonezu</author><author>Akiko Uyeda</author><author>Haruki Watanabe</author><author>Tatsunori Suzuki</author><author>Hidemi Misawa</author><author>Rieko Muramatsu</author>
        <description><![CDATA[Brain pericytes play essential roles in vascular homeostasis, including capillary stabilization and maintenance of the blood–brain barrier. Lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria, is known to trigger inflammatory responses not only systemically but also within the central nervous system. In this study, we investigated the effects of LPS on the phenotype and transcriptome of brain vascular pericytes. LPS promoted bromodeoxyuridine incorporation in the primary culture of human brain pericytes as well as increased the number of Ki67-positive cells, indicating enhanced pericyte proliferation. Morphological analysis revealed that LPS decreased the cellular aspect ratio, suggesting altered cellular elongation. Transcriptomic profiling showed that LPS-induced differentially expressed genes were enriched for terms related to cell proliferation, angiogenesis, and blood–brain barrier function. Because pericytes critically regulate neurovascular coupling and metabolic support for active neurons, these LPS-induced alterations may ultimately perturb the microvascular control of neural circuits. These results suggest that LPS has the potential to regulate brain vascular function by inducing morphological and functional changes in pericytes.]]></description>
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