Journal of neurophysiology最新文献

Based on item-method directed forgetting (DF) task, 60 participants were recruited to explore the influence of emotion (negative, neutral, and positive) on memory encoding processing, with all data referring to the encoding phase of the task. Behavioral results showed that participants were more successful at remembering negative pictures that needed to be forgotten, with both higher recognition rates and discrimination accuracy (Pr) compared with neutral pictures. In the brain, parietal activities reflected preferential processing during negative picture viewing through enhanced late parietal positive potentials (LPP) relative to neutral ones. In addition, "Remember" (R) instruction evoked a larger parietal P3 component, whereas "Forget" (F) instruction evoked a stronger frontal N2 component, each of which component was significantly associated with the DF effect (i.e., more recognized items of R-cue than that of F-cue), reflecting the fact that inhibitory control and selective rehearsal mechanisms were jointly responsible for the directed forgetting of emotional materials. Finally, we showed the presence of instruction-evoked low-frequency phase synchronization between frontal and parietal regions, and that these synchronization patterns differed between R-cue and F-cue in an emotion-dependent manner. Together, these findings reveal cognitive mechanisms and specific patterns of large-scale phase synchronization underlying active forgetting of emotional memories, deepening our comprehension of the interplay between cognition and emotion.NEW & NOTEWORTHY This study provides experimental evidence that emotional memories, especially negative ones, are more difficult to intentionally forget than neutral memories within the item-method directed forgetting paradigm. It explores the cognitive mechanisms underlying this process, highlighting the role of selective rehearsal and inhibitory control. In addition, it reveals emotion-dependent low-frequency phase synchronization between frontal and parietal regions, offering new insights into active forgetting of emotional memories.

Stress is a fundamental adaptive response that invokes amygdala and hypothalamus-pituitary-adrenal (HPA) axis along with other brain regions. Extreme or chronic stress, however, can result in a multitude of neuropsychiatric disorders, including anxiety, paranoia, bipolar disorder (BP), major depressive disorder (MDD), and posttraumatic stress disorder (PTSD). Despite widespread exposure to trauma (70.4%), the incidence of PTSD is relatively low (6.8%), suggesting that either individual susceptibility or adaptability driven by epigenetic and genetic mechanisms are likely at play. PTSD takes hold from exposure to traumatic events, such as death threats or severe abuse, with its severity being impacted by the magnitude of trauma, its frequency, and the nature. This comprehensive review examines how traumatic experiences and epigenetic modifications in hypothalamic-pituitary axis (HPA), such as DNA methylation, histone modifications, noncoding RNAs, and chromatin remodeling, are transmitted across generations, and impact genes such as FKBP prolyl isomerase 5 (FKBP5), nuclear receptor subfamily 3 group C member 1 (NR3C1), brain-derived neurotrophic factor (BDNF), and solute carrier family 6 member 4 (SLC6A4). It also provides a comprehensive overview on trauma reversal, resilience mechanisms, and pro-resilience factors such as histone acetyltransferases (HATs)/histone deacetylases (HDACs) ratio, dehydroepiandrosterone (DHEA)/cortisol ratio, testosterone levels, and neuropeptide Y, thus highlighting potential therapeutic approaches for trauma-related disorders. The studies highlighted here underscore the narrative, for the first time, that the examination and treatment of PTSD and other depressive disorders must invoke a multitude of approaches to seek out the most effective and personalized strategies. We also hope that the discussion emanating from this review will also inform government policies directed toward intergenerational trauma and PTSD.

Many individuals with incomplete spinal cord injury (SCI) exhibit reduced volitional control of trunk muscles, such as impaired voluntary contractions of the erector spinae (ES), due to damage to the neural pathways regulating sensorimotor function. Studies using conventional bipolar electromyography (EMG) showed alterations in the overall, or global, activation of the trunk muscles in people with SCI. However, how activation varied across specific regions within the ES, referred to as regional activation, remains unknown. The aim of the study was to investigate the regional distribution of the ES activity below the level of injury in individuals with incomplete SCI during postural tasks and multidirectional reaching tasks using high-density EMG. Twenty-one individuals with incomplete SCI and age-matched controls were recruited. The EMG amplitude of the thoracic ES and displacement of the arm, trunk, and center of pressure were recorded during the tasks. Activation was more in the lower region of the ES in individuals with SCI than in the controls during the postural tasks. In addition, activation was limited to a small area of the ES during the reaching tasks. The EMG amplitude was greater during reaching forward than returning to the upright posture in the controls; however, this phase-dependent difference in the EMG amplitude was not present in individuals with SCI. Our findings demonstrate changes in regional activation of the thoracic ES during postural and reaching tasks, likely reflecting injury-induced changes in selective neural control to activate residual muscle fibers of the ES for postural control and function after SCI.NEW & NOTEWORTHY We demonstrate that individuals with chronic incomplete spinal cord injury (SCI) recruit lower part of the thoracic erector spinae (ES) for postural control of the trunk. We also show that activation was restricted in a smaller part of the ES, and the discrete control of the ES was lost during functional reaching movements in individuals with SCI. Our study provides evidence of alterations in neural control between vertebral levels in individuals with SCI.

Anatomical studies have revealed a prominent role for feedback projections in the primate visual cortex. Theoretical models suggest that these projections support important brain functions such as attention, prediction, and learning. However, these models make different predictions about the relationship between feedback connectivity and neuronal stimulus selectivity. We have therefore performed simultaneous recordings in different regions of the primate dorsal visual pathway. Specifically, we recorded neural activity from the medial superior temporal (MST) area, and one of its main feedback targets, the middle temporal (MT) area. We estimated functional connectivity from correlations in the single-neuron spike trains and performed electrical microstimulation in MST to determine its causal influence on MT. Both methods revealed that inhibitory feedback occurred more commonly when the source and target neurons had very different stimulus preferences. At the same time, the strength of feedback suppression was greater for neurons with similar preferences. Excitatory feedback projections, in contrast, showed no consistent relationship with stimulus preferences. These results suggest that corticocortical feedback could play a role in shaping sensory responses according to behavioral or environmental context.NEW & NOTEWORTHY Here, we show that corticocortical feedback influences are often determined by the selectivity of the individual neurons. A common motif is the occurrence of inhibitory feedback among neurons with very different stimulus preferences. This results in strong suppression of responses in area MT when MST is electrically stimulated. Interestingly, this feedback shows a complex interaction with ongoing visual stimulation, being powerfully suppressive when visual inputs are strong, yet excitatory when visual inputs are weak.

Obesity and comorbid sleep disordered breathing (SDB) lead to high cardiovascular morbidity and mortality via multiple mechanisms including hypertension. Obesity also leads to high levels of leptin, which is produced in adipocytes. Increased leptin levels have also been implicated in increased sympathetic activity and the pathogenesis of hypertension in obesity. However, mechanisms for the effects of leptin on blood pressure are unclear. The carotid bodies (CB) express leptin receptor (Lepr^b), and diet-induced obesity (DIO) increases Lepr^b expression levels, but the mechanisms and consequences of leptin action in CB are poorly understood. We hypothesize that leptin signaling in CB in obesity leads to hypertension, which can be treated by Lepr^b knockdown specifically in CB. DIO male and female mice and lean male C57BL/6J mice were implanted with telemetry in the left femoral artery for continuous blood pressure monitoring. The adenoviral vectors carrying antisense RNA, Ad-LepR shRNA or Ad-scrambled control shRNA, were administered locally to the CB region. Blood pressure measurements were performed at baseline and 9-11 days after CB infection with the adenoviral vector. DIO male mice showed increased blood pressure compared with lean males and DIO females. Ad-LepR shRNA induced a twofold decrease in Lepr^b mRNA level in CB and abolished obesity-induced hypertension. Lepr^b knockdown was particularly effective during the light phase, when animals were predominantly asleep, decreasing mean arterial pressure by 8.5 mmHg. Control shRNA had no effect on DIO-induced hypertension. We conclude that inhibition of Lepr^b in the carotid bodies abolished obesity-induced hypertension.NEW & NOTEWORTHY Obesity and comorbid sleep apnea are key predisposing factors to hypertension. Obesity increases circulating leptin levels and hyperleptinemia may contribute to hypertension but mechanisms are not clear. Here, we have shown that knockdown of the leptin receptor LepR^b in the carotid body decreased blood pressure and treated hypertension in diet-induced obese mice. Thus, we identified a novel mechanism of obesity hypertension and a novel drug target, LepR^b in the carotid body.

Orientation selectivity is a prominent feature of neurons in the mammalian primary visual cortex (V1), yet its emergence along the visual pathway varies across species. In carnivores and primates, neurons with elongated and orientation-selective receptive fields (RFs) emerge in V1, whereas in mice such RFs appear earlier, in the retina or dorsal lateral geniculate nucleus (dLGN). Here, we investigate the RF properties of neurons in the dLGN of a marsupial, the wallaby (Macropus eugenii) (n = 2; males), using multichannel electrodes and nonlinear input model (NIM) analysis. Do dLGN RFs resemble those of carnivores and primates or exhibit unique characteristics, particularly regarding orientation selectivity? We found that 82% of neurons have a predominant ON-center response. We identified two main cell types: X-cells (n = 15/22), which exhibit linear properties, and Y-cells (n = 7/22), which display nonlinear characteristics. Most dLGN RFs were blob-like and lacked the oriented structures seen in cortical neurons but some had slightly elongated central areas. These results indicate that robust orientation selectivity develops fully in V1 (76% of neurons). However, mild orientation biases were observed in 41% of dLGN neurons. This study enhances our understanding of visual processing in marsupials and underscores the evolutionary significance of orientation selectivity in mammalian visual pathways.NEW & NOTEWORTHY This study examines receptive field (RF) properties of neurons in the dorsal lateral geniculate nucleus (dLGN) of wallabies using multichannel electrodes and nonlinear input model (NIM) analysis. We identified two main cell types: X-cells (linear) and Y-cells (nonlinear). Most dLGN RFs were blob-like, with mild orientation biases in 41% of neurons, indicating robust orientation selectivity develops fully in primary visual cortex (V1) (76% of neurons).

The hippocampus has a known role in learning and memory, with the ventral subregion supporting many learning tasks involving affective responding, including fear conditioning. Altered neuronal intrinsic excitability reflects experience-dependent plasticity that supports learning-related behavioral changes. Such changes have previously been observed in the dorsal hippocampus following fear conditioning, but little work has examined the effect of fear conditioning on ventral hippocampal intrinsic plasticity. The present study tested the hypothesis that acquisition of trace and context fear conditioning alters intrinsic excitability of specific classes of ventral hippocampal CA1 neurons in male rats. We observed distinct changes in excitability that were specific to cell type and learning paradigm. Specifically, regular-spiking ventral hippocampal CA1 neurons demonstrated increased excitability following context fear conditioning, and these changes were correlated with context fear retrieval. In contrast, trace fear conditioning resulted in increased excitability of ventral hippocampal CA1 late-spiking neurons from good learners relative to poor learners. Together, these data demonstrate ventral hippocampal CA1 neuronal excitability is finely tuned to support fear memory in a learning- and firing type-specific manner.NEW & NOTEWORTHY This study is the first to characterize ventral hippocampal CA1 physiological firing types in associative fear learning. Distinct intrinsic excitability changes among these populations suggest they contribute uniquely to trace and context fear memory. These findings have important implications for anxiety disorders that depend on the ventral hippocampus and pave the way for future studies to examine how these populations might coordinate with the larger ventral hippocampal network in forming fear associations.

Ballet shows numerous physiological benefits for dancers, with adaptations in posture, power, strength, stamina, and balance. A recent study from Simpkins and Yang (J Neurophysiol 132: 1115-1125, 2024) showed that 45% of ballet-trained dancers experienced a fall during a standing-slip perturbation, compared with 82.6% of nondancers, along with shorter step latencies, durations, and speeds, which were accompanied by shorter electromyographic latencies in several leg muscles. This study demonstrates the viability of ballet training in aiding fall prevention in elderly individuals.

Donor nerve health likely underlies much variability in nerve transfer outcomes. Standard electromyography (EMG) and clinical examination suffer from subjectivity and a lack of standardization when assessing nerve health. Quantitative electromyography promises to assess nerve health more accurately. The objective of this retrospective pilot study was to evaluate rapid and feasible quantitative electromyography methods in determining donor nerve health for planning nerve transfer surgery and its correlation with functional outcomes. For this study, the branch of the radial nerve supplying the supinator muscle was chosen as the donor nerve and the recipient nerve was the posterior interosseous nerve supplying finger extensors. Fifteen supinator muscle electromyographic recordings from 12 patients were analyzed using quantitative electromyography techniques and compared with the most readily available gold standard neurophysiology metric (full electromyographic signal decomposition) and the average finger extensor Medical Research Council (MRC) grading scores at least 12 mo after surgery. Two multiple regression models were developed to predict MRC grade and decomposition results. Moderate to good correlation was observed between the quantitative electromyography techniques and both the gold standard decomposition-based neurophysiology metric and average MRC finger extension strength outcomes. Both regression models were highly significant. This pilot study highlights the importance of understanding the degree of innervation within the donor nerve and introduces a promising novel quantitative electromyography technique, stimulation-free concentric needle-based motor unit number estimation. Automation and rapid application, using standard EMG signals and widely available software, lowers the threshold for clinical uptake to potentially benefit surgical outcomes.NEW & NOTEWORTHY We introduce a novel quantitative electromyography technique, stimulation-free concentric needle-based motor unit number estimation, which could potentially aid surgical planning in the management of peripheral nerve injury. The ability to apply this technique to any muscle as part of a standard electromyography protocol without imposing additional time burden suggests this technique may represent a practical and feasible approach to optimize surgical outcomes.

The purpose was to assess whether visual feedback of torque contributes to motor unit (MU) firing rate reduction observed during postactivation potentiation (PAP) of skeletal muscle. From 15 participants 23 MUs were recorded with intramuscular fine-wire electrodes from the tibialis anterior during isometric dorsiflexion contractions at 20% of maximum, with and without both PAP and visual feedback of torque. A 5-s maximal voluntary contraction (MVC) was used to induce PAP, and evoked twitch responses were assessed before and after. After the MVC twitch torque was 188% of baseline (P < 0.001). Without visual feedback of torque and with participants targeting 20% MVC, torque, MU firing rates and rating of perceived exertion (RPE) were 22.8 ± 5.3%MVC, 14.3 ± 2.6 Hz, 1.79 ± 0.93 a.u., respectively. Inducing PAP without feedback but targeting 20% MVC torque was overestimated by 50% (P < 0.001) despite similar firing rates and RPE as baseline (both P values ≥ 0.3). With visual feedback, torque was not overestimated during PAP (P = 0.14), however, firing rates and RPE were lower (13% and 20%, respectively) than baseline (both P values ≤0.008). Therefore, no compensatory modifications in MU output occurred despite muscle potentiation. This indicates lower voluntary drive, reflected additionally by reduced RPE, was responsible for the reduced firing rates so that torque did not exceed the required task, compared with modified peripheral feedback. During PAP, the motoneuron is not sensitive to alterations in the active state of the muscle unit per se, but rather compensatory adjustments to optimize contractile output are due to reductions in descending input.NEW & NOTEWORTHY Without visual feedback of torque, no modification in motor unit output occurred despite peripheral muscle potentiation. Therefore, reduced voluntary drive lowered firing rates so that torque did not exceed the task demand, rather than peripheral muscle afferent feedback. During muscle potentiation, the motoneuron is not sensitive to acute enhanced changes in the active state of the muscle unit per se, but rather compensatory adjustments in neuromuscular output are due to perceptual reductions in descending input.