Neural Plasticity最新文献

[This retracts the article DOI: 10.1155/2021/7506754.].

While infant cues are often assumed to innately motivate maternal response, recent research highlights how the neural coding of infant cues is altered through maternal care. Infant vocalizations are important social signals for caregivers, and evidence from mice suggests that experience caring for mouse pups induces inhibitory plasticity in the auditory cortex (AC), though the molecular mediators for such AC plasticity during the initial pup experience are not well delineated. Here, we used the maternal mouse communication model to explore whether transcription in AC of a specific, inhibition-linked, memory-associated gene, brain-derived neurotrophic factor (Bdnf) changes due to the very first pup caring experience hearing vocalizations, while controlling for the systemic influence of the hormone estrogen. Ovariectomized and estradiol or blank-implanted virgin female mice hearing pup calls with pups present had significantly higher AC exon IV Bdnf mRNA compared to females without pups present, suggesting that the social context of vocalizations induces immediate molecular changes at the site of auditory cortical processing. E2 influenced the rate of maternal behavior but did not significantly affect Bdnf mRNA transcription in the AC. To our knowledge, this is the first time Bdnf has been associated with processing social vocalizations in the AC, and our results suggest that it is a potential molecular component responsible for enhancing future recognition of infant cues by contributing to AC plasticity.

Objective: Many stroke victims have severe swallowing problems. Previous neuroimaging studies have found that several brain regions scattered in the frontal, temporal, and parietal lobes, such as Brodmann's areas (BA) 6, 21, and 40, are associated with swallowing function. This study sought to investigate changes in swallowing function and resting-state functional magnetic resonance imaging (rs-fMRI) in stroke patients with dysphagia following action observation treatment. It also sought to detect changes in brain regions associated with swallowing in stroke patients.

Methods: In this study, 12 healthy controls (HCs) and 12 stroke patients were recruited. Stroke patients were given 4 weeks of action observation therapy. In order to assess the differences in mfALFF values between patients before treatment and HCs, the fractional amplitude of low-frequency fluctuations (fALFF) in three frequency bands (conventional frequency band, slow-4, and slow-5) were calculated for fMRI data. The significant brain regions were selected as regions of interest (ROIs) for subsequent analysis. The mfALFF values were extracted from ROIs of the three groups (patients before and after treatment and HCs) and compared to assess the therapeutic efficacy.

Results: In the conventional band, stroke patients before treatment had higher mfALFF in the inferior temporal gyrus and lower mfALFF in the calcarine fissure and surrounding cortex and thalamus compared to HCs. In the slow-4 band, there was no significant difference in related brain regions between stroke patients before treatment and HCs. In the slow-5 band, stroke patients before treatment had higher mfALFF in inferior cerebellum, inferior temporal gyrus, middle frontal gyrus, and lower mfALFF in calcarine fissure and surrounding cortex compared to HCs. We also assessed changes in aberrant brain activity that occurred both before and after action observation therapy. The mfALFF between stroke patients after therapy was closed to HCs in comparison to the patients before treatment.

Conclusion: Action observation therapy can affect the excitability of certain brain regions. The changes in brain function brought about by this treatment may help to further understand the potential mechanism of network remodeling of swallowing function.

Background: Prolonged disorders of consciousness (pDOC) are common in neurology and place a heavy burden on families and society. This study is aimed at investigating the characteristics of brain connectivity in patients with pDOC based on quantitative EEG (qEEG) and extending a new direction for the evaluation of pDOC.

Methods: Participants were divided into a control group (CG) and a DOC group by the presence or absence of pDOC. Participants underwent magnetic resonance imaging (MRI) T1 three-dimensional magnetization with a prepared rapid acquisition gradient echo (3D-T1-MPRAGE) sequence, and video EEG data were collected. After calculating the power spectrum by EEG data analysis tool, DTABR ((δ + θ)/(α + β) ratio), Pearson's correlation coefficient (Pearson r), Granger's causality, and phase transfer entropy (PTE), we performed statistical analysis between two groups. Finally, receiver operating characteristic (ROC) curves of connectivity metrics were made.

Results: The proportion of power in frontal, central, parietal, and temporal regions in the DOC group was lower than that in the CG. The percentage of delta power in the DOC group was significantly higher than that in the CG, the DTABR in the DOC group was higher than that in the CG, and the value was inverted. The Pearson r of the DOC group was higher than that of CG. The Pearson r of the delta band (Z = -6.71, P < 0.01), theta band (Z = -15.06, P < 0.01), and alpha band (Z = -28.45, P < 0.01) were statistically significant. Granger causality showed that the intensity of directed connections between the two hemispheres in the DOC group at the same threshold was significantly reduced (Z = -82.43, P < 0.01). The PTE of each frequency band in the DOC group was lower than that in the CG. The PTE of the delta band (Z = -42.68, P < 0.01), theta band (Z = -56.79, P < 0.01), the alpha band (Z = -35.11, P < 0.01), and beta band (Z = -63.74, P < 0.01) had statistical significance.

Conclusion: Brain connectivity analysis based on EEG has the advantages of being noninvasive, convenient, and bedside. The Pearson r of DTABR, delta, theta, and alpha bands, Granger's causality, and PTE of the delta, theta, alpha, and beta bands can be used as biological markers to distinguish between pDOC and healthy people, especially when behavior evaluation is difficult or ambiguous; it can supplement clinical diagnosis.

Objective: Epilepsy may cause chronic cognitive impairment by disturbing sleep plasticity. Sleep spindles play a crucial role in sleep maintenance and brain plasticity. This study explored the relationship between cognition and spindle characteristics in adult epilepsy.

Methods: Participants underwent one-night sleep electroencephalogram recording and neuropsychological tests on the same day. Spindle characteristics during N2 sleep were extracted using a learning-based system for sleep staging and an automated spindle detection algorithm. We investigated the difference between cognitive subgroups in spindle characteristics. Multiple linear regressions were applied to analyze associations between cognition and spindle characteristics.

Results: Compared with no/mild cognitive impairment, epilepsy patients who developed severe cognitive impairment had lower sleep spindle density, the differences mainly distributed in central, occipital, parietal, middle temporal, and posterior temporal (P < 0.05), and had relatively long spindle duration in occipital and posterior temporal (P < 0.05). Mini-Mental State Examination (MMSE) was associated with spindle density (pars triangularis of the inferior frontal gyrus (IFGtri): β = 0.253, P = 0.015, and P.adjust = 0.074) and spindle duration (IFGtri: β = -0.262, P = 0.004, and P.adjust = 0.030). Montreal Cognitive Assessment (MoCA) was associated with spindle duration (IFGtri: β = -0.246, P = 0.010, and P.adjust = 0.055). Executive Index Score (MoCA-EIS) was associated with spindle density (IFGtri: β = 0.238, P = 0.019, and P.adjust = 0.087; parietal: β = 0.227, P = 0.017, and P.adjust = 0.082) and spindle duration (parietal: β = -0.230, P = 0.013, and P.adjust = 0.065). Attention Index Score (MoCA-AIS) was associated with spindle duration (IFGtri: β = -0.233, P = 0.017, and P.adjust = 0.081).

Conclusions: The findings suggested that the altered spindle activity in epilepsy with severe cognitive impairment, the associations between the global cognitive status of adult epilepsy and spindle characteristics, and specific cognitive domains may relate to spindle characteristics in particular brain regions.

CX3CR1 is a G protein-coupled receptor that is expressed exclusively by microglia within the brain parenchyma. The only known physiological CX3CR1 ligand is the chemokine fractalkine (FKN), which is constitutively expressed in neuronal cell membranes and tonically released by them. Through its key role in microglia-neuron communication, the FKN/CX3CR1 axis regulates microglial state, neuronal survival, synaptic plasticity, and a variety of synaptic functions, as well as neuronal excitability via cytokine release modulation, chemotaxis, and phagocytosis. Thus, the absence of CX3CR1 or any failure in the FKN/CX3CR1 axis has been linked to alterations in different brain functions, including changes in synaptic and network plasticity in structures such as the hippocampus, cortex, brainstem, and spinal cord. Since synaptic plasticity is a basic phenomenon in neural circuit integration and adjustment, here, we will review its modulation by the FKN/CX3CR1 axis in diverse brain circuits and its impact on brain function and adaptation in health and disease.

The structural connectivity from the primary olfactory cortex to the main secondary olfactory areas was previously reported as relatively increased in the medial orbitofrontal cortex in a cohort of 27 recently SARS-CoV-2-infected (COV+) subjects, of which 23/27 had clinically confirmed olfactory loss, compared to 18 control (COV-) normosmic subjects, who were not previously infected. To complement this finding, here we report the outcome of an identical high angular resolution diffusion MRI analysis on follow-up data sets collected in 18/27 COV+ subjects (10 males, mean age ± SD: 38.7 ± 8.1 years) and 10/18 COV- subjects (5 males, mean age ± SD: 33.1 ± 3.6 years) from the previous samples who repeated both the olfactory functional assessment and the MRI examination after ~1 year. By comparing the newly derived subgroups, we observed that the increase in the structural connectivity index of the medial orbitofrontal cortex was not significant at follow-up, despite 10/18 COV+ subjects were still found hyposmic after ~1 year from SARS-CoV-2 infection. We concluded that the relative hyperconnectivity of the olfactory cortex to the medial orbitofrontal cortex could be, at least in some cases, an acute or reversible phenomenon linked to the recent SARS-CoV-2 infection with associated olfactory loss.

Long-term hypoxia can induce oxidative stress and apoptosis in hippocampal neurons that can lead to brain injury diseases. Astragaloside IV (AS-IV) is widely used in the antiapoptotic therapy of brain injury diseases. However, its mechanism of action is still not fully understood. In this study, we investigated the effect of AS-IV on hypoxia-induced oxidative stress and apoptosis in hippocampal neurons and explored its possible mechanism. In vivo, mice were placed in a hypoxic circulatory device containing 10% O₂ and gavaged with AS-IV (60 and 120 mg/kg/d) for 4 weeks. In vitro, mouse hippocampal neuronal cells (HT22) were treated with hypoxia (1% O₂) for 24 hours in the presence or absence of AS-IV, MDL-28170 (calpain-1 inhibitor), or YC-1 (HIF-1α inhibitor). The protective effect of AS-IV on brain injury was further explored by examining calpain-1 knockout mice. The results showed that hypoxia induced damage to hippocampal neurons, impaired spatial learning and memory abilities, and increased oxidative stress and apoptosis. Treatment with AS-IV or calpain-1 knockout improved the damage to hippocampal neurons and spatial learning and memory, attenuated oxidative stress and inhibited cell apoptosis. These changes were verified in HT22 cells. Overexpression of calpain-1 abolished the improvement of AS-IV on apoptosis and oxidative stress. In addition, the effects of AS-IV were accompanied by decreased calpain-1 and HIF-1α expression, and YC-1 showed a similar effect as AS-IV on calpain-1 and caspase-3 expression. In conclusion, this study demonstrates that AS-IV can downregulate the calpain-1/HIF-1α/caspase-3 pathway and inhibit oxidative stress and apoptosis of hippocampal neurons induced by hypoxia, which provides new ideas for studying the antiapoptotic activity of AS-IV.

Sound stimulation is generally used for tinnitus and hyperacusis treatment. Recent studies found that long-term noise exposure can change synaptic and firing properties in the central auditory system, which will be detected by the acoustic startle reflex. However, the perceptual consequences of long-term low-intensity sound exposure are indistinct. This study will detect the effects of moderate-level noise exposure (83 dB SPL) on auditory loudness, and temporal processing was evaluated using CBA/CaJ mice. C-Fos staining was used to detect neural activity changes in the central auditory pathway. With two weeks of 83 dB SPL noise exposure (8 hours per day), no persistent threshold shift of the auditory brainstem response (ABR) was identified. On the other hand, noise exposure enhanced the acoustic startle response (ASR) and gap-induced prepulse inhibition significantly (gap-PPI). Low-level noise exposure, according to the findings, can alter temporal acuity. Noise exposure increased the number of c-Fos labeled neurons in the dorsal cochlear nucleus (DCN) and caudal pontine reticular nucleus (PnC) but not at a higher level in the central auditory nuclei. Our results suggested that noise stimulation can change acoustical temporal processing presumably by increasing the excitability of auditory brainstem neurons.

Objective: This study is aimed at exploring alteration in motor-related effective connectivity in individuals with transient ischemic attack (TIA).

Methods: A total of 48 individuals with TIA and 41 age-matched and sex-matched healthy controls (HCs) were recruited for this study. The participants were scanned using MRI, and their clinical characteristics were collected. To investigate motor-related effective connectivity differences between individuals with TIA and HCs, the bilateral primary motor cortex (M1) was used as the regions of interest (ROIs) to perform a whole-brain Granger causality analysis (GCA). Furthermore, partial correlation was used to evaluate the relationship between GCA values and the clinical characteristics of individuals with TIA.

Results: Compared with HCs, individuals with TIA demonstrated alterations in the effective connectivity between M1 and widely distributed brain regions involved in motor, visual, auditory, and sensory integration. In addition, GCA values were significantly correlated with high- and low-density lipoprotein cholesterols in individuals with TIA.

Conclusion: This study provides important evidence for the alteration of motor-related effective connectivity in TIA, which reflects the abnormal information flow between different brain regions. This could help further elucidate the pathological mechanisms of motor impairment in individuals with TIA and provide a new perspective for future early diagnosis and intervention for TIA.