Journal of neurophysiology最新文献

Visual cross-modal plasticity after deafness describes when the sensory cortex compensates for auditory deprivation by increasing sensitivity to visual information. Cross-modal plasticity is evident in humans and animal models with deafness and is linked to improved visual perception, but it is unclear whether this occurs for mild, partial hearing loss. Here, we investigated cross-modal plasticity in adults with mixed levels of high-frequency hearing loss, but normal mid- and low-frequency hearing sensitivity, and whether this plasticity was associated with visual short-term memory recall. A total of 25 participants (aged 18-78) completed a modified Sternberg task with text-based words. Participants viewed a five-word sentence presented word-by-word during an encoding period and held these words in short-term memory during a retention period. After, they reported whether a target word probe was present in the encoding period. Multichannel electroencephalogram recorded visual cortical activity throughout. Results showed separate effects of high-frequency hearing and age on visual cortical responses. Visual N1 amplitudes were larger with worse sensitivity, and P2 latencies were longer. In contrast, age was associated with shorter P2 latencies. Source analysis found that the N1 amplitude increased with worse high-frequency hearing sensitivity in the right auditory cortex, but no effects were found in the visual cortex. Hearing sensitivity and visual encoding activity did not correlate with behavioral performance or neural oscillations during the retention period. Results suggest that even a mild decline of high-frequency hearing sensitivity is associated with increased visual activation of the right auditory cortex during an active visual processing task, consistent with cross-modal plasticity.NEW & NOTEWORTHY By recording the electroencephalogram and analyzing visual cortical potentials, we provide evidence for enhanced visual cortical sensitivity and recruitment of the auditory cortex during visual text perception in individuals with worse high-frequency hearing sensitivity. These individuals otherwise had normal middle- and lower-frequency hearing sensitivity, suggesting that visual cross-modal plasticity is initiated in early stages of hearing loss.

In the core of a stroke, cell death occurs within minutes. In the penumbra, activity quickly drops, but cells typically remain viable for several hours. Improving neuronal survival in the penumbra is crucial for enhancing recovery in patients with stroke. Earlier work showed that mild activation may improve recovery, but the mechanisms are unclear. Brain-derived neurotrophic factor (BDNF) is well recognized for its neuroprotective functions via activation of tyrosine receptor kinase B (TrkB) receptors, and its release is activity-dependent. This study explored the role of BDNF/TrkB signaling in neuronal survival under hypoxic conditions, using cultures of dissociated cortical rat neurons. When exposed to hypoxia, activity quickly drops and cells become apoptotic after ∼12 h, similar to observations in the ischemic penumbra. Inhibition of the TrkB receptor in healthy, normoxic cultures led to a fivefold increase in apoptosis, confirming the importance of BDNF/TrkB signaling for cell viability in these preparations. The addition of BDNF to hypoxic cultures significantly improved neuronal survival, comparable with the effects of mild activation. These findings suggest that the beneficial effect of mild stimulation to prevent apoptosis in hypoxic cultures is mediated by BDNF/TrkB signaling, offering insights for potential therapeutic strategies aimed at promoting neuronal recovery after a stroke.NEW & NOTEWORTHY Low activity in the ischemic penumbra has been suggested as a critical factor leading to apoptosis. BDNF excretion is activity-dependent and has been shown to be neuroprotective. Blockade of TrkB receptors induced apoptosis in cultured neurons, comparable with the effects of hypoxia. BDNF administration was effective in mitigating hypoxia-induced apoptosis, suggesting that the beneficial effect of mild activation to prevent apoptosis in hypoxic cultures is mediated by BDNF-TrkB signaling.

Arm choice can be altered by introducing an energy imbalance between two arms by asymmetrically changing the visual feedback of their movements. Theoretically, the choice of an arm can be promoted by virtually increasing its range of motion (ROM) (energetic reward), or by decreasing ROM of the other arm (energetic penalty), but it remains unclear whether they would result in similar adaptation patterns. Fourteen neurologically intact subjects participated in an experiment where they reached toward visual targets in a virtual-reality environment. Their nondominant arm choice was encouraged by either amplifying its ROM (energetic reward) or by reducing the ROM of their dominant arm (energetic penalty). The impact of energetic penalty was found to be greater, as the change in the nondominant arm choice induced by imposing energetic penalty on the dominant arm was significantly larger than the change created by energetic reward on the nondominant arm (P < 0.01). Kinematic changes were found mostly in the promoted arm under both conditions (energetic reward/penalty), as the energetic reward on the nondominant arm increased its movement vigor (peak velocity), whereas the energetic penalty on the dominant arm reduced the reaction time of the nondominant arm. Individual differences in adaptation (i.e., arm choice change) were also explained by the change in the kinematics of the encouraged arm, particularly reaction time. These results suggest that avoidance learning via energetic penalty has a greater impact on arm choice, and the changes in arm choice were indicated by the changes in the kinematics of the encouraged arm, regardless of how the energetic imbalance was created.NEW & NOTEWORTHY We report that imposing an energetic penalty on the nontarget arm may have a greater impact on arm choice than applying an energetic reward to the targeted arm. A training strategy to promote more-impaired arm choice by imposing an energetic penalty on the less-impaired arm could be effective in reversing its learned nonuse for individuals affected by neurological disorders.

Glial cells play an essential role in the development, function, and plasticity of the central nervous system (CNS). Once regarded as passive support cells, glia are now recognized as highly dynamic and responsive participants in neural circuitry, a shift in understanding largely attributed to recent advances in in vivo imaging. This review highlights key discoveries from the past three decades that have transformed our understanding of glial cell functions, while also addressing the key obstacles ahead. We first discuss the technical challenges in imaging glial cells, including glial reactivity, accessing deeper brain regions, phototoxicity, anesthesia effects, and the need for glia-specific analysis tools. We then review major imaging-based discoveries across the four major glial subtypes in the mammalian CNS. For astrocytes, genetically encoded calcium indicators have visualized intracellular Ca²⁺ activity linked to neuromodulation and behavior. Microglia display continuous surveillance and intimate interactions with neurons and vasculature, contributing to synapse formation and network regulation. Oligodendrocyte precursor cells (OPCs), once considered mere resident progenitors for myelinating oligodendrocytes, exhibit rich structural and Ca²⁺ dynamics modulated by neurotransmitters. Finally, longitudinal imaging of oligodendrocytes has revealed ongoing myelin remodeling throughout life, supporting the theory that myelin is a plastic structure influenced by circuit activity. Together, these in vivo imaging approaches have illuminated the highly dynamic nature of glial cells, revealing multifunctional roles beyond structural support. Continued technological innovation will be critical to fully uncovering the multifaceted contributions of glia to brain function and plasticity.

In this study, we aimed to determine whether the semitendinosus (ST) and biceps femoris long head (BF) exhibit systematically distinct preferred directions (PDs) and to evaluate the biomechanical mechanisms underlying the PDs. A total of 21 healthy young adults performed isometric torque tasks in 16 sagittal-plane directions while surface electromyography (EMG) signals were recorded from six lower limb muscles. Joint torque was estimated with inverse dynamics, and muscle PDs were determined through linear regression of EMG against torque data. Optimal PDs were predicted with static optimization modeling that incorporated both moment arm and physiological cross-sectional areas. Mechanical-only PDs were also estimated based solely on moment arm geometry. Experimentally derived PDs differed significantly between ST and BF (P < 0.001). The ST exhibited significantly greater alignment with optimization-based predictions (mean cosine similarity = 0.96 ± 0.08) than with mechanical-only predictions (0.82 ± 0.15, P = 0.0007), whereas the BF showed comparable levels of agreement with both models (optimization = 0.70 ± 0.35, mechanical = 0.76 ± 0.20, P = 0.3096). These findings indicate that muscle-specific neural modulation contributes to directional tuning, particularly in the ST, and highlight the necessity of incorporating both biomechanical and neural factors to understand spatial organization of muscle activity during complex multijoint motor tasks.NEW & NOTEWORTHY This study demonstrates that the semitendinosus and biceps femoris long head exhibit distinct preferred directions during multijoint isometric torque tasks. Whereas biceps femoris shows high interindividual variability despite anatomical alignment, semitendinosus consistently deviates from mechanical predictions, suggesting stable neural modulation. These findings reveal how the central nervous system selectively tunes muscle activity in a muscle-specific manner, balancing anatomical structure and task-dependent control across multijoint muscles.

The fluid efficiency of everyday hand actions such as reaching-to-grasp is underpinned by finely calibrated, anticipatory, in-flight control of the hand. Peripheral nerve dysfunction could affect this control. We used Carpal Tunnel Syndrome (CTS), a compressive neuropathy of the median nerve, as a model of nerve dysfunction. Whether CTS affects in-flight aspects of reaching-to-grasp is unknown. We compared kinematics of movements in CTS and healthy controls, using motion capture. We varied object properties to determine whether anticipatory signatures of reaching-to-grasp are preserved in CTS. We also examined the effect of removing visual feedback at movement onset. This manipulation forces greater reliance on non-visual control signals, which should highlight impairments due to CTS, while indexing how much movements rely on vision. Participants also completed standardised clinical tests of sensorimotor function. Reaching-to-grasp in CTS showed normal anticipatory signatures, including reliable scaling of movement speed and hand opening with object distance and size, respectively. Removing visual feedback caused both patients and controls to increase hand opening by similar amounts, to compensate for increased probability of errors. Distinct from controls, however, CTS patients also showed slower movement speeds and longer movement onset times without visual feedback. These CTS-specific responses suggest that CTS causes greater reliance on vision for reaching-to-grasp. They also demonstrate adaptive compensation for nerve dysfunction (consistent with normative, statistical-decision-theoretic accounts of movement control). The qualitative similarity of reaching-to-grasp in CTS and controls suggests that normal control processes are preserved in moderate peripheral nerve dysfunction, taking the effects of injury into account appropriately.

The purpose of our study was to determine the influence of load compliance on the discharge characteristics of the same motor units in the first dorsal interosseus (FDI) muscle during submaximal isometric contractions. Motor unit activity in FDI was recorded using high-density, surface electromyography while participants performed isometric contractions either by pushing against a rigid force transducer (force task) or supporting an equivalent inertial load (position task). The coefficient of variation for force decreased as the target force increased from 10% to 30% of maximal FDI force (index finger abduction) during the force task, whereas the standard deviation (SD) of acceleration increased with corresponding loads during the position task (both p < 0.001). The variability in discharge rate was greater during the position task and at the higher target (p < 0.001). There were two main findings: (1) factor analysis of the smoothed discharge rates yielded one motor unit mode for both compliance tasks and the two target forces, and (2) the SD of the discharge rates for the motor units included in the mode were more correlated with fluctuations in force or acceleration (0.52 - 0.84) than was the SD of the cumulative spike train (0.48 - 0.76). The emergence of a single motor unit mode for both tasks suggests that load compliance did not have a significant influence on the distribution of shared synaptic input to the involved motor neurons at either target force.

Developing an animal model that more closely represents the human multidimensional pain experience is an important step toward addressing the current chronic pain crisis. The common marmoset has potential as a model species, given its biological, neurological, and phylogenetic similarity to humans. Here, we developed a model of myofascial temporomandibular disorder (TMD) in the marmoset by injecting nerve growth factor (NGF) into the superficial masseter. Following injection, animals showed reduced mechanical withdrawal thresholds at 5 μg and 10 μg doses of NGF and changes in circadian rhythm and feeding initiation following injection of 10 μg of NGF. Animals did not show evidence of other TMD-related pain behaviors, including jaw dysfunction, masticatory alterations, or grimace during novel behavioral assays. The model is transient, with pain resolution occurring approximately 7 days after onset, which allows for repeated testing on the same animal. This same NGF-TMD model has been previously validated in rodents and humans and presents an opportunity for forward and reverse translation to examine mechanisms, develop relevant pain assessment tools, and ultimately test novel treatments for TMD and other musculoskeletal pain conditions.NEW & NOTEWORTHY We developed a long-lasting but transient (∼7 days) model of myofascial temporomandibular disorder (TMD) pain in marmosets. Mechanical hypersensitivity and changes to circadian activity and spontaneous eating behaviors were observed. There was no evidence of jaw dysfunction, altered food preference, or changes in grimace. The nerve growth factor (NGF)-TMD model can be translated to the marmoset with the potential for investigating mechanisms and novel interventions for TMD.

Many studies require a reliable estimation of when neural activity is modulated by sensory, cognitive, or behavioral events. Standard methods often rely on arbitrary parameter choices such as bin widths or response thresholds, limiting reproducibility and comparability. Here, we introduce two nonparametric, binning-free methods: latenZy, which estimates response onset latency, and latenZy2, which detects when spiking activity diverges between experimental conditions. Both methods analyze spike times directly using cumulative statistics and iterative refinement, without assuming any specific response shape. Validated on electrophysiological datasets from mouse visual cortex, latenZy produced more precise and stable latency estimates than conventional bin-based methods, reliably capturing contrast-dependent latency shifts and hierarchical timing differences across visual areas. Power analyses showed it required fewer neurons to detect significant latency differences, thereby enhancing statistical efficiency. LatenZy2 revealed earlier attentional modulation in macaque higher visual cortex, consistent with top-down feedback, and outperformed bin-based methods in sensitivity and sample size efficiency. Together, these tools offer scalable, parameter-free solutions for reliable latency estimation in large-scale neural recordings. Open-source implementations are available in Python and MATLAB.NEW & NOTEWORTHY We present latenZy and latenZy2, two nonparametric, binning-free methods for precise latency estimation from neural spiking data. Unlike traditional approaches, our tools avoid arbitrary parameters, enhancing reproducibility and comparability. Validated on real electrophysiological datasets, these methods outperform conventional techniques by providing less variable estimates and more accurately capturing known physiological timing effects. Crucially, statistical tests based on latenZy estimates require fewer neurons to detect significant latency differences, boosting efficiency in neural population analyses.

Reactive saccades are rapid eye movements performed toward salient stimuli. Saccadic adaptation maintains the accuracy of visual reactive saccades throughout life and is thought to occur at the motor level of the saccade circuitry. Recently, we revealed that saccadic adaptation also emerges with non-visual, namely tactile targets (Batikh et al. J Neurophysiol 132: 1183-1197, 2024). In addition, such adaptation of tactile saccades transferred partially to nonadapted visual reactive saccades of similar amplitude, compared with a complete visual-to-tactile transfer, suggesting the adaptation occurred upstream of the motor level common to all saccade modalities. Here, we test whether and how saccadic adaptation and transfer occur for auditory saccades. Experiment 1 tested the visual-to-auditory transfer of both backward and forward adaptation whereas experiment 2 investigated the possibility of adapting auditory saccades and the extent to which such adaptation transfers to visual saccades. Experiment 1 revealed a strong visual-to-auditory transfer of both forward and backward adaptations. In experiment 2, stepping the auditory target to another location while the saccade was in flight induced backward adaptation, but could not elicit any significant forward adaptation. Furthermore, we found a partial auditory-to-visual transfer of backward adaptation, in agreement with our previous findings regarding tactile saccades adaptation. This work brings additional insights into our understanding of saccadic adaptation, highlighting the adaptive functional levels of the different saccade modalities.NEW & NOTEWORTHY In this study, we showed that both backward and forward adaptations of visual reactive saccades transfer to nonadapted auditory saccades. Furthermore, we were able to induce a decrease in auditory saccades amplitude when stepping the target sound backward while the saccade was inflight. This indicates that auditory saccades can be subject to adaptive amplitude changes, which, however, are transferred only partially to visual saccades, pointing to the presence of modality-specific adaptation sites.