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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.
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.
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Emergence of Beta Oscillations of a Resonance Model for Parkinson’s Disease
In Parkinson’s disease, the excess of beta oscillations in cortical-basal ganglia (BG) circuits has been correlated with normal movement suppression. In this paper, a physiologically based resonance model, generalizing an earlier model of the STN-GPe circuit, is employed to analyze critical dynamics of the occurrence of beta oscillations, which correspond to Hopf bifurcation. With the experimentally measured parameters, conditions for the occurrence of Hopf bifurcation with time delay are deduced by means of linear stability analysis, center manifold theorem, and normal form analysis. It is found that beta oscillations can be induced by increasing synaptic transmission delay. Furthermore, it is revealed that the oscillations originate from interaction among different synaptic connections. Our analytical results are consistent with the previous experimental and simulating findings, thus may provide a more systematic insight into the mechanisms underlying the transient beta bursts.
Does Measurement of Corticospinal Tract Involvement Add Value to Clinical Behavioral Biomarkers in Predicting Motor Recovery after Stroke?
Background. The prediction of motor recovery after stroke is an important issue, and various prediction models have been proposed using either clinical behavioral or neurological biomarkers. This study sought to identify the effects of clinical behavioral biomarkers combined with corticospinal tract (CST) injury measurement on the prediction of motor recovery after stroke. Methods. The region of interest was drawn on the normalized brain magnetic resonance imaging scans of patients with first-ever unilateral hemispheric stroke, and the degree of CST injury was calculated in a total of 67 such subjects. Patients who had initial minor deficits and showed a ceiling effect on motor recovery were excluded. To predict the follow-up Fugl-Meyer assessment (FMA) scores, correlation and regression analyses were performed using various clinical behavioral biomarkers, including age, sex, lesion location, and initial FMA scores and CST injury measurements. Results. Only the initial FMA-upper extremity (UE) score was statistically correlated with the follow-up FMA-UE score at ≥2 months after the onset (adjusted ), and the relationship between CST injury and follow-up FMA-UE score was unclear (). Hierarchical clustering between the initial and follow-up FMA-UE scores showed three clusters. After exclusion of a cluster with an initial FMA-UE ≥ 35, the prediction of the follow-up FMA-UE score was possible by incorporating the initial FMA-UE score and CST injury measurements (). However, the explanatory power decreased (adjusted ), and the unique contribution of the CST injury (10.1%) was lower than that of the initial FMA-UE score (26.7%). With respect to the FMA-lower extremity score, CST injury was not related to recovery. Conclusions. Motor recovery of the upper and lower extremities after stroke could be predicted using the initial FMA score. CST injury was significant for the prediction of motor recovery of the upper extremity in patients with severe initial motor deficits (FMA-UE < 35); however, its portion of prediction of motor recovery was low. The prediction of poststroke motor recovery using the initial motor deficit was not improved by the addition of CST injury measurements.
Exploring Cortical Thickness Alteration in Parkinson Disease Patients with Freezing of Gaits
Background: Freezing of gait (FoG) is a disabling gait disorder that commonly occurs in advanced stages of Parkinson’s disease (PD). The neuroanatomical mechanisms underlying FoG in PD are still unclear. The present study aims to explore alterations of structural gray matter (GM) in PD patients with FoG. Method: Twenty-four PD patients with FoG (FoG+), 37 PD patients without FoG (FoG-) and 24 healthy controls (HC) were included. All subjects underwent a standardized MRI protocol. The cortical thickness (CTh), segmentation volume without ventricles (BrainSegVolNotVent) and estimated total intracranial volume (eTIV) were analysed using the FreeSurfer pipeline. Results: CTh differences were found in the right middle temporal gyrus (rMTG) generally. Compared to that in HCs, the CTh of the rMTG in both the FoG+ and FoG- groups was smaller, while no significant difference between the FoG+ and FoG- groups. Correlation analyses demonstrated a negative correlation between the CTh of the rMTG and the UPDRS part II score in PD subjects, and a borderline significant correlation between the score of Freezing of Gait Questionnaire (FoGQ) and rMTG CTh. Additionally, receiver operating characteristic curve (ROC) analysis revealed a cut-off point of CTh =3.08 mm in the rMTG that could be used to differentiate PD patients and HCs (AUC =0.79, P <0.01). There were no differences in the BrainSegVolNotVent or eTIV among the 3 groups. Conclusions: Our findings currently suggest no significant difference between FoG+ and FoG- patients in terms of structural gray matter changes. However, decreased CTh in the rMTG related to semantic control may be used as a biomarker to differentiate PD patients and HCs.
Changes in Hippocampal Plasticity in Depression and Therapeutic Approaches Influencing These Changes
Depression is a common neurological disease that seriously affects human health. There are many hypotheses about the pathogenesis of depression, and the most widely recognized and applied is the monoamine hypothesis. However, no hypothesis can fully explain the pathogenesis of depression. At present, the brain-derived neurotrophic factor (BDNF) and neurogenesis hypotheses have highlighted the important role of plasticity in depression. The plasticity of neurons and glial cells plays a vital role in the transmission and integration of signals in the central nervous system. Plasticity is the adaptive change in the nervous system in response to changes in external signals. The hippocampus is an important anatomical area associated with depression. Studies have shown that some antidepressants can treat depression by changing the plasticity of the hippocampus. Furthermore, caloric restriction has also been shown to affect antidepressant and hippocampal plasticity changes. In this review, we summarize the latest research, focusing on changes in the plasticity of hippocampal neurons and glial cells in depression and the role of BDNF in the changes in hippocampal plasticity in depression, as well as caloric restriction and mitochondrial plasticity. This review may contribute to the development of antidepressant drugs and elucidating the mechanism of depression.
Cytokine-, Neurotrophin-, and Motor Rehabilitation-Induced Plasticity in Parkinson’s Disease
Neuroinflammation and cytokine-dependent neurotoxicity appear to be major contributors to the neuropathology in Parkinson’s disease (PD). While pharmacological advancements have been a mainstay in the treatment of PD for decades, it is becoming increasingly clear that nonpharmacological approaches including traditional and nontraditional forms of exercise and physical rehabilitation can be critical adjunctive or even primary treatment avenues. Here, we provide an overview of preclinical and clinical research detailing the biological role of proinflammatory molecules in PD and how motor rehabilitation can be used to therapeutically modulate neuroinflammation, restore neural plasticity, and improve motor function in PD.
Hyperexcitability of the Nucleus Accumbens Is Involved in Noise-Induced Hyperacusis
Reduced tolerance to sound stimuli (hyperacusis) is commonly seen in tinnitus patients. Dysfunction of limbic systems, such as the nucleus accumbens (NAc), may be involved in emotional reactions to the sound stimuli in tinnitus patients. To study the functional changes in the NAc in hyperacusis, we have examined the neural activity changes of the NAc using c-Fos staining in an animal model of hyperacusis. The c-Fos staining was also examined in the medial geniculate nucleus (MGN), a central auditory pathway which has neural projections to the NAc. Postnatal rats (14 days) were exposed to loud noise (115 dB SPL, 4 hours for two consecutive days) to induce hyperacusis (). Rats without noise exposure were used as the controls (). After P35, rats in both groups were put in a behavioral training for sound detection. After they were trained to detect sound stimuli, their reaction time to noise bursts centered at 2 kHz (40-110 dB SPL) was measured. Rats in the noise group showed a significantly shorter reaction time than those in the control group to the noise bursts at high intensities, suggesting the noise exposure induced hyperacusis behavior. The c-Fos expressions in the NAc and the MGNs of the noise group were significantly higher than those of the control group. Our results suggested that early-age noise exposure caused hyperactivity in the NAc and the MGNs which may induce the loudness increase in these rats.