Changes In Neural Plasticity Research Articles

Impact of Weekly Community-Based Dance Training Over 8 Months on Depression and Blood Oxygen Level-Dependent Signals in the Subcallosal Cingulate Gyrus for People With Parkinson Disease: Observational Study.

Dance has emerged as a complementary treatment that may promote adaptive neural plasticity while improving symptoms of Parkinson disease (PD), such as balance, gait, posture, and walking. Understanding brain changes that arise from participation in dance interventions is important as these neural plastic changes play an important role in protecting and healing the brain. Although dance has been shown to improve PD motor and nonmotor symptoms, the neural mechanisms underlying these changes, specifically depression and mood, remain elusive. Further, many side effects of PD drug treatments can be exacerbated or even induced by dopaminergic drugs, particularly depression and anxiety, making these nonmotor symptoms more noticeable throughout the progression of the disease. In this study, we focused on the impact of dance interventions on PD nonmotor symptoms by conducting an 8-month observational study, tracking the relationship between depression scores and functional neuroimaging measures for people with PD. A total of 34 dancers-23 (68%) people with PD and 11 (32%) healthy controls-completed the Geriatric Depression Scale (GDS) before and after attending weekly community-based dance classes, referred to as Dance for PD classes. Specifically, we examined changes within the functional magnetic resonance imaging signal from the subcallosal cingulate gyrus (SCG), an important node within the depression network and a controversial target for deep brain stimulation in the treatment of major depressive disorder. Depression scores on the GDS decreased in each preintervention to postintervention comparison (all P<.025). In addition, GDS scores also improved over the 8-month dance period (all P<.01). Blood oxygen level-dependent signals from frontal cortex brain region implicated for emotional regulation within the SCG decreased at each testing time point (all P<.05). Also, a significant decrease in depression scores (GDS) was correlated with reduced blood oxygen level-dependent signals from the SCG (P=.02). This study contributes to an improved understanding of the neural mechanisms that are involved in depression, as well as the beneficial contribution that longitudinal dance interventions have in reducing nonmotor symptoms associated with PD, particularly in depression symptoms.

Effects of high-definition tDCS targeting individual motor hotspot with EMG-driven robotic hand training on upper extremity motor function: a pilot randomized controlled trial

BackgroundDelivering HD-tDCS on individual motor hotspot with optimal electric fields could overcome challenges of stroke heterogeneity, potentially facilitating neural activation and improving motor function for stroke survivors. However, the intervention effect of this personalized HD-tDCS has not been explored on post-stroke motor recovery. In this study, we aim to evaluate whether targeting individual motor hotspot with HD-tDCS followed by EMG-driven robotic hand training could further facilitate the upper extremity motor function for chronic stroke survivors.MethodsIn this pilot randomized controlled trial, eighteen chronic stroke survivors were randomly allocated into two groups. The HDtDCS-group (n = 8) received personalized HD-tDCS using task-based fMRI to guide the stimulation on individual motor hotspot. The Sham-group (n = 10) received only sham stimulation. Both groups underwent 20 sessions of training, each session began with 20 min of HD-tDCS and was then followed by 60 min of robotic hand training. Clinical scales (Fugl-meyer Upper Extremity scale, FMAUE; Modified Ashworth Scale, MAS), and neuroimaging modalities (fMRI and EEG-EMG) were conducted before, after intervention, and at 6-month follow-up. Two-way repeated measures analysis of variance was used to compare the training effect between HDtDCS- and Sham-group.ResultsHDtDCS-group demonstrated significantly better motor improvement than the Sham-group in terms of greater changes of FMAUE scores (F = 6.5, P = 0.004) and MASf (F = 3.6, P = 0.038) immediately and 6 months after the 20-session intervention. The task-based fMRI activation significantly shifted to the ipsilesional motor area in the HDtDCS-group, and this activation pattern increasingly concentrated on the motor hotspot being stimulated 6 months after training within the HDtDCS-group, whereas the increased activation is not sustainable in the Sham-group. The neuroimaging results indicate that neural plastic changes of the HDtDCS-group were guided specifically and sustained as an add-on effect of the stimulation.ConclusionsStimulating the individual motor hotspot before robotic hand training could further enhance brain activation in motor-related regions that promote better motor recovery for chronic stroke.Trial registrationThis study was retrospectively registered in ClinicalTrials.gov (ID NCT05638464).

Acoustic Processing and the Origin of Human Vocal Communication

Humans have inherited from their remotest mammalian ancestors an integration of the sensory and motor systems that permits the exchange of signals and information, led by an instinctive response to harmonicity. The transition, from capacity for animal communication involving calls, facial expression and gestures, to modern human culture that embraces language, music, and dance, has resulted from anatomical adaptations such as upright posture, a distinct oro-facial and respiratory tract arrangement, and important changes in neural architecture, connectivity and plasticity. A key development on which modern human vocal abilities depend was the achievement of a feedback loop between the perception and production of voiced sound that allows precise matching, imitation, and meaningful variation, of the acoustic properties: fundamental frequency, duration, amplitude, and timbre; all contributing to the capacity to coordinate simultaneous participation. These are the four specific properties that influence our sensations of sound. They play parallel and complementary roles in both language and vocal music, represented in blended synchrony such as unison song and collective speech as well as temporally organised and coordinated sequences such as call-and-response and polyphony. In turn, responding especially to the properties of the Harmonic Series, such features inform the musical employment of tools – musical instruments – that make use of materials available in the local environment (skin, bone, stone, bamboo, wood, etc.) to provide increased range and loudness as well as alternative timbres to those produced by the voice. We propose a framework by which the adaptations essential to such universal behaviours may have arisen, drawing on an extensive and varied literature to explore the potential of this position for illuminating the nature of human musicality and its relationship to language development.

Exploring the versatility of miRNA-128: a comprehensive review on its role as a biomarker and therapeutic target in clinical pathways.

MicroRNAs (miRNAs/ miRs) are short, noncoding RNAs, usually consisting of 18 to 24 nucleotides, that control gene expression after the process of transcription and have crucial roles in several clinical processes. This article seeks to provide an in-depth review and evaluation of the many activities of miR-128, accentuating its potential as a versatile biomarker and target for therapy; The circulating miR-128 has garnered interest because of its substantial influence on gene regulation and its simplicity in extraction. Several miRNAs, such as miR-128, have been extracted from circulating blood cells, cerebrospinal fluid, and plasma/serum. The miR-128 molecule can specifically target a diverse range of genes, enabling it to have intricate physiological impacts by concurrently regulating many interrelated pathways. It has a vital function in several biological processes, such as modulating the immune system, regulating brain plasticity, organizing the cytoskeleton, and inducing neuronal death. In addition, miR-128 modulates genes associated with cell proliferation, the cell cycle, apoptosis, plasma LDL levels, and gene expression regulation in cardiac development. The dysregulation of miR-128 expression and activity is associated with the development of immunological responses, changes in neural plasticity, programmed cell death, cholesterol metabolism, and heightened vulnerability to autoimmune illnesses, neuroimmune disorders, cancer, and cardiac problems; The paper highlights the importance of studying the consequences of miR-128 dysregulation in these specific locations. By examining the implications of miRNA-128 dysregulation in these areas, the article underscores its significance in diagnosis and treatment, providing a foundation for research and clinical applications.

Bidirectional remodeling of the central auditory system caused by unilateral auditory deprivation.

Unilateral auditory deprivation (UAD) results in cross-modal reorganization of the auditory cortex (AC), which can impair auditory and cognitive functions and diminish the recovery effect of cochlear implantation. Moreover, the subcortical areas provide extensive ascending projections to the AC. To date, a thorough systematic study of subcortical auditory neural plasticity has not been undertaken. Therefore, this review aims to summarize the current evidence on the bidirectional remodeling of the central auditory system caused by UAD, particularly the changes in subcortical neural plasticity. Lateral changes occur in the cochlear nucleus, lateral superior olive, medial nucleus of the trapezoid body, inferior colliculus, and AC of individuals with UAD. Moreover, asymmetric neural activity becomes less prominent in the higher auditory nuclei, which may be due to cross-projection regulation of the bilateral pathway. As a result, subcortical auditory neural plasticity caused by UAD may contribute to the outcomes of cochlear implantation in patients with single-sided deafness (SSD), and the development of intervention strategies for patients with SSD is crucial. Considering that previous studies have focused predominantly on the neural plasticity of the AC, we believe that bidirectional remodeling of subcortical areas after UAD is also crucial for investigating the mechanisms of interventions.

Andrographolide exhibits antinociceptive effects in neuropathic rats via inhibiting class Ⅱ MHC associated response and regulating synaptic plasticity

BackgroundNeuropathic pain (NP) due to nerve injury, disrupts neural plasticity by triggering the release of inflammatory mediators. Alongside the hypothesis that neuro-inflammation contributes to this disruption, Andrographolide (Andro), a traditional bioactive compound derived from Andrographis paniculata, has garnered attention for its potent anti-inflammatory properties. However, whether Andro could ameliorate NP by regulating neuroinflammation remains unknown. PurposeThis study aimed to investigate whether and how Andro regulates neuroinflammation and alleviates NP. MethodsThe analgesic effects of Andro on NP were evaluated using both the spinal nerve ligation (SNL) and formalin rat models. A combination of network pharmacology, RNA sequencing, and experimental validation was employed to elucidate the underlying mechanism behind Andro's analgesic effects. Additionally, various techniques such as functional ultrasound, immunohistochemistry, quantitative real-time polymerase chain reaction (qPCR), patch clamp, and electron microscopy were employed to investigate the specific neural cell types, neural functions, and changes in neural plasticity influenced by Andro. ResultsNetwork pharmacology analysis unveiled the crucial roles played by shared targets of Andro and pain in regulating pain-related inflammation, including microglia activation, neuroinflammation, immune modulation, and synaptic transmission. Furthermore, we confirmed Andro's superior efficacy in pain relief compared to the traditional analgesic drug, Gabapentin. In these models, Andro was observed to modulate the haemodynamic response triggered by SNL. Transcriptome analysis and molecular docking studies indicated the involvement of major histocompatibility complex class II (MHCII) genes (Db1, Da, and Bb). Electron microscopy revealed improvements in synaptic ultrastructure, and electrophysiological investigations showed a selective reduction in glutamatergic transmission in neuropathic rats after following Andro treatment. The integration of systems pharmacology analysis and biological validation collectively demonstrated that the mechanism of pain relief involves immune modulation, enhancement of synaptic plasticity, and precise regulation of excitatory neurotransmission. ConclusionIn conclusion, this study has demonstrated that Andro, by targeting MHCII genes, may serve as a promising therapeutic candidate for neuropathic pain.

Trigeminal neuralgia.

Trigeminal neuralgia (TN) is a facial pain disorder characterized by intense and paroxysmal pain that profoundly affects quality of life and presents complex challenges in diagnosis and treatment. TN can be categorized as classical, secondary and idiopathic. Epidemiological studies show variable incidence rates and an increased prevalence in women and in the elderly, with familial cases suggesting genetic factors. The pathophysiology of TN is multifactorial and involves genetic predisposition, anatomical changes, and neurophysiological factors, leading to hyperexcitable neuronal states, central sensitization and widespread neural plasticity changes. Neurovascular compression of the trigeminal root, which undergoes major morphological changes, and focal demyelination of primary trigeminal afferents are key aetiological factors in TN. Structural and functional brain imaging studies in patients with TN demonstrated abnormalities in brain regions responsible for pain modulation and emotional processing of pain. Treatment of TN involves a multifaceted approach that considers patient-specific factors, including the type of TN, with initial pharmacotherapy followed by surgical options if necessary. First-line pharmacological treatments include carbamazepine and oxcarbazepine. Surgical interventions, including microvascular decompression and percutaneous neuroablative procedures, can be considered at an early stage if pharmacotherapy is not sufficient for pain control or has intolerable adverse effects or contraindications.

Decoded EEG neurofeedback-guided cognitive reappraisal training for emotion regulation.

Neurofeedback, when combined with cognitive reappraisal, offers promising potential for emotion regulation training. However, prior studies have predominantly relied on functional magnetic resonance imaging, which could impede its clinical feasibility. Furthermore, these studies have primarily focused on reducing negative emotions while overlooking the importance of enhancing positive emotions. In our current study, we developed a novel electroencephalogram (EEG) neurofeedback-guided cognitive reappraisal training protocol for emotion regulation. We recruited forty-two healthy subjects (20 females; 22.4 ± 2.2 years old) who were randomly assigned to either the neurofeedback group or the control group. We evaluated the efficacy of this newly proposed neurofeedback training approach in regulating emotions evoked by pictures with different valence levels (low positive and high negative). Initially, we trained an EEG-based emotion decoding model for each individual using offline data. During the training process, we calculated the subjects' real-time self-regulation performance based on the decoded emotional states and fed it back to the subjects as feedback signals. Our results indicate that the proposed decoded EEG neurofeedback-guided cognitive reappraisal training protocol significantly enhanced emotion regulation performance for stimuli with low positive valence. Additionally, wavelet energy and differential entropy features in the high-frequency band played a crucial role in emotion classification and were associated with neural plasticity changes induced by emotion regulation. These findings validate the beneficial effects of the proposed EEG neurofeedback protocol and offer insights into the neural mechanisms underlying its training effects. This novel decoded neurofeedback training protocol presents a promising cost-effective and non-invasive treatment technique for emotion-related mental disorders.

Mirror Therapy Reduces Pain and Preserves Corticomotor Excitability in Human Experimental Skeletal Muscle Pain.

Approaches to preserve corticomotor excitability (CE) are attracting interest as a treatment for pain-induced changes in neural plasticity. We determined the effects of mirror therapy (MT) on skeletal muscle pain. Fifteen healthy adults who received hypertonic saline injections (5.8% NaCl, 0.2 mL) into the first dorsal interosseous (FDI) muscle of the right hand to induce experimental skeletal muscle pain were assigned to either the "MT and injection" or "injection only" group. Post-injection, the "MT and injection" group observed their left index finger abducting and adducting for 4 min, creating the illusion that the right index finger was moving. The "injection only" group remained at rest. CE and pain were assessed by measuring motor-evoked potentials (MEPs) of the right FDI triggered by transcranial magnetic stimulation and the numerical rating scale (NRS), respectively. MEP amplitudes were significantly higher in the "MT and injection" group, a trend that persisted post-MT intervention (MT intervention; p < 0.01, post-1; p < 0.05). The time for the NRS score to reach 0 was notably shorter in the "MT and injection" group (p < 0.05). Our preliminary results suggested that MT decreases CE and pain in skeletal muscles, potentially preventing neural plasticity changes associated with skeletal muscle pain and providing early pain relief.

Cognitive Dysfunction and Exercise: From Epigenetic to Genetic Molecular Mechanisms.

Maintaining good health is crucial, and exercise plays a vital role in achieving this goal. It offers a range of positive benefits for cognitive function, regardless of age. However, as our population ages and life expectancy increases, cognitive impairment has become a prevalent issue, often coexisting with age-related neurodegenerative conditions. This can result in devastating consequences such as memory loss, difficulty speaking, and confusion, greatly hindering one's ability to lead an ordinary life. In addition, the decrease in mental capacity has a significant effect on an individual's physical and emotional well-being, greatly reducing their overall level of contentment and causing a significant financial burden for communities. While most current approaches aim to slow the decline of cognition, exercise offers a non-pharmacological, safe, and accessible solution. Its effects on cognition are intricate and involve changes in the brain's neural plasticity, mitochondrial stability, and energy metabolism. Moreover, exercise triggers the release of cytokines, playing a significant role in the body-brain connection and its impact on cognition. Additionally, exercise can influence gene expression through epigenetic mechanisms, leading to lasting improvements in brain function and behavior. Herein, we summarized various genetic and epigenetic mechanisms that can be modulated by exercise in cognitive dysfunction.

The Effect and Mechanism of Mindfulness Training on Psychological Stress in College School Students

This present research delves into the multifaceted world of mindfulness, exploring its definition and emphasizing its pivotal role in promoting mental health, especially for the utilisation of college students. Investigating various research methodologies, including behavioral and neuroimaging studies, the paper unveils the effects of mindfulness on psychological well-being. Noteworthy findings include compelling evidence supporting its ability to reduce stress and anxiety, enhance emotional regulation, and bolster resilience and coping mechanisms. The article further dissects the intricate mechanisms underlying mindfulness, encompassing psychological aspects such as exposure and confrontation, acceptance of experiences, and changes in thinking patterns, as well as neurological factors like impacts on brain structure and function, neural plasticity, cognitive enhancement, and neurochemical changes associated with the stress response. In conclusion, the article underscores the significance of mindfulness in fostering mental well-being, providing a succinct summary of observed effects and mechanisms. It also acknowledges study limitations and proposes potential future research directions, underscoring the enduring relevance of mindfulness in advancing mental health across diverse populations.

Mindfulness-based therapy improves brain functional network reconfiguration efficiency

Mindfulness-based interventions are showing increasing promise as a treatment for psychological disorders, with improvements in cognition and emotion regulation after intervention. Understanding the changes in functional brain activity and neural plasticity that underlie these benefits from mindfulness interventions is thus of interest in current neuroimaging research. Previous studies have found functional brain changes during resting and task states to be associated with mindfulness both cross-sectionally and longitudinally, particularly in the executive control, default mode and salience networks. However, limited research has combined information from rest and task to study mindfulness-related functional changes in the brain, particularly in the context of intervention studies with active controls. Recent work has found that the reconfiguration efficiency of brain activity patterns between rest and task states is behaviorally relevant in healthy young adults. Thus, we applied this measure to investigate how mindfulness intervention changed functional reconfiguration between rest and a breath-counting task in elderly participants with self-reported sleep difficulties. Improving on previous longitudinal designs, we compared the intervention effects of a mindfulness-based therapy to an active control (sleep hygiene) intervention. We found that mindfulness intervention improved self-reported mindfulness measures and brain functional reconfiguration efficiency in the executive control, default mode and salience networks, though the brain and behavioral changes were not associated with each other. Our findings suggest that neuroplasticity may be induced through regular mindfulness practice, thus bringing the intrinsic functional configuration in participants’ brains closer to a state required for mindful awareness.

THE INFLUENCE OF A PERIPHERAL TUMOR ON THE BEHAVIOR OF ANIMALS AND THE STRUCTURE OF NEURONS IN THE PREFRONTAL CORTEX

Melanoma is the most aggressive of the common forms of skin cancer. Proinflammatory cytokines produced by the tumor and delivered via the circulatory and lymphatic systems can lead to damage to the structures of the central nervous system. Damage to the blood-brain barrier and the endothelium of blood capillaries can cause dysfunction of neurons in the cerebral cortex, induce changes in neural plasticity, cognitive functions and result in the development of depression. Depression is observed in 20% of the cancer patients, and it affects quality of life, treatment effectiveness and survival. Depression has been linked to damage to the prefrontal cortex, which plays an important role in many brain functions, including cognition, emotion regulation, motivation and sociability.

Neural Plasticity Changes Induced by Motor Robotic Rehabilitation in Stroke Patients: The Contribution of Functional Neuroimaging.

Robotic rehabilitation is one of the most advanced treatments helping people with stroke to faster recovery from motor deficits. The clinical impact of this type of treatment has been widely defined and established using clinical scales. The neurofunctional indicators of motor recovery following conventional rehabilitation treatments have already been identified by previous meta-analytic investigations. However, a clear definition of the neural correlates associated with robotic neurorehabilitation treatment has never been performed. This systematic review assesses the neurofunctional correlates (fMRI, fNIRS) of cutting-edge robotic therapies in enhancing motor recovery of stroke populations in accordance with PRISMA standards. A total of 7, of the initial yield of 150 articles, have been included in this review. Lessons from these studies suggest that neural plasticity within the ipsilateral primary motor cortex, the contralateral sensorimotor cortex, and the premotor cortices are more sensitive to compensation strategies reflecting upper and lower limbs' motor recovery despite the high heterogeneity in robotic devices, clinical status, and neuroimaging procedures. Unfortunately, the paucity of RCT studies prevents us from understanding the neurobiological differences induced by robotic devices with respect to traditional rehabilitation approaches. Despite this technology dating to the early 1990s, there is a need to translate more functional neuroimaging markers in clinical settings since they provide a unique opportunity to examine, in-depth, the brain plasticity changes induced by robotic rehabilitation.

Neuropharmacological insight into preventive intervention in posttraumatic epilepsy based on regulating glutamate homeostasis.

Posttraumatic epilepsy (PTE) is one of the most critical complications of traumatic brain injury (TBI), significantly increasing TBI patients' neuropsychiatric symptoms and mortality. The abnormal accumulation of glutamate caused by TBI and its secondary excitotoxicity are essential reasons for neural network reorganization and functional neural plasticity changes, contributing to the occurrence and development of PTE. Restoring glutamate balance in the early stage of TBI is expected to play a neuroprotective role and reduce the risk of PTE. To provide a neuropharmacological insight for drug development to prevent PTE based on regulating glutamate homeostasis. We discussed how TBI affects glutamate homeostasis and its relationship with PTE. Furthermore, we also summarized the research progress of molecular pathways for regulating glutamate homeostasis after TBI and pharmacological studies aim to prevent PTE by restoring glutamate balance. TBI can lead to the accumulation of glutamate in the brain, which increases the risk of PTE. Targeting the molecular pathways affecting glutamate homeostasis helps restore normal glutamate levels and is neuroprotective. Taking glutamate homeostasis regulation as a means for new drug development can avoid the side effects caused by direct inhibition of glutamate receptors, expecting to alleviate the diseases related to abnormal glutamate levels in the brain, such as PTE, Parkinson's disease, depression, and cognitive impairment. It is a promising strategy to regulate glutamate homeostasis through pharmacological methods after TBI, thereby decreasing nerve injury and preventing PTE.

The Effect of Physical Exercise on People with Psychosis: A Qualitative Critical Review of Neuroimaging Findings.

Recently, genuine motor abnormalities have been recognized as prodromal and predictive signs of psychosis onset and progression. Therefore, physical exercise could represent a potentially relevant clinical tool in promoting the reshaping of neural connections in motor circuitry. The aim of this review is to provide an overview of the literature on neuroimaging findings as a result of physical treatment in psychosis cohorts. Twenty-one studies, all research articles, were included and discussed in this narrative review. Here, we first outlined how the psychotic brain is susceptible to structural plastic changes after aerobic physical training in pathognomic brain areas (i.e., temporal, hippocampal and parahippocampal regions). Secondly, we focused on functional changes, both region-specific and in terms of connections, to gain insights into the involvement of distant but inter-related neural regions in the plastic process occurring after treatment. Third, we attempted to bridge neural plastic changes occurring after physical interventions with clinical and cognitive outcomes of psychotic patients in order to assess the relevance of such neural reshaping in the psychiatric rehabilitation field. In conclusion, we suggest that the current state of the art is presenting physical intervention as effective in promoting neural changes for patients with psychosis; it is not only useful at the onset of the pathology but also in improving the course of the illness and its functional outcome. However, more evidence is needed to improve our knowledge of the efficacy of physical exercise in plastically reorganizing the psychotic brain in the long term, especially within regions lacking specific investigations, such as motor circuitry.

Neural plasticity and depression treatment.

Depression is one of the most common mental disorders, which can lead to a variety of emotional problems and even suicide at its worst. As this neuropsychiatric disorder causes the patients to suffer a lot and function poorly in everyday life, it is imposing a heavy burden on the affected families and the whole society. Several hypotheses have been proposed to elucidate the pathogenesis of depression, such as the genetic mutations, the monoamine hypothesis, the hypothalamic-pituitary-adrenal (HPA) axis hyperactivation, the inflammation and the neural plasticity changes. Among these models, neural plasticity can occur at multiple levels from brain regions, cells to synapses structurally and functionally during development and in adulthood. In this review, we summarize the recent progresses (especially in the last five years) on the neural plasticity changes in depression under different organizational levels and elaborate different treatments for depression by changing the neural plasticity. We hope that this review would shed light on the etiological studies for depression and on the development of novel treatments.

Changes in Visual Long-Term Potentiation Show Preserved Cyclicity in Human Females Taking Combined Oral Contraceptives

Introduction: The combined oral contraceptive (COC) pill is often employed to address physical and neurological symptoms in menstrual cycle-related disorders by suppressing shifts in endogenous gonadal hormone fluctuations. Symptom persistence, especially in the lead up to the hormone-free interval (HFI), suggests an underlying neurobiological mechanism of preserved cycling. Our study utilised a non-invasive method of visually inducing long-term potentiation (LTP) to index changes in neural plasticity in the absence of hormonal fluctuations. Methods: Visually induced LTP was recorded using electroencephalography in 24 healthy female COC users across three sessions: days 3 and 21 during active hormone pills, and day 24 during the HFI. The Daily Record of the Severity of Problems (DRSP) questionnaire tracked premenstrual symptoms. Dynamic causal modelling (DCM) was used to elucidate the neural connectivity and receptor activity changes associated with LTP across different days of COC. Results: Visually induced LTP was greater on day 21 than day 3 (p = 0.011) and was localised to the P2 visually evoked potential. There was no effect of the HFI (day 24) on LTP. DCM of differences between days 3 and 21 showed changes to inhibitory interneuronal gating of LTP in cortical layer VI. The DRSP only showed a significant increase in symptoms in the HFI, meaning the LTP result appeared more sensitive to cyclicity. Conclusions: This study provides objective evidence of preserved cyclicity in COC users through enhanced LTP on day 21 compared to day 3 of a 28-day COC regimen, indicating that relatively higher excitation in the brain despite peripheral gonadal suppression may underlie and exacerbate menstrual cycle-related disorders.

Plasticity After Hearing Rehabilitation in the Aging Brain.

Age-related hearing loss, presbycusis, is an unavoidable sensory degradation, often associated with the progressive decline of cognitive and social functions, and dementia. It is generally considered a natural consequence of the inner-ear deterioration. However, presbycusis arguably conflates a wide array of peripheral and central impairments. Although hearing rehabilitation maintains the integrity and activity of auditory networks and can prevent or revert maladaptive plasticity, the extent of such neural plastic changes in the aging brain is poorly appreciated. By reanalyzing a large-scale dataset of more than 2200 cochlear implant users (CI) and assessing the improvement in speech perception from 6 to 24 months of use, we show that, although rehabilitation improves speech understanding on average, age at implantation only minimally affects speech scores at 6 months but has a pejorative effect at 24 months post implantation. Furthermore, older subjects (>67 years old) were significantly more likely to degrade their performances after 2 years of CI use than the younger patients for each year increase in age. Secondary analysis reveals three possible plasticity trajectories after auditory rehabilitation to account for these disparities: Awakening, reversal of deafness-specific changes; Counteracting, stabilization of additional cognitive impairments; or Decline, independent pejorative processes that hearing rehabilitation cannot prevent. The role of complementary behavioral interventions needs to be considered to potentiate the (re)activation of auditory brain networks.

Affective touch in the context of development, oxytocin signaling, and autism.

Touch represents one of our most important senses throughout life and particularly in the context of our social and emotional experiences. In this review, we draw on research on touch processing from both animal models and humans. Firstly, we briefly describe the cutaneous touch receptors and neural processing of both affective and discriminative touch. We then outline how our sense of touch develops and summarize increasing evidence demonstrating how essential early tactile stimulation is for the development of brain and behavior, with a particular focus on effects of tactile stimulation in infant animals and pediatric massage and Kangaroo care in human infants. Next, the potential mechanisms whereby early tactile stimulation influences both brain and behavioral development are discussed, focusing on its ability to promote neural plasticity changes and brain interhemispheric communication, development of social behavior and bonding, and reward sensitivity through modulation of growth factor, oxytocin, and opioid signaling. Finally, we consider the implications of evidence for atypical responses to touch in neurodevelopmental disorders such as autism spectrum disorder and discuss existing evidence and future priorities for establishing potential beneficial effects of interventions using massage or pharmacological treatments targeting oxytocin or other neurochemical systems.