Neural Plasticity
 Journal metrics
Acceptance rate45%
Submission to final decision82 days
Acceptance to publication40 days
CiteScore3.330
Impact Factor3.591
 Submit

Effect of Electroacupuncture Treatment at Dazhui (GV14) and Mingmen (GV4) Modulates the PI3K/AKT/mTOR Signaling Pathway in Rats after Spinal Cord Injury

Read the full article

 Journal profile

Neural Plasticity is an interdisciplinary journal dedicated to the publication of articles related to all aspects of neural plasticity, with special emphasis on its functional significance as reflected in behavior and in psychopathology.

 Editor spotlight

Chief Editor, Professor Baudry, is currently University Professor at Western University of Health Sciences in Pomona, CA. His research focuses on understanding the molecular/cellular mechanisms of learning and memory and neurodegeneration.

 Special Issues

We currently have a number of Special Issues open for submission. Special Issues highlight emerging areas of research within a field, or provide a venue for a deeper investigation into an existing research area.

Latest Articles

More articles
Research Article

Crocin Alleviates Pain Hyperalgesia in AIA Rats by Inhibiting the Spinal Wnt5a/β-Catenin Signaling Pathway and Glial Activation

At present, most of the drugs have little effect on the pathological process of rheumatoid arthritis (RA). Analgesia is an important measure in the treatment of RA and is also one of the criteria to determine the therapeutic effects of the disease. Some studies have found that crocin, a kind of Chinese medicine, can effectively alleviate pain sensitization in pain model rats, but the mechanism is not clear. Emerging evidence indicates that crocin may inhibit the metastasis of lung and liver cancer cells from the breast by inhibiting Wnt/β-catenin and the Wnt signaling pathway is closely related to RA. Wnt5a belongs to the Wnt protein family and was previously thought to be involved only in nonclassical Wnt signaling pathways. Recent studies have shown that Wnt5a has both stimulatory and inhibitory effects on the classical Wnt signaling pathway, and so, Wnt5a has attracted increasing attention. This study demonstrated that crocin significantly increased the mechanical thresholds of adjuvant-induced arthritis (AIA) rats, suggesting that crocin can alleviate neuropathic pain. Crocin significantly decreased the levels of pain-related factors and glial activation. Foxy5, activator of Wnt5a, inhibited the above effects of crocin in AIA rats. In addition, intrathecal injection of a Wnt5a inhibitor significantly decreased hyperalgesia in AIA rats. This research shows that crocin may alleviate neuropathic pain in AIA rats by inhibiting the expression of pain-related molecules through the Wnt5a/β-catenin pathway, elucidating the mechanism by which crocin relieves neuropathic pain and provides a new way of thinking for the treatment of AIA pain.

Clinical Study

Cerebral Blood Flow Alterations in High Myopia: An Arterial Spin Labeling Study

Objective. The aim of this study was to explore cerebral blood flow (CBF) alterations in subjects with high myopia (HM) using three-dimensional pseudocontinuous arterial spin labeling (3D-pcASL). Methods. A total of sixteen patients with bilateral HM and sixteen age- and sex-matched healthy controls (HCs) were recruited. All subjects were right-handed. Image data preprocessing was performed using SPM8 and the DPABI toolbox. Clinical parameters were acquired in the HM group. Two-sample -tests and Pearson correlation analysis were applied in this study. Results. Compared to HCs, patients with HM exhibited significantly increased CBF in the bilateral cerebellum, and no decreases in CBF were detected in the brain. However, no relationship was found between the mean CBF values in the different brain areas and the disease duration (). Conclusions. Using ASL analysis, we detected aberrant blood perfusion in the cerebellum in HM patients, contributing to a better understanding of brain abnormalities and brain plasticity through a different perspective.

Review Article

Functional Brain Plasticity Associated with ACL Injury: A Scoping Review of Current Evidence

Anterior cruciate ligament (ACL) injury is a common problem with consequences ranging from chronic joint instability to early development of osteoarthritis. Recent studies suggest that changes in brain activity (i.e., functional neuroplasticity) may be related to ACL injury. The purpose of this article is to summarize the available evidence of functional brain plasticity after an ACL injury. A scoping review was conducted following the guidelines of the Joanna Briggs Institute and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses. The terms “brain,” “activity,” “neuroplasticity,” “ACL,” “injury,” and “reconstruction” were used in an electronic search of articles in PubMed, PEDro, CINAHL, and SPORTDiscus databases. Eligible studies included the following criteria: (a) population with ACL injury, (b) a measure of brain activity, and (c) a comparison to the ACL-injured limb (contralateral leg or healthy controls). The search yielded 184 articles from which 24 were included in this review. The effect size of differences in brain activity ranged from small (0.05, ACL-injured vs. noninjured limbs) to large (4.07, ACL-injured vs. healthy control). Moreover, heterogeneity was observed in the methods used to measure brain activity and in the characteristics of the participants included. In conclusion, the evidence summarized in this scoping review supports the notion of functional neuroplastic changes in people with ACL injury. The techniques used to measure brain activity and the presence of possible confounders, as identified and reported in this review, should be considered in future research to increase the level of evidence for functional neuroplasticity following ACL injury.

Research Article

Altered Brain Structure and Functional Connectivity Associated with Pubertal Hormones in Girls with Precocious Puberty

Pubertal hormones play an important role in brain and psychosocial development. However, the role of abnormal HPG axis states in altering brain function and structure remains unclear. The present study is aimed at determining whether there were significant differences in gray matter volume (GMV) and resting state (RS) functional connectivity (FC) patterns in girls with idiopathic central precocious puberty (CPP) and peripheral precocious puberty (PPP). We further explored the correlation between these differences and serum pubertal hormone levels. To assess this, we recruited 29 idiopathic CPP girls and 38 age-matched PPP girls. A gonadotropin-releasing hormone (GnRH) stimulation test was performed, and pubertal hormone levels (including luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E2), prolactin, and cortisol) were assessed. All subjects underwent multimodal magnetic resonance imaging of brain structure and function. Voxel-based morphometry (VBM) analysis was paired with seed-to-voxel whole-brain RS-FC analysis to calculate the GMV and RS-FC in idiopathic CPP and PPP girls. Correlation analyses were used to assess the effects of pubertal hormones on brain regions with structural and functional differences between the groups. We found that girls with CPP exhibited decreased GMV in the left insula and left fusiform gyrus, while connectivity between the left and right insula and the right middle frontal gyrus (MFG), as well as the left fusiform gyrus and right amygdala, was reduced in girls with CPP. Furthermore, the GMV of the left insula and peak FSH levels were negatively correlated while higher basal and peak E2 levels were associated with increased bilateral insula RS-FC. These findings suggest that premature activation of the HPG axis and pubertal hormone fluctuations alter brain structure and function involved in the cognitive and emotional process in early childhood. These findings provide vital insights into the early pathophysiology of idiopathic CPP.

Research Article

Changes in the Fluorescence Tracking of NaV1.6 Protein Expression in a BTBR T+Itpr3tf/J Autistic Mouse Model

The axon initial segment (AIS), the site of action potential initiation in neurons, is a critical determinant of neuronal excitability. Growing evidence indicates that appropriate recruitment of the AIS macrocomplex is essential for synchronized firing. However, disruption of the AIS structure is linked to the etiology of multiple disorders, including autism spectrum disorder (ASD), a condition characterized by deficits in social communication, stereotyped behaviors, and very limited interests. To date, a complete understanding of the molecular components that underlie the AIS in ASD has remained elusive. In this research, we examined the AIS structure in a BTBR T+Itpr3tf/J mouse model (BTBR), a valid model that exhibits behavioral, electrical, and molecular features of autism, and compared this to the C57BL/6J wild-type control mouse. Using Western blot studies and high-resolution confocal microscopy in the prefrontal frontal cortex (PFC), our data indicate disrupted expression of different isoforms of the voltage-gated sodium channels (NaV) at the AIS, whereas other components of AIS such as ankyrin-G and fibroblast growth factor 14 (FGF14) and contactin-associated protein 1 (Caspr) in BTBR were comparable to those in wild-type control mice. A Western blot assay showed that BTBR mice exhibited a marked increase in different sodium channel isoforms in the PFC compared to wild-type mice. Our results provide potential evidence for previously undescribed mechanisms that may play a role in the pathogenesis of autistic-like phenotypes in BTBR mice.

Review Article

The Role of Descending Pain Modulation in Chronic Primary Pain: Potential Application of Drugs Targeting Serotonergic System

Chronic primary pain (CPP) is a group of diseases with long-term pain and functional disorders but without structural or specific tissue pathologies. CPP is becoming a serious health problem in clinical practice due to the unknown cause of intractable pain and high cost of health care yet has not been satisfactorily addressed. During the past decades, a significant role for the descending pain modulation and alterations due to specific diseases of CPP has been emphasized. It has been widely established that central sensitization and alterations in neuroplasticity induced by the enhancement of descending pain facilitation and/or the impairment of descending pain inhibition can explain many chronic pain states including CPP. The descending serotonergic neurons in the raphe nuclei target receptors along the descending pain circuits and exert either pro- or antinociceptive effects in different pain conditions. In this review, we summarize the possible underlying descending pain regulation mechanisms in CPP and the role of serotonin, thus providing evidence for potential application of analgesic medications based on the serotonergic system in CPP patients.

Neural Plasticity
 Journal metrics
Acceptance rate45%
Submission to final decision82 days
Acceptance to publication40 days
CiteScore3.330
Impact Factor3.591
 Submit