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Results for “Neuronal Plasticity”

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At least 19 recordsLinked to original sources
PubMed1978

Neuronal plasticity in the limbic system during classical conditioning of the rabbit nictitating membrane response. II: Septum and mammillary bodies.

Neuronal unit activity was recorded from several limbic system structures during classical conditioning of the rabbit nictiating membrane response to a tone CS. Air puff to cornea was used as a UCS. The present and past investigations of hippocampal activity using this paradigm show a neuronal plasticity which develops early in training, increases rapidly and shifts forward in time as behavioral conditioning develops. Recordings from the lateral septal region demonstrate the same within-trial pattern of unit discharge seen in hippocampus, indicating a projection of hippocampal plasticity over precommissural fornix pathways. Medial septal neurons, on the other hand, respond in an excitatory manner to the onsets of tone and air puff stimulation. While unit discharges seen in hippocampus and lateral septum occur only during the paired (learning) paradigm, medial septal activity is identical under both paired and unpaired (control) conditions. The latter fact lends support for a sensory interpretation of medial septal responses, and is consistent with anatomical evidence of a major septohippocampal projection originating from this region. In contrast to results for lateral septum, recordings from medial and lateral mammillary nuclei indicate only small, diffuse excitation that exhibits no consistent changes over training, and is not related to activity seen in hippocampal or septal regions. The apparent lack of correspondence between learning dependent unit measures obtained from pre- and postcommissural fornix structures is entirely consistent with current modified descriptions of limbic system anatomy.

Action Potentials↗
PubMed1978

Neuronal plasticity in primate telencephalon: anomalous projections induced by prenatal removal of frontal cortex.

When the dorsolateral prefrontal cortex in one hemisphere of a rhesus monkey is resected 6 weeks before birth and the fetus survives to postnatal ages, neurons of the corresponding cortex in the intact hemisphere issue a greatly expanded projection to the contralateral caudate nucleus in addition to a normal projection to the ipsilateral caudate. The enhancement of the crossed prefronto-caudate pathway after prenatal neurosurgery provides direct evidence for lesion-induced neuronal rearrangement in the primate telencephalon.

Animals↗
PubMed2026

Genome-Wide Association Analysis of Hippocampal Neuroplasticity as an Indicator of Stress Responsiveness in Laying Hens (Gallus gallus domesticus).

Environmental stressors in commercial poultry systems can negatively affect bird welfare, although individuals vary considerably in their responses. Neuroplasticity within the hippocampus, measured through the density of doublecortin-positive (DCX+) neurons, provides a potential biomarker of stress experience in laying hens. However, the genetic basis underlying variation in this biomarker remains poorly understood. A total of 42 H&N and Hy-Line Brown hens housed in a multitier free range and enriched cage system, respectively, were genotyped using Genotyping by Sequencing, yielding over 200 000 SNP markers after initial filtering. Hippocampal tissue sections were immunostained for DCX to quantify the density of highly plastic neurons. A genome-wide association analysis identified 19 genomic regions across eight chromosomes within the top 1% of windows explaining the greatest proportion of genetic variance in the neuroplasticity phenotype. Within ±100 kb of these regions, 39 annotated genes were identified, several of which are involved in cellular regulation and genetic information processing pathways. Notably, PIK3R6, VPS37D, STX1A, BAZ1B, HGH1, MAF1, MAPK15, and PIT54 emerged as positional candidate genes potentially contributing to variation in stress responsiveness. These findings provide preliminary insight into the genetic architecture of hippocampal neuroplasticity in laying hens and highlight candidate genes that may contribute to individual differences in stress response, with potential implications for breeding strategies aimed at improving poultry welfare.

Animals↗
PubMed1979

[The morphologic diversity and complexity of synapses and microcircuits].

After mentioning the dendrite arborizations and the dendritic spines which represent an important site of synaptic interactions and neuronal plasticity, the main synaptic types, chemical and electrical, excitatory and inhibitory are mentioned and their morphological characteristics and dynamic properties are discussed. In the second part, the synaptic connections between several nerve cells, and the module principle of cerebellar and cerebral cortex are described. Significant progress is expected from the application of the 14C-deoxyglucose technique which is used as a histochemical marker of neuronal activity.

Animals↗
PubMed1975

Neurochemical changes in the cat's spinal cord due to orthodromic tetanic stimuli. I: phospholipids.

Posttetanic potentiation of monosynaptic reflexes has been used as a paradigm for neuronal plasticity. The explanation for this phenomenon is an increased responsiveness of the synaptic junctions. This would basically require chemical changes of the nervous structures involved. The ventral horn area of the spinal cord was therefore analyzed neurochemically. The determination of the phospholipids revealed an alteration of their composition. Sphingomyelin, phosphatidylcholine and phosphatidylinositide/serine behaved differently, whereas phosphatidylethanolamine and the total phospholipid content remained unchanged.

Animals↗
PubMed1979

The crossed cortico-caudate projection in the rhesus monkey.

In the normal young adult rhesus monkey, reduced silver staining of degenerating axons revealed that the lateral prefrontal cortex projects to the caudate nucleus of the contralateral hemisphere. This crossed prefronto-caudate projection provides a means whereby the prefrontal cortex can affect the neuronal activity of the extrapyramidal motor systems in both hemispheres. These findings also support the concept that apparent neuronal plasticity in this primate telencephalic system is a result of expanded projections of axons that normally issue a minor projection to the contralateral caudate nucleus.

Animals↗
PubMed2026

Activity-dependent DNA methylation and demethylation: epigenetic regulators of learning and memory.

Learning and memory are fundamental cognitive processes that rely on activity-dependent epigenetic mechanisms to shape synaptic and neuronal plasticity. Among these, DNA methylation and demethylation have emerged as pivotal regulators that convert transient neural activity into enduring transcriptional programs. In mammals, DNA methylation marks include 5-methylcytosine (5mC) as well as the less well-established N6-methyladenine (6mA) and the more enigmatic N4-methylcytosine (4mC). Compared with 5mC, the abundance, genomic distribution, and regulatory role of 6mA and 4mC remain incompletely defined, partly due to low abundance and technical challenges, yet these non-canonical marks may provide an additional regulatory layer in specific biological contexts. Accordingly, this review focuses on the best-characterized pathway in the nervous system, 5mC and its activity-regulated oxidative turnover. This system comprises a dynamic spectrum of cytosine modifications, including 5mC, 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC), orchestrated by distinct enzyme families such as DNMTs, TETs, and TDG. We review current insights about how these regulators shape activity-induced gene expression programs underlying learning and memory, and we discuss how dysregulated DNA (de) methylation contributes to impaired transcriptional control and cognitive decline in neurodegenerative diseases, particularly Alzheimer's disease. Finally, we highlight recent advances in high-resolution mapping technologies for DNA modifications, which are expanding our ability to resolve cell type- and locus-specific epigenetic dynamics in the brain. A deeper understanding of these pathways may inform targeted strategies to preserve or restore cognitive function in neurological disorders.

Alzheimer’s disease↗
PubMed2026

Age-dependent reorganization of behavioral and striatal function in Cntnap2 knockout mice.

Autism spectrum disorder (ASD) is characterized by persistent deficits in social communication and the presence of restricted and repetitive behaviors. While ASD has a neurodevelopmental origin, it remains a lifelong condition, yet little is known about how its behavioral and neural features evolve across adulthood. Here, we investigated behavioral, synaptic, and structural alterations across the transition from early to mature adulthood in Cntnap2 knockout mice, a widely used model of ASD. Using a longitudinal behavioral approach combined with electrophysiological recordings and morphological analysis, we show that KO mice exhibit increased stereotyped and repetitive behaviors and reduced exploratory activity at both ages. However, detailed analysis of behavioral patterns revealed age-dependent differences, with early adult KO mice displaying increased behavioral persistence that later evolved into distinct patterns of behavioral sequences. These behavioral changes were associated with alterations in inhibitory synaptic transmission in the dorsolateral striatum (DLS), including changes in spontaneous inhibitory postsynaptic current (sIPSC) frequency and temporal structure. In parallel, mature adult KO mice showed structural remodeling of spiny projection neurons, characterized by increased distal dendritic arborization and age-dependent organization of dendritic spines. Together, our findings demonstrate that ASD-related alterations are not static but evolve across adulthood, revealing a multi-level reorganization of behavioral, synaptic, and structural features. These results highlight the importance of considering adulthood stages in ASD and provide new insights into the dynamic nature of the condition.

Animals↗
PubMed2026

Shielding the First 24 Postnatal Months of Life: A Proposal for a Prospective Cohort Study of Early-Life Electromagnetic Exposure and Autism Risk.

BACKGROUND: Autism Spectrum Disorder (ASD) involves Mirror Neuron System (MNS) dysfunction, driving core social and imitative impairments. Systemic physiological alterations such as autonomic dysregulation, mitochondrial dysfunction and neuroinflammation are known to impair synchronization and plasticity of neuronal clusters. A less-evident environmental cofactor, coinciding with rising ASD prevalence, is the considerable world-wide increase in electromagnetic radiation (EMR) overall exposure among children. Experimental evidence shows how low-intensity EMR influences cellular processes, via voltage-gated calcium channels (VGCCs), oxidative stress, and mitochondrial metabolism. The Resonant Convergence framework, allow to predict how chronic EMR exposure during the first 24 postnatal months of life can act as a factor in ASD pathogenesis. The best candidate mechanism is chronic Ion Cyclotron Resonance (ICR) detuning the Ca2+-calmodulin pathway, thus disrupting MNS synchronization. METHODS AND ANALYSIS: A prospective observational pilot cohort study (24-month follow-up) proposes to enroll 1000 full-term newborns into two arms: an EMR-reduced cohort (n = 500, rest and sleep-phase Faraday shielding) and a standard exposure cohort (n = 500). Exposure is quantified via radiofrequency (RF)/extremely low frequency(ELF) measurements, proximity analysis, device inventories and wearable dosimetry. The primary endpoint is a continuous neurodevelopmental trajectory score (joint attention, language, electroencephalogram (EEG) mu-rhythm); binary ASD diagnosis (Autism Diagnostic Observation Schedule, Second Edition (ADOS-2), Autism Diagnostic Interview-Revised (ADI-R)) is a secondary, exploratory endpoint. Moreover, an optional genomic screening will evaluate gene-environment interactions within extremely low-frequency electromagnetic field (ELF-EMF) vulnerable pathways, including ASD-associated genes upregulated by RF via bromodomain and extraterminal protein (BET)-mediated epigenetic mechanisms. Analyses will employ risk ratios, Fisher's exact tests and logistic regression adjusted for confounders; mixed-effects and Bayesian modeling will evaluate longitudinal outcomes and exposure reduction effects. Given a 2-3% baseline prevalence, approximately 20-30 ASD cases are expected. The study is therefore powered for exploratory signal detection rather than definitive causal inference, providing the critical baseline data required to justify and design future confirmatory trials. Sex-stratified modeling will address the 4:1 male-to-female prevalence ratio. ETHICS AND DISSEMINATION: Ethics committee approval is not yet sought; full protocol review and approval will be obtained prior to the study initiation, in strict accordance with the Declaration of Helsinki. Written parental informed consent will be mandatory for all participants prior to enrollment. Study findings and methodological milestones will be disseminated through peer-reviewed international scientific publications. This protocol provides a structured methodological framework for the first prospective investigation of sleep-phase EMR reduction as a potential modulator of ASD incidence during early neurodevelopment. Results will inform adequately powered confirmatory trials in electromagnetic neurodevelopmental epidemiology.

autism spectrum disorder↗
PubMed2026

Effects of strength and balance training on the structure of the aging brain.

BACKGROUND: While it is established that motor training induces structural changes in the brains of young adults, structural adaptations in aging brains are less studied. METHODS: This randomized controlled study investigated the impact of long-term strength and balance training on the structural plasticity in 60 elderly adults (64 - 82 years old, 70.6 ± 4.7) using multi-modal neuroimaging. We compared the effects of three months of strength training to balance training of the same duration and to a passive control group. Voxel-based morphometry (VBM) and tract-based spatial statistics (TBSS) were used to assess grey matter (GM) and white matter (WM) plasticity. White matter tract integrity (WMTI) modelling was employed to explore the microstructural underpinnings of white matter alterations. RESULTS: We found that strength training was associated with changes in diffusion metrics consistent with white matter microstructural remodeling, specifically increased extra-axonal axial diffusivity in the bilateral inferior fronto-occipital and longitudinal fasciculi. Additionally, both balance and strength training mitigated reductions in axonal water fraction in the splenium of the corpus callosum and the right posterior corona radiata observed in the control group. CONCLUSION: These results underscore the potential relevance of strength and balance training to induce beneficial neural plasticity by counteracting aging-related demyelination in the corpus callosum and highlight the specific role of strength training in facilitating white matter reorganization in key transmission fiber pathways.

Humans↗
PubMed2026

Adaptations to breath-hold diving: from traditional divers to elite athletes.

Breath-hold diving exposes humans to repeated episodes of profound hypoxia and hypercapnia, eliciting physiological adaptations that enable prolonged underwater performance. This article summarises current knowledge on chronic adaptations in elite breath-hold athletes and traditional diving populations, including the Bajau sea nomads of Southeast Asia and the Korean Haenyeo divers. Evidence indicates that repeated apnoea induces adaptations across multiple physiological systems. Haematological changes include increased spleen size and enhanced splenic contraction, augmenting circulating haemoglobin and oxygen stores during apnoea. In elite divers, structured training can increase resting spleen volume, whereas the Bajau exhibit genetically associated splenic enlargement linked to variants near the PDE10A gene. Cardiopulmonary adaptations include modified pulmonary vascular responses to hypoxia, improved oxygen conservation, and metabolic shifts favoring efficient mitochondrial energy production. Molecular adaptations involve enhanced antioxidant defenses and activation of hypoxia-responsive pathways that may mitigate oxidative stress associated with repeated hypoxia-reoxygenation cycles. Emerging evidence also suggests neural plasticity and possible structural brain adaptations, although the long-term neurological consequences of chronic intermittent hypoxia exposure remain uncertain. Studies of traditional diving populations indicate that both phenotypic plasticity and genetic selection contribute to diving capacity, highlighting interactions between training and evolution. Despite these benefits, breath-hold diving also carries risks, including hypoxic blackout, decompression sickness, and potential neurological injury. Understanding the mechanisms underlying human tolerance to extreme hypoxia may have implications beyond diving physiology, including applications in cardiovascular medicine, hypoxic diseases, and rehabilitation. Further longitudinal, genomic, and mechanistic studies are needed to clarify the limits, benefits, and clinical relevance of these adaptations.

Humans↗
PubMed2026

Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools.

Ketogenic diet (KD) is used for the treatment of drug-resistant childhood epilepsy and has been proposed to improve outcomes in neurodegenerative diseases. However, the mechanisms by which KD alters brain circuitry remain unclear. Here, we investigated the impact of KD on hippocampal function through integrative analysis of gene expression and neurotransmission. We found that KD induces extensive transcriptional reprogramming, including altered expression of numerous synaptic genes. Proteomic and genomic profiling revealed significant changes in histone modifications, particularly at promoters of KD-regulated genes. Electrophysiological recordings showed that KD reduces excitatory synaptic gain and short-term plasticity at CA3-CA1 synapses, dampening the summation of excitatory inputs and enhancing the summation of inhibitory inputs. These functional changes were driven, in part, by a reduction in the readily releasable vesicle pool at excitatory synapses under KD. Together, our findings demonstrate that KD drives transcriptional remodeling of hippocampal circuits, leading to synaptic adaptations that may underlie its anti-epileptic and neuroprotective effects.

Animals↗
PubMed2026

Genome-wide mapping of stress-responsive lncRNA, uc.104, reveals the chromatin-mediated regulation of stress and plasticity-related genes in the hippocampus of chronic restraint rats.

Chronic stress significantly impacts hippocampal function through transcriptional and epigenetic mechanisms. While the roles of lncRNAs in stress-related transcriptional and epigenetic regulation have recently been recognized, their genome-wide functions controlling the transcriptional network remain largely unclear. Evidence indicates that the lncRNA uc.104 is involved in stress responses; however, its genome-wide chromatin interactions and gene regulatory effects are yet to be explored. To examine this, we combined chromatin isolation by RNA purification sequencing (ChIRP-seq) and RNA sequencing (RNA-seq) in the hippocampus from handled control and chronic restraint stress (CRS) rats. ChIRP-seq identified 6,664 uc.104 binding peaks under CRS, including 6,517 enriched and 149 reduced. Many peaks were mapped to intronic and promoter-proximal regions of protein-coding genes. Integration of ChIRP-seq with RNA-seq data revealed 1,839 differentially expressed genes associated with uc.104 binding sites, with 106 high-confidence overlaps. Several genes (Gabra3, Htr7, Irs1, Gpr37, Clu, Hspa1b, Ppp3r2, Nfasc, Pcdhac2, and Cysltr2) identified as regulatory targets of uc.104, have been directly implicated in stress responses, synaptic plasticity, and neuroinflammation. Gene ontology and Synapse GO (SynGO) analyses revealed significant enrichment for processes involving dendritic spine formation, synapse organization, and pre- and postsynaptic signaling. Protein-protein interaction analysis identified hub genes, including EGFR, CDC42, IGF1R, CTNNB1, CALM1, CALM3, POLR2A, MDM2, TBP, and CSNK1E, several of which have been linked to stress-responsive pathways. Together, our findings reveal that uc.104 binding to chromatin near stress- and synapse-related genes may act as a regulator of stress-responsive transcriptional networks in the hippocampus. By linking uc.104 occupancy to stress and synaptic responsive genes, this study highlights uc.104 as a potential mediator of stress-induced hippocampal malfunctions.

Animals↗
PubMed2026

Faster N1 latency in response to homeostatic-like plasticity of PREPs is impaired during pain: A randomized-placebo capsaicin-pain study.

INTRODUCTION: Homeostatic-like plasticity (HP-like) stabilizes cortical excitability through long-term potentiation and depression-like mechanisms. The efficacy of homeostatic regulation in the corticomotor system is impaired during pain, which may have functional relevance for chronic pain. This study investigated whether a cortical HP-like response could be assessed by nociceptive stimulation, and if such response was impaired by experimental tonic pain. METHODS: Twenty-eight healthy participants completed placebo and capsaicin sessions, with 11 sham controls for time and design. HP-like plasticity was induced with two blocks of anodal tDCS over the primary motor cortex. The N1 (TP7) and N2P2 (Cz) components of electrically induced pain-related evoked potentials (PREPs) were assessed from the volar forearm before and after patch application, and again immediately and 20 min after HP-like induction. An HP-like response was defined by PREP decrease after induction, and further normalization to baseline. RESULTS: Anodal tDCS did not induce an HP-like regulation of PREP amplitudes. Interestingly, an HP-like response was observed as a fastening of N1 latency after HP-like induction, which returned to baseline values after 20 min. The latter effect was impaired during capsaicin-induced pain, where N1 was slower. The N2P2 component showed habituation over time in all sessions. CONCLUSION: This is the first study that investigates the HP-like regulation of nociceptive-evoked responses. An HP-like response was observed as a shortening of N1 latency, suggesting that early nociceptive processing may be susceptible to homeostatic regulation. In contrast, the later component, N2P2, showed habituation over time, which prevented evaluation of HP-like effects.

Humans↗
PubMed2026

Effectiveness of passive vs. assistive robotic gait training on functional recovery and neuroplasticity post-stroke: A randomized controlled trial.

OBJECTIVE: This study seeks to compare the impacts of various robotic gait training (RAGT) modes on lower limb motor function recovery in stroke patients while exploring the corresponding neural mechanisms. DESIGN: A single-blind, randomized controlled trial. SETTING: Inpatient Rehabilitation Facility. PARTICIPANTS: Forty-eight patients aged 18-80 who had experienced their first unilateral subacute stroke accompanied by walking impairments were included. INTERVENTIONS: Participants were randomly assigned to: (1) assistive mode training, (2) passive mode training, or (3) control group receiving only traditional rehabilitation. Clinical and neurological outcomes were assessed at pre-intervention (T0), and post-2-week intervention (T1). MAIN OUTCOME MEASURES: Outcomes were evaluated using the Fugl-Meyer Assessment for Lower Extremity, Berg Balance Scale, Modified Barthel Index, the Functional Ambulatory Category, and functional near-infrared spectroscopy. RESULTS: Among the 48 patients recruited, significant time effects were observed across all groups in FMA-LE scores (p&#x202f;<&#x202f;0.001). Notable improvements were detected in the conventional group (MD = 2.69, p&#xff1c;0.01) and the passive group (MD = 3.67, p&#x202f;<&#x202f;0.001), with the assistive mode also demonstrating a significant effect (MD = 1.79, p&#x202f;<&#x202f;0.05). BBS scores improved across all groups; however, no significant differences were noted between the groups (p&#x202f;=&#x202f;0.11). Similarly, MBI scores showed a significant time effect (p&#x202f;<&#x202f;0.001), without notable group differences (p&#x202f;=&#x202f;0.29). CONCLUSION: All training modalities effectively enhanced motor function, balance, and daily living skills in stroke patients. Distinct cortical activation and connectivity patterns were observed between training modalities, which may reflect different neuroplastic mechanisms. These preliminary neural differences may help inform personalized rehabilitation strategies, although no clinical superiority of one mode over another can be concluded from the present data.

Humans↗