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Results for “Cortical plasticity”

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At least 19 recordsLinked to original sources
PubMed1979

Restoration of visual cortical plasticity by local microperfusion of norepinephrine.

Using a newly developed technique of continuous microperfusion, we obtained further evidence in support of our hypothesis that the neocortical catecholamines (CAs), particularly norepinephrine (NE), are responsible for a high level of cortical plasticity. We used the visual cortical changes in ocular dominance which follow a brief monocular deprivation as a simple and reliable index of cortical plasticity. Local perfusion of kitten visual cortex with 1 mg/ml (4.0 mM) 6-hydroxydopamine (6-OHDA) prevented the effects of monocular deprivation in kittens, thus replicating the results we had obtained using intraventricular injections (Kasamatsu and Pettigrew, '76b, '79). Locally perfused NE at a concentration of of 10(-2) mg/ml (48.6 micron) restored visual cortical plasticity in animals which were no longer susceptible to brief monocular lid-suture. These numbers refer to the concentration of solutions in the cannula/minipump system. The effective concentrations at the site of recording (about 2 mm away) are probably much lower than these. This effect of NE perfusion was seen both in kittens which had received prior 6-OHDA treatment as well as in older animals which had outgrown the susceptible period. In the kittens we obtained as a nearly complete shift in ocular dominance toward the open eye and in the older animals a decrease in binocularity was obtained. The changes were found only in the local region of visual cortex perfused with either NE or 6-OHDA, while nearby cortical regions in the same animals were unaffected. There were no obvious changes in receptive field properties of individual neurons other than ocularity, and externally perfused NE did not itself reduce binocularity in normal animals: the effects of NE described about only occurred when the animal's visual experience was simultaneously altered. These results support the view that NE plays an important role in cortical plasticity.

Age Factors↗
PubMed1979

Cortical plasticity in monocularly deprived immobilized kittens depends on eye movement.

A marked reduction of binocular cells in striate cortex is found if 4-week-old kittens are visually stimulated monocularly while anesthetized and held in a stereotaxic apparatus. If the kittens are paralyzed and artificially respirated, changes are not found unless an eye is moved mechanically. It appears that eye movement and visual stimulation are necessary conditions for deactivation of binocular connections, but neither is sufficient to induce such changes alone.

Animals↗
PubMed2026

Altered Excitation-Inhibition Balance and mGluR1/5-Driven Plasticity in the Motor Cortical Surface in a Rat Model of Parkinson's Disease.

Parkinson's disease (PD) is characterized by progressive dopaminergic degeneration and maladaptive motor cortical plasticity. However, the cellular pathways underlying cortical surface activity in the primary motor cortex (M1) remain unclear, despite serving as a potential target for electrotherapy. We investigated the excitatory-inhibitory (E-I) balance and synaptic plasticity of superficial M1 circuits in a unilateral 6-hydroxydopamine (6-OHDA)-induced rat model of PD. Using extracellular local field potential and whole-cell patch recordings from the contralateral and ipsilateral M1 hemispheres of hemi-parkinsonian rats, we observed a significantly elevated field excitatory postsynaptic potential (fEPSP) input-output function but unchanged intrinsic neuronal excitability in the M1 superficial layer. An altered relative contribution between alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and N-methyl-D-aspartate receptor (NMDAR)-mediated transmission was reflected by a significantly increased AMPA/NMDA ratio. Markedly reduced inhibitory synaptic tone was also evidenced by the decreased amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs), supporting an E-I imbalance favoring excitation in PD. Furthermore, group I metabotropic glutamate receptor (mGluR1/5)-dependent long-term depression (LTD) was abolished in the ipsilateral PD hemisphere, whereas NMDAR-dependent LTD remained intact. In summary, dopamine depletion appears to enhance network excitation and disrupt mGluR1/5-mediated control of M1 surface circuitry. Our findings identify altered cortical surface mGluR-dependent plasticity in the hemi-parkinsonian model; however, the relationship between these electrophysiological alterations and individual motor outcomes remains to be determined.

Animals↗
PubMed1979

Preservation of binocularity after monocular deprivation in the striate cortex of kittens treated with 6-hydroxydopamine.

The results of single unit recordings from Area 17 of monocularly deprived kittens were compared with similar ones from littermates who had been monocularly lid-sutured for the same period of time, but who had in addition been given intraventricular injections of 6-hydroxydopamine (6-OHDA) to deplete brain catecholamines. This visual cortices of all catecholamine-depleted kittens showed high proportions of binocular neurons, in contrast to the control group, a majority of whose visual cortical neurons were driven exclusively by the non-deprived eye. Preservation of binocularity in 6-OHDA-treated kittens was dose-related. Even after a 1 to 2-week period of lidsuture which reduced binocularity to 20% in controls, normal proportions of binocular neurons (greater than 75%) were preserved if the cumulative dose had been 10 mg 6-OHDA or more. The density of single neurons sampled from electrode tracks through the cortex of drug-treated kittens was high and did not differ significantly from controls. Neurons were isolated every 100 micron on the average. There was some indication that the drug's effect in preventing an ocular dominance shift disappears by six weeks following cessation of 6-OHDA treatment. This reversal of the physiological effects in cortex is preceded by recovery from the behavioral manifestations of 6-OHDA treatments. Binocularity was only slightly increased in a kitten who received large doses of 6-OHDA after a period of monocular deprivation. This observation, together with control recordings from normal kittens and adults treated with 6-OHDA, indicates that the direct effects of 6-OHDA on cortical neurons' response properties play a minor role in comparison to its effects in reducing the sensitivity of the cortex to monocular deprivation. The overwhelming majority of cortical neurons in 6-OHDA-treated kittens remained normal in receptive field properties after a period of monocular deprivation. These data support the hypothesis that catecholamines are required for the maintenance of visual cortical plasticity during the critical period.

Animals↗
PubMed1976

Depletion of brain catecholamines: failure of ocular dominance shift after monocular occlusion in kittens.

Monocularly deprived kittens were compared with littermates that had had their eyelids sutured for the same time but that had, in addition, been treated with 6-hydroxydopamine to deplete their forebrains of catecholamines. The visual cortices of all the catecholamine-depleted kittens showed high proportions of binocular neurons, in contrast to the control group, most of whose visual cortical neurons were driven exclusively by the nondeprived eye. Catecholamines may play an important role in the maintenance of cortical plasticity during the critical period.

Animals↗
PubMed2026

A single session of high-definition transcranial direct current stimulation does not modulate effects of knee two-point discrimination training or sensorimotor function in healthy adults: Double-blind randomised controlled trial.

BACKGROUND: Benefits of sensory-training interventions on sensorimotor outcomes are inconsistent, and it is unclear whether transcranial direct current stimulation (tDCS) can enhance proprioception, which is fundamental to neuromuscular control. Existing evidence is dominated by upper-limb studies, so transferability to the knee is unclear. This study investigated whether a single session of anodal high-definition (HD)-tDCS, alone or combined with brief two-point discrimination (TPD) training, enhances knee sensorimotor function and performance in healthy adults. METHODS: In a double-blind randomised-controlled trial, 57 healthy participants received (1) 20-min, 1&#xa0;mA anodal HD-tDCS over the knee primary somatosensory (S1) map or sham stimulation, and (2) 15-min knee TPD training or no training. Knee somatosensory, sensorimotor, and functional performance measures were assessed pre- and immediately post-intervention. Three-way mixed-design ANOVAs, equivalence testing (smallest effect size of interest &#x3b7;2&#xa0;=&#xa0;0.02), Bayes factors, and linear mixed-effects models quantified effects. RESULTS: HD-tDCS, TPD training, and their sequential combination had no effect on any outcome measure (p&#xa0;&#x2265;&#xa0;0.05; &#x3b7;2&#xa0;&#x2264;&#xa0;0.015). Confidence intervals spanned equivalence bounds, and equivalence testing results were non-significant (p&#xa0;&#x2265;&#xa0;0.05). Bayes factors (<0.33) showed moderate evidence for the null (no effect). Mixed-effects modelling attributed &#x2264;8% of total variance to intervention fixed effects, with the remainder captured by participant-level random effects. CONCLUSION: A single 20-minute session of 1&#xa0;mA HD-tDCS, with or without brief TPD training, does not acutely modify knee somatosensory, sensorimotor, or functional performance in healthy adults. Existing evidence at the hand may not translate to the lower limb. Future work should investigate higher-dose, multi-session, task-concurrent, or network-targeted strategies in clinical populations.

Humans↗
PubMedDate not supplied

[Plastic transformation of the activity of cortical neurons upon pairing a signal stimulus with microiontophoresis or electrocutaneous stimulation].

Substantial differences have been found in the plastic reorganizations of neuronal activity of the rat sensorimotor cortex at local and systemic reinforcements. In nineteen (95%) out of 20 neurones stable and one-type changes of response to CS (electrical stimulation of the cortex) developed in the course of pairings with local ionophoretic application of L-glutamate in the vicinity of the studied neurone. Twenty two units were studied during the pairings of electrical stimulation of the cortex with pain electrocutaneous stimulation: plastic reorganizations in response to CS were revealed only in eight (36.4%) units; they were, however, of long duration and were more diverse in pattern, than in the series with local reinforcement. It is assumed that different plastic reorganizations in these two model situations of learning depend on the number and reactive properties of the participating units.

Animals↗
PubMed1976

Cortical blindness after overlapping retinal-striate lesions: a limit to plasticity in the central visual system.

Lesions in cats, rats, and monkeys that spare more than 2% of the optic tract or visual cortex cause trivial deficits on most measures of vision. Overlap in the topography of the visual system may allow the spared remnant to 'see' a wider field of vision than the physiological map predicts. We tested whether monkeys left with only the lower retinal-field portion of their striate map could see with information coming from the upper half of the retina. In 6 rhesus monkeys the ganglion fibers exiting from the lower half of both retinae were cut with a photocoagulator. Later, the portion of area 17 which, according to the electrophysiological map, controls upper retinal vision, was ablated bilaterally. The combined retinal and striate lesions overlapped to include the entire visual field. Together they produced cortical blindness. The monkeys' performance of two pattern and object tasks remained at chance throughout the survival period. A previous study has described considerable sparing of vision after combined optic tract and visual cortex lesions in cats. Differences in the lesion methods and in the anatomy of the cat and monkey visual system may explain the disagreement.

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&#xa0;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&#xa0;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

Genome-Wide and Rare Variant Association Studies of Amblyopia in Admixed American and African Ancestry Groups.

OBJECTIVE: To identify genetic variants associated with amblyopia in African (AFR) and Admixed American (AMR) ancestry groups, expanding on previous studies conducted in European ancestry. DESIGN: Retrospective ancestry-stratified genome-wide association study (GWAS) and gene-level rare variant association study (RVAS). PARTICIPANTS: Participants in the All of Us Research Program from AFR and AMR ancestry groups who had whole-genome sequencing available. Cases and controls were distinguished based on the presence of International Classification of Diseases 9/10/SNOMED diagnosis codes for amblyopia in electronic health records. This yielded ancestry-stratified subsets of 269 cases and 71 585 controls of AMR ancestry and 366 cases and 79 460 controls of AFR ancestry. METHODS: Stratified logistic regression models were adjusted for age, biological sex, and the top 10 principal components of genomic ancestry. GWAS was limited to common variants (minor allele frequency &#x2265;1%), and RVAS was limited to rare variants with coding sequence-altering effects (minor allele frequency >1%, exonic only, excluding synonymous variants) aggregated at the gene level using the SKAT algorithm. Downstream analyses of the significant variants were performed using KEGG and GO pathway analysis and STRING database queries for protein-protein interactions and gene-gene interactions. MAIN OUTCOME MEASURES: Single-nucleotide polymorphisms were determined to have genome-wide significance if P < 5e-8 in the GWAS, and genes were determined to have significant association with amblyopia in the RVAS if P < 8.0 &#xd7; 10-4. RESULTS: In the AMR GWAS, 245 unique single-nucleotide polymorphisms mapping to 97 distinct loci were identified, notably within neurodevelopmental and axonal guidance genes, including ROBO1, SEMA4B, PTPRD, NRXN1, and CAMK2D. The AFR GWAS identified 11 significant variants corresponding to 6 loci mapping primarily to long noncoding RNAs and pseudogenes. The AMR RVAS identified 15 genes, including axonal transport genes (KIF1B and KIF7) and growth factor signaling genes (EGF, ERBIN, and AKAP17A). The AFR RVAS identified a single gene, DLG2, which encodes the postsynaptic protein PSD-93, which promotes the closure of the sensitive period of neuroplasticity for vision in early childhood. CONCLUSIONS: Genetic risk architectures for amblyopia differ across ancestries but fundamentally converge on neurodevelopmental signaling, cortical synapse assembly, and sensitive period plasticity rather than ocular structural dynamics. FINANCIAL DISCLOSURE(S): The authors have no proprietary or commercial interest in any materials discussed in this article.

Amblyopia↗
PubMed1978

Facilitatory and inhibitory effects of electrochemical stimulation of the amygdala on the release of luteinizing hormone.

The effect of amygdaloid stimulation on the release of luteinizing hormone (LH) was studied in unanesthetized, unrestrained rats. Electrochemical stimulation (anodic D.C.) was applied at 11.30 h through stainless steel electrodes chronically implanted into different amygdaloid nuclei; medial (Men.), cortical (Con.), central (Cn.), or basolateral (Bln.). A plastic cannula inserted into the jugular vein was used for obtaining blood samples at different times of the experimental procedure. In rats on the day of proestrus, stimulation (100 micronA/30 sec) in the Bln. resulted in blockade of spontaneous ovulation and of the preovulatory LH release and that in the Cn. produced a delay in the hormone discharge. On the contrary, stimulation in the Men. was effective in advancing the time of the normal LH surge, while no change of the normal pattern occurred from the Con. Stimulation (100 micronA/60 sec) of ovariectomized estrogen primed rats applied in the Men. or the Con. induced LH release, while that in the Bln. or the Cn. had no effect. The release of LH by Men. stimulation and the blocking effect of Bln. showed a close relationship with the amount of current delivered. Lower thresholds were required for inhibition than for activation. The release of LH induced by stimulation in the Men. of ovariectomized estrogen primed rats occurred at the same time of the day whether the stimulus was applied at 8.30 h, 11.30 h or 14.00 h, indicating a modulatory effect of the amygdala. No changes in serum LH concentration were observed after stimulation of the Men. of castrated estrogen primed male rats or in the Bln. of ovariectomized non-primed rats. The present results indicate that the amygdala exerts a dual effect on the release of LH, the Bln. being inhibitory and the Men. and Con. facilitatory.

Amygdala↗
PubMed2025

Druggable genome CRISPRi screen in 3D hydrogels reveals regulators of cortactin-driven actin remodeling in invading glioblastoma cells.

To identify new therapeutic targets that limit glioblastoma (GBM) invasion, we applied druggable-genome CRISPR screens to patient-derived GBM cells in micro-dissectible biomimetic 3D hydrogel platforms that permit separation and independent analysis of core vs. invasive fractions. We identified 12 targets whose suppression limited invasion, of which ACP1 (LMW-PTP) and Aurora Kinase B (AURKB) were validated in neurosphere assays. Proximity labeling analysis identified cortactin as an ACP1-AURKB link, as cortactin undergoes serine phosphorylation by AURKB and tyrosine dephosphorylation by ACP1. Suppression of ACP1 or AURKB in culture and in vivo shifted the balance of cortactin phosphorylation in GBM and reduced actin polymerization and actin-cortactin co-localization. Additional biophysical analysis implicated AURKB in GBM cell adhesion and cortical stiffness, and ACP1 in resistance to mechanical stress and shape plasticity needed for 3D migration. These findings reveal a novel targetable axis that balances kinase and phosphatase activities to regulate actin polymerization during GBM invasion.

CRISPR↗
PubMed1978

Histomorphometric analysis of normal bone from the iliac crest.

Bone specimens from a standardized area of the iliac crest were obtained at autopsy in 105 individuals after sudden unexpected death and at biopsy in 30 living volunteers. Seven micron thick sections of the plastic embedded undecalcified material were produced and stained. The amount of cancellous and cortical bone and the parameters attached to description of bone remodelling were determined by point counting and simple measurements, in order to establish normal mean values and range in a Danish population. A decrease in the amount of bone, trabecular as well as cortical, was found with increasing age in both males and females. The extent, volume and width of osteoid seams and the osteoclastic resorption were found to be age-independent. The osteoclastic resorption in cortical bone in males decreased, however, with increasing age. The reported values are of the greatest importance for the use of histomorphometric analysis of bone biopsies as a diagnostic tool in metabolic bone diseases. It is stressed, however, that supplementary information of the dynamic aspects of the bone remodelling would be necessary for the understanding of the pathogenesis of bone changes. Such information might be obtained by using tetracyline double labelling.

Adolescent↗
PubMed1978

The juxtaglomerular apparatus in a human kidney with polar artery stenosis.

Juxtaglomerular apparatuses (JGA) of a human kidney with stenosis of a polar artery from a hypertensive 18-year-old male patient were studied qualitatively and quantitatively on 2 mu thick serial sections from plastic embedded renal tissue. 11 JGA from juxtamedullary and 9 JGA from subcapsular cortical zones were photographed serially, the copies taped together and the cells and relationships within the JGA studied. On the copies the lenght of contact between the different juxtaglomerular structures and the basement membrane of the macula densa was measured. Futhermore we calculated the areas of surface contact and the macula densa basal area. In the juxtamedullary JGA affected by the polar artery stenosis all Goormaghtigh cells were transformed into epitheloid cells and the Goormaghtigh cell field was significantly larger than in the JGA of the subcapsular cortex, which obviously had been exposed to the systemic hypertension. The macula densa basal area was significantly greater in the juxtamedullary JGA than in the subcapsular JGA, but neither of these differed significantly from the macula densa in the normal JGA reported previously.

Adolescent↗