Journal of integrative neuroscience最新文献

Declining fertility due to ovarian dysfunction is a critical concern for population sustainability. Acupuncture shows potential for ovarian functional restoration, primarily mediated through its neuromodulatory effects on the hypothalamic-pituitary-ovarian (HPO) axis. Accumulating evidence from clinical and animal studies suggests that acupuncture modulates ovarian function through multiple neuroendocrine pathways. Specifically, acupuncture regulates hypothalamic activity by influencing the release of reproduction-associated neuropeptides (e.g., kisspeptin, neuropeptide Y, and gonadotropin-releasing hormone) and neurotransmitters (e.g., gamma-aminobutyric acid, serotonin, glutamate, and dopamine). Additionally, it may affect peripheral-to-central sensory nerve pathways as well as sympathetic and parasympathetic neural activity, which collectively enhance ovarian function. In this article, we comprehensively reviewed the neuroendocrine regulatory pathways through which acupuncture exerts its therapeutic effects in ovarian diseases, thereby providing a deeper understanding of the mechanisms involved and the directions for future research.

Background: Global developmental delay (GDD) is a common childhood neurodevelopmental disorder characterized by the core symptoms of cognitive impairment. However, the underlying neural mechanisms of the cognitive impairment remain unclear. This study aimed to both analyze differences in electroencephalography (EEG) connectivity patterns between children with GDD and typical development (TD) using brain functional connectivity and to explore the neural mechanisms linking these differences to cognitive impairment.

Methods: The study enrolled 60 children with GDD and 60 TD children. GDD participants underwent clinical assessment via the Gesell Developmental Schedule (GDS). Resting-state EEG data were subjected to brain functional connectivity analysis and graph theory metric-based network analysis, with intergroup functional differences compared. Subsequently, correlation analysis characterized the relationships between GDD subject's brain network metrics and GDS-derived cognitive developmental quotient (DQ). Finally, three support vector machine (SVM) models were constructed for GDD classification and feature weight factors were calculated to screen potential EEG biomarkers.

Results: The two groups exhibited complex differences in functional connectivity. Compared with the TD group, the GDD group showed a large number of increased functional connections in the θ, α, and γ-bands, along with a small number of decreased functional connections in the α and γ-bands (all p < 0.025). Brain network analysis revealed lower global efficiency, local efficiency, clustering coefficient and small-world coefficient, as well as higher characteristic path length in GDD children across multiple bands (all p < 0.05). Correlation analysis indicated that global efficiency and small-world coefficient in θ and γ-bands were positively correlated with the DQ, while the characteristic path length in α and γ-bands was negatively correlated with DQ in the GDD group (all p < 0.05). Machine learning models showed that a quantum particle swarm optimization SVM (QPSO-SVM) achieved the highest classification performance, with characteristic path length in the γ-band being the highest weighted metric.

Conclusions: Children with GDD exhibit abnormal patterns of brain functional connectivity, characterized by global hypo-connectivity and local hyper-connectivity. Specific network metrics under these abnormal patterns are significantly correlated with cognitive impairment in GDD. This study also highlights the potential of the γ-band characteristic path length as an EEG biomarker for diagnosing GDD.

Background: Neuroplasticity and synaptic homeostasis are essential in regulating neuronal activity and behavioral functions within the hippocampus. Alzheimer's disease (AD) is characterized by progressive cognitive decline, pathological accumulation of amyloid β (Aβ) plaques and tau neurofibrillary tangles, neuroinflammation, and synaptic dysfunction. However, the temporal progression of neuroplasticity-related impairments in the hippocampus, a region particularly vulnerable to AD pathology, is not completely understood.

Methods: This study examined age-dependent changes in behavioral performance and hippocampal structural plasticity in the 5×FAD (five familial Alzheimer's disease) mouse model at 3, 6, and 12 months of age.

Results: The 5×FAD mice exhibited progressive impairments in fine motor coordination and hippocampal-dependent working memory compared to control. Corresponding increases were observed in the accumulation of Aβ and phosphorylated tau, glial activation, and inflammatory cytokine production in the hippocampus across all time points. Golgi staining revealed significant age-related reductions in dendritic complexity, including fiber crossing counts, total dendritic length, and branch points in the cornu ammonis 1 (CA1) and dentate gyrus (DG) hippocampal subregions. Dendritic spine density and morphology exhibited significant alterations in the CA1 apical/basal and DG subregions with advancing age. Furthermore, the expression of synaptic proteins, including activity-regulated cytoskeleton-associated protein (Arc) and postsynaptic density protein-95 (PSD-95), significantly declined at 6 and 12 months of age.

Conclusions: Our findings suggest a potential relationship between AD-related protein pathology, neuroinflammation, and structural plasticity impairments in the hippocampus. Collectively, these changes may contribute to disrupted synaptic transmission and behavioral deficits associated with AD pathology.

Background: There are divergent viewpoints on how Chinese compound words undergo morphological processing-especially regarding the role and timing of morphemic semantics during word recognition. Whether-and in what way-lexical and sublexical semantics influence the recognition of Chinese compound words remains unclear; this issue is central to the debate between form-then-meaning and form-and-meaning processing models.

Method: We investigated morphological effects on compound processing by recording event-related potentials (ERPs) to Chinese compound targets that were preceded by five prime types: W+M+, W-M+, W-M- (W = whole-word semantics, M = morphemic meaning, "+" = congruent, "-" = incongruent), a purely semantic prime, and an unrelated prime. This design simultaneously controlled prime-target relatedness at both the morphemic and whole-word levels.

Results: The results showed that, across both the 100-300 ms and 300-500 ms windows, the W-M+ and W-M- conditions produced statistically equivalent priming effects, suggesting that the semantic content of individual morphemes contributes only minimally to recognizing the compound as a whole.

Conclusions: These findings align more closely with morphological models proposing parallel processing of form and meaning, as opposed to frameworks that assume a strictly hierarchical or step-by-step sequence.

Background: Migraine is the most common primary headache disorder encountered in clinical practice and is associated with a significantly reduced quality of life. Despite abundant research, the underlying pathophysiological mechanisms behind migraine development remain unclear. Literature reviews indicate that most studies utilized functional magnetic resonance imaging (fMRI) and electroencephalography (EEG), often yielding inconsistent results. In contrast magnetoencephalography (MEG) offers superior temporal and spatial resolution, making it better suited for capturing the neural dynamics underlying migraine without aura (MwoA).

Methods: MEG data were obtained from 33 migraine cases and 22 healthy controls (HC). We used Minimum norm estimation (MNE) combined with Welch's technique for spectral power analysis, and graph theory for network topology analysis.

Results: Significant group differences were observed in the theta and alpha bands spectral power, with the MwoA group exhibiting increased theta power and decreased alpha power relative to HC. Graph theory analysis revealed a higher path length in the MwoA group compared to the HC group.

Conclusions: Individuals with MwoA demonstrate distinct alterations in cortical excitability and functional network organization. These findings suggest that MwoA is associated with impaired information integration. The opposing patterns of increased and decreased cortical excitability across frequency bands further underscore the complex and multifaceted nature of MwoA pathology. These findings may contribute to a deeper understanding of the neural mechanisms and functional network disruptions underlying MwoA pathophysiology.

Background: The objective of this study was to map the topography, morphology, connectivity, and correlative anatomy of the ansa lenticularis (AL) in the human brain since there is a paucity of direct structural evidence from cadaveric studies.

Methods: Twenty normal adult formalin-fixed cerebral hemispheres were treated with Klingler's method and subsequently explored through the fiber microdissection technique. Basal and medial dissections focusing on the anterior perforated substance, subthalamic, and mesencephalic areas were carried out in a stepwise manner. Hemispheric asymmetries were recorded, and the spatial relationship of the AL with the surrounding fiber tracts and nuclei was investigated.

Results: The AL and its segments were consistently identified sweeping around the cerebral peduncle in a medial direction posterior to the anterior commissure and dorsal to the optic tract and ansa peduncularis after arising from the ventral-posterior margin of the globus pallidus. Then it made an almost right angle to reach the thalamus (dorsal segment), subthalamic nucleus (dorsal segment), red nucleus (middle segment), and substantia nigra (ventral segment), respectively. Additionally, the dorsal segment of the AL intermingled with the fasciculus lenticularis (FL) at the level of the zona incerta (ZI) to form the thalamic fasciculus (H1 field of Forel), which travelled slightly lateral to the cerebellothalamic fibers, ascended through the prerubral field, and terminated in the area of the anterior and ventral thalamus.

Conclusions: We provide structural evidence of the topography, morphology, and connectional anatomy of the ansa lenticularis. From our review of the literature this is the first cadaveric study using white matter microdissection to delineate the comprehensive composition of the ansa lenticularis. Fiber microdissection studies are integral for the extrapolation of accurate anatomical conclusions which subsequently inform clinical practice. Combined with tractography and histology, these studies enhance our understanding of delicate pathways that can act as surgical targets in fields such as stereotactic neurosurgery.

Background: Hypothalamic corticotropin-releasing factor (CRF) has been implicated in the formation of false contextual fear memory. Here, we examined the involvement of glucocorticoid (GR) and mineralocorticoid receptors (MR) in this process.

Methods: Adult male C57BL/6J mice were exposed to Context B, similar but distinct from Context A, 3 h (B-3 h) after electric foot shock (FS) in Context A, and re-exposed to Context B either 24 h (B-24 h) or 9 days (B-9 d) after FS in Context A. To assess the effect of B-3 h exposure on the specificity of original memory, freezing levels were also measured in Context A (A-24 h or A-9 d) in a separate group, following the B-3 h exposure after FS. GR and MR protein levels in the hippocampal nuclear fractions were analyzed by western blotting. In pharmacological studies, dexamethasone (a GR agonist), fludrocortisone (an MR agonist), and mifepristone (a GR antagonist) were subcutaneously administered to hypothalamic CRF knockdown mice.

Results: When mice were exposed to B-3 h after FS, they exhibited increased freezing at B-24 h compared with B-3 h and showed further increases at B-9 d compared with B-24 h, indicating a time-dependent intensification of false contextual fear memory. In contrast, freezing behavior in Context A was reduced at A-24 h and A-9 d after B-3 h exposure compared with mice that were not exposed to B-3 h, suggesting diminished precision of the original memory. Immunoblotting revealed increased nuclear GR levels at B-3 h and decreased MR levels at B-24 h and B-9 d. In CRF knockdown mice, dexamethasone enhanced freezing at B-3 h, whereas fludrocortisone reduced freezing at B-24 h and B-9 d. Co-administration of mifepristone and fludrocortisone suppressed both the formation of false memory at B-3 h and its subsequent enhancement. However, this treatment increased freezing in Context A at A-24 h and A-9 d following B-3 h exposure.

Conclusion: Exposure to a similar but distinct context shortly after FS induces false contextual fear memory via GR activation and promotes its time-dependent potentiation through MR inactivation. Such early exposure may also impair the specificity of the original fear memory.

Encoding a key 'hub' scaffolding protein, the 'Disrupted-In-Schizophrenia-1' (DISC1) gene has been strongly implicated in brain development and functions. Genetic variance in this gene is associated with major neuropsychiatric disorders, including schizophrenia, bipolar disorder, and major depression. DISC1 is abundantly expressed in the brain of humans and various model organisms. Here, we discuss currently available animal models of DISC1-related brain deficits and their clinical relevance. We focus on evolutionarily conserved (shared) mechanisms and species-specific phenotypes, especially in newly developed zebrafish (Danio rerio) models, to better understand the uniquely complex role of DISC1 in the molecular pathogenesis of neurobehavioral abnormalities relevant to human neuropsychiatric disorders.