SEARCH · PubMed Health

Results for “Neuronal Plasticity”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources

PubMed2004

The role of neurotrophins in bronchial asthma: contribution of the pan-neurotrophin receptor p75.

Allergic bronchial asthma is characterized by chronic inflammation of the airways, development of airway hyperreactivity and recurrent reversible airway obstruction. Target and effector cells responsible for airway hyperresponsiveness and airway obstruction include sensory and motor neurons as well as epithelial and smooth muscle cells. Although it is well established that the inflammatory process is controlled by T-helper-2 (Th2) cells, the mechanisms by which immune cells interact with neurons, epithelial cells or smooth muscle cells still remain uncertain. Due to growing evidence for extensive communication between neurons and immune cells, the mechanisms of this neuroimmune crosstalk in lung and airways of asthmatic patients are becoming the focus of asthma research. Neurotrophins represent molecules potentially responsible for regulating and controlling the crosstalk between the immune and peripheral nervous system. They are constitutively expressed by resident lung cells and produced in increasing concentrations by immune cells invading the airways under pathological conditions. Neurotrophins modify the functional activity of sensory and motor neurons, leading to enhanced and altered neuropeptide and tachykinin production. These effects are defined as neuronal plasticity. The consequences are the development of neurogenic inflammation.

Animals↗

PubMed2003

Immunohistochemical changes induced by repeated footshock stress: revelations of gender-based differences.

As a growing literature has proven, adverse experiences, particularly when severe and persistent, play a pivotal role in the development of neuronal dysfunctions and psychopathology. In the present study, the neurochemical changes induced by acute and repeated footshock exposure were investigated at the molecular and cellular level, using c-fos and phospho-ERK1/2 immunoreactivity and gene expression arrays. Marked gender-related differences were found following both acute and prolonged footshock exposure. Acute aversive conditioning resulted in significant immunohistochemical changes that might be critically involved in the modulation of fear-related responses, especially in males. Prolonged footshock exposure, on the contrary, was associated with sustained hypothalamic-pituitary-adrenal axis hyperactivity, differential gender-related patterns of cortical-limbic activity, and abnormal neuronal plasticity, especially in medial prefrontocortical regions. These data may provide additional insights into the understanding of the neural circuits underlying the effects of acute and repeated footshock exposure as well as clarify some of the mechanisms involved in the development of stress-related neuronal abnormalities.

Animals↗

PubMed1992

Protein kinase C modulation of NMDA currents: an important link for LTP induction.

A brief high frequency tetanic stimulation of afferent fibers induces a long-term potentiation (LTP) of synaptic transmission, which is manifested by an increase in the size of the synaptic response elicited by low frequency stimulation of the same synapse. LTP persists for several hours in vitro and up to several weeks in vivo, and is at present the most extensively studied form of activity-dependent synaptic plasticity. This article focuses on the relationship between two key elements in the induction of LTP--the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor and the Ca(2+)-phospholipid-dependent protein kinase C (PKC). In view of several recent findings that describe a direct positive modulation of NMDA currents by PKC, we suggest that PKC activity may, in fact, determine the threshold of LTP induction. Enhanced kinase activity may underlie the central role of the NMDA receptor--channel complex in neuronal plasticity.

Animals↗

PubMed2001

Enriched rehabilitative training promotes improved forelimb motor function and enhanced dendritic growth after focal ischemic injury.

Chronic impairment of forelimb and digit movement is a common problem after stroke that is resistant to therapy. Previous studies have demonstrated that enrichment improves behavioral outcome after focal ischemia; however, postischemic enrichment alone is not capable of enhancing fine digit and forelimb function. Therefore, we combined environmental enrichment with daily skilled-reach training to assess the effect of intensive task-specific rehabilitation on long-term functional outcome. Rats were subjected to either endothelin-1-induced focal ischemia or sham surgery and subsequently designated to enriched-rehabilitation or standard-housing treatment groups starting 15 d after ischemia. Functional assessment of the affected forelimb at 4 and 9 weeks after treatment revealed that ischemic plus enrichment (IE) animals had improved approximately 30% on the staircase-reaching task and were indistinguishable from sham animals for both latency and foot faults in a beam-traversing task. In contrast, ischemic plus standard (IS) animals remained significantly impaired on both tasks. Interestingly, both ischemic groups (IE and IS) relied on the nonaffected forelimb during upright weight-bearing movements, a pattern that persisted for the duration of the experiment. Dendritic arborization of layer V pyramidal cells within the undamaged motor cortex was examined using a Golgi-Cox procedure. IE animals showed enhanced dendritic complexity and length compared with both IS and sham groups. These results suggest that enrichment combined with task-specific rehabilitative therapy is capable of augmenting intrinsic neuronal plasticity within noninjured, functionally connected brain regions, as well as promoting enhanced functional outcome.

Animals↗

PubMedDate not supplied

[Memory model based on the plasticity of inhibiting neurons].

A stochastic memory model based on the net of excitatory and inhibitory neurons is considered. Its learning ability is due to a decrease of the reactivity of inhibitory elements. Information capacity of such neuron net was estimated in relation to its structure parameters. It has been shown that in the definite range of their change the information capacity of the net under consideration significantly exceeds that of the neuron net with the memory based on the plasticity of excitatory elements.

Animals↗

PubMed1996

The sexually dimorphic medial preoptic nucleus of quail: a key brain area mediating steroid action on male sexual behavior.

About 10 years ago, a sexually differentiated nucleus was identified in the preoptic area (POA) of the Japanese quail in the course of studies analyzing the dimorphic mechanisms involved in the activation of sexual behavior. In this species, males exposed to testosterone copulate while females never show this masculine behavior. The present paper reviews anatomical, neurochemical, and functional data that have been collected since that time about the quail dimorphic nucleus. The medial preoptic nucleus (POM) is significantly larger in adult male than in adult female quail. Its volume is also steroid-sensitive in adulthood: it decreases when circulating levels of testosterone are low (castration, exposure to short-days) and it increases when testosterone levels are high (treatment with testosterone, exposure to long-days). The POM is a necessary and sufficient site of steroid action for the activation of male copulatory behavior. The volumetric difference of the POM results from a difference in the adult hormonal milieu of males and females (activational effect) and is not affected by embryonic treatments that permanently modify sexual behavior (no organizational effects on POM). In contrast, the size of neurons in the dorsolateral part of POM appears to be irreversibly affected by embryonic steroids and this feature is therefore a better correlate of the behavioral sex difference. The POM is characterized by the presence of a wide variety of neurotransmitters, neuropeptides, and receptors. It can, in addition, be specifically distinguished from the surrounding POA by the presence of aromatase-immunoreactive cells, by a high density of alpha 2-adrenergic receptors, and by a dense vasotocinergic innervation. Some of these neurochemical markers of the dimorphic nucleus are themselves modulated by steroids. In particular, the aromatase-immunoreactive cells of the lateral POM appear to be a key target for steroids in the activation of male copulatory behavior. The POM is bidirectionally connected to many brain areas. It receives inputs from a variety of sensory areas and from a number of regulatory areas (e.g., catecholaminergic cell groups). This nucleus also sends outputs to "neurovegetative" centers and to brain regions directly connected to the motor pathways. These connections fully support the role of the POM as an integrative center for the control of male sexual behavior. The available data indicate that there is a high degree of steroid-induced neuronal plasticity in the POM, including changes in neuronal function, in protein synthesis, and in specific inputs. These phenomena can easily be studied in the POM because they are of a large magnitude, they are localized in a specific brain site, and they develop rapidly after exposure to steroids. They are also directly related to a clear functional output, the activation of male sexual behavior. The quail POM therefore constitutes an exceptional model for the analysis of steroid-induced brain plasticity in a functionally relevant context.

Androgens↗

PubMed1984

[Interneuronal relations in elementary neuronal assemblies].

Mechanisms of integrating cortical neurons into discrete modules--elementary ensembles--as functional units involved in formation of mosaic activity, in which input information is coded, were studied. Neurons primarily activated by specific afferent terminals and consistently responding with minimal latencies form the center of the ensemble while its periphery consists of secondary activated cells with variable long-latency reaction. Probabilistic participation of the latter in the ensemble structure underlies the cortical mechanism of plasticity. Neurons inhibited intracortically and, probably, by ascending inhibitory ways are situated in the periphery and at output ensemble elements.

Animals↗

PubMed1995

[The doctrine of brain localization and its development in the 20th century].

The discovery of the cerebral motor cortex in the last third of the 19th century has decisively influenced the doctrine of cerebral localization. It has dominated brain research from there on. Its considerable practical importance for focalized local diagnosis was recognized from the clinical point of view. As a consequence, interdisciplinary institutions for brain research developed in Europe and in the USA for the study of functional localization in the brain by means of cyto- and myeloarchitecture, electrical brain stimulation and lesion experiments in close connection with clinico-neurologic centers. From this research resulted the cerebral cortical maps with more or less numerous areas linked to either sensory, motor or 'higher' psychic functions. An intensive, emotional critique developed against the brain-localization theory from its onset. This article demonstrates that the arguments of the anti-localizationists gave rise in part to new knowledge about some principles of cerebral function. Some of these are the concept of 'diaschisis' (distant effects of acute lesions and functional recovery, von Monakow, 1902), the concept of 'motor equivalence' (Lashley, 1930) and of neuronal plasticity of the cerebral cortex (Cajal, 1911). Furthermore, modern imaging techniques (position emission tomography, functional nuclear spin resonance) show that complex functions in particular, such as the natural, targeted arm and grasp synergy, are not 'localized' within a small area of the cortex but do activate multiple neuronal networks interconnected dynamically and in alternating composition in the process of movement initiation and execution.

Brain↗

PubMed2006

Cyclic AMP response element binding protein and brain-derived neurotrophic factor: molecules that modulate our mood?

Depression is the major psychiatric ailment of our times, afflicting approximately 20% of the population. Despite its prevalence, the pathophysiology of this complex disorder is not well understood. In addition, although antidepressants have been in existence for the past several decades, the mechanisms that underlie their therapeutic effects remain elusive. Building evidence implicates a role for the plasticity of specific neuro-circuitry in both the pathophysiology and treatment of depression. Damage to limbic regions is thought to contribute to the etiology of depression and antidepressants have been reported to reverse such damage and promote adaptive plasticity. The molecular pathways that contribute to the damage associated with depression and antidepressant-mediated plasticity are a major focus of scientific enquiry. The transcription factor cyclic AMP response element binding protein (CREB) and the neurotrophin brain-derived neurotrophic factor (BDNF) are targets of diverse classes of antidepressants and are known to be regulated in animal models and in patients suffering from depression. Given their role in neuronal plasticity, CREB and BDNF have emerged as molecules that may play an important role in modulating mood. The purpose of this review is to discuss the role of CREB and BDNF in depression and as targets/mediators of antidepressant action.

Affect↗

PubMed2004

Volume transmission in activity-dependent regulation of myelinating glia.

The importance of neural impulse activity in regulating neuronal plasticity is widely appreciated; increasingly, it is becoming apparent that activity-dependent communication between neurons and glia is critical in regulating many aspects of nervous system development and plasticity. This communication takes place not only at the synapse, but also between premyelinating axons and glia, which form myelin in the PNS and CNS. Recent work indicates that neural impulse activity releases ATP and adenosine from non-synaptic regions of neurons, which activates purinergic receptors on myelinating glia. Acting through this receptor system, neural impulse activity can regulate gene expression, mitosis, differentiation, and myelination of Schwann cells (SCs) and oligodendrocytes, helping coordinate nervous system development with functional activity in the perinatal period. ATP and adenosine have opposite effects on differentiation of Schwann cells and oligodendrocytes, providing a possible explanation for the opposite effects of impulse activity reported on myelination in the CNS and PNS.

Adenosine Triphosphate↗

PubMed2002

Low levels of estrogen significantly diminish axonal sprouting after entorhinal cortex lesions in the mouse.

This study tested the hypothesis that estrogen enhances axonal sprouting in the hippocampal formation in the female mouse. The entorhinal cortex was unilaterally lesioned with ibotenic acid in control mice and in ovariectomized mice that were treated with a high dose of, a moderate dose of, or zero estrogen supplementation pellets. Four weeks later the density of staining for synaptophysin immunoreactivity and acetylcholinesterase (AChE) histochemistry was measured in the molecular layer of the dentate gyrus. In control mice, lesions of the lateral part of the entorhinal cortex increased synaptophysin and acetylcholinesterase staining (i.e., indicative of axonal sprouting) in the outer one-third of the molecular layer of the dentate gyrus. Mice receiving high and moderate estrogen supplementation displayed the same sprouting response; however, in ovariectomized mice the sprouting response was significantly reduced (to nearly nothing). Thus, in ovariectomized compared with control mice the lesion-induced sprouting response is severely blunted, and this effect is reversed by estrogen supplementation. Together, these findings suggest that estrogen plays a prominent role in promoting neuronal plasticity and remodeling in the dentate gyrus.

Acetylcholinesterase↗

PubMed2001

Dynamics and plasticity of peptidergic control centres in the retino-brain-pituitary system of Xenopus laevis.

This review deals particularly with the recent literature on the structural and functional aspects of the retino-brain-pituitary system that controls the physiological process of background adaptation in the aquatic toad Xenopus laevis. Taking together the large amount of multidisciplinary data, a consistent picture emerges of a highly plastic system that efficiently responds to changes in the environmental light condition by releasing POMC-derived peptides, such as the peptide alpha-melanophore-stimulating hormone (alpha-MSH), into the circulation. This plasticity is exhibited by both the central nervous system and the pituitary pars intermedia, at the level of molecules, subcellular structures, synapses, and cells. Signal transduction in the pars intermedia of the pituitary gland of Xenopus laevis appears to be a complex event, involving various environmental factors (e.g., light and temperature) that act via distinct brain centres and neuronal messengers converging on the melanotrope cells. In the melanotropes, these messages are translated by specific receptors and second messenger systems, in particular via Ca(2+) oscillations, controlling main secretory events such as gene transcription, POMC-precursor translation and processing, posttranslational peptide modifications, and release of a bouquet of POMC-derived peptides. In conclusion, the Xenopus hypothalamo-hypophyseal system involved in background adaptation reveals how neuronal plasticity at the molecular, cellular and organismal levels, enable an organism to respond adequately to the continuously changing environmental factors demanding physiological adaptation.

Adaptation, Physiological↗

PubMed1998

Factors governing activity-dependent structural plasticity of the hypothalamoneurohypophysial system.

1. The adult hypothalamoneurohypophysial system (HNS) undergoes reversible morphological changes in response to physiological stimulation. 2. In the hypothalamus, stimulation of neurohormone secretion results in reduced astrocytic coverage of oxytocinergic somata and dendrites so that their surfaces become directly juxtaposed. Concurrently, there is a significant increase in the number of GABAergic, glutamatergic. and noradrenergic synapses impinging on the neurons. 3. In the neurohypophysis, stimulation induces retraction of pituicyte processes from the perivascular area and enlargement and multiplication of neurosecretory terminals. 4. These neuronal-glial and synaptic changes are reversible with cessation of stimulation, thus rendering the HNS an excellent model to study physiologically linked structural neuronal plasticity in the adult CNS. 5. We still do not know the cellular mechanisms and factors underlying such plasticity. Recent studies indicate, however, that the adult HNS expresses molecular characteristics normally associated with histogenesis and/or tissue reorganization in developing or regenerating neural systems. They include expression of cell adhesion molecules such as the highly sialylated isoform of the neural cell adhesion molecule, PSA-NCAM, and the glycoproteins, F3 and tenascin-C. 6. The expression of PSA-NCAM and tenascin-C does not show striking differences in terms of age, sex or physiological condition but that of F3 varies considerably with neurohypophysial stimulation. 7. We postulate that such molecular features allow magnocellular neurons and their glia to undergo neuronal-glial and synaptic plasticity throughout life, provided the proper stimulus intervenes. 8. Thus, in the hypothalamic nuclei, centrally released oxytocin acting in synergy with steroids can induce such plasticity, while adrenaline, acting through beta-adrenergic mechanisms, does so in the neurohypophysis.

Animals↗

PubMed1999

Effects of nerve growth factor on visual cortical plasticity require afferent electrical activity.

It is known that administration of nerve growth factor (NGF) prevents the ocular dominance shift induced by monocular deprivation in the rat. To determine whether electrical activity in the visual afferent pathway is required for NGF effects on ocular dominance, we infused NGF into the cortex of animals subjected to complete monocular blockade of retinal discharges. Rats at the peak of the critical period received intravitreal tetrodotoxin (TTX) injections to silence activity in one eye for a period of 6-7 days; NGF was concurrently delivered into the visual cortex by means of osmotic minipumps. At the end of the treatment period, the ocular dominance distribution of cortical neurons was assessed by single-cell recordings. The results demonstrate that while infusion of NGF is effective in preventing the ocular dominance shift in lid-sutured rats, virtually no rescue can be observed in TTX-injected animals. Identical results were obtained when a specific agonist of the NGF receptor TrkA, the bivalent anti-rat TrkA IgG (RTA), was infused into the cortex in place of NGF. We conclude that NGF signalling via the TrkA receptor must be coupled to afferent electrical activity to produce its effects on the eye preference of cortical neurons. This suggests a generalized mechanism in which high-affinity neurotrophin receptor activation and afferent discharge interact to modulate neuronal plasticity in the developing visual cortex.

Animals↗

PubMed1996

Immediate early gene expression in cat visual cortex during and after the critical period: differences between EGR-1 and Fos proteins.

Immediate early gene (IEG) expression in the cat visual cortex is highly responsive to visual input and may initiate genetic mechanisms responsible for neuronal plasticity. The present study used immunohistochemical methods to address two issues regarding IEG expression in response to visual input. One was to define the differential response of distinct IEG families by comparing EGR-1 (also termed zif-268, NGFI-A, and Krox-24) and Fos proteins. The second was to determine whether IEG expression, in addition to reflecting neural activity, is related to the state of plasticity by comparing young and adult visual cortex. Immunoreactivity of the two IEG proteins was compared between 5-week-old and adult cats under three conditions of visual input: ambient light to assess basal levels of expression, 1 week of darkness to assess the effect of reduced activity, and exposure to light after 1 week of darkness to determine rapid changes in expression as a result of visual input. At both ages, there were marked differences in the expression of the two IEG proteins. EGR-1 responded to visual input with sustained changes in its level of expression. It showed high basal levels, reduced expression in darkness, and a rapid return to high constitutive levels with the introduction of light. Fos showed a markedly different profile. It had very low basal expression which was not demonstrably affected by darkness and its principal response was a marked transient induction upon exposure to light after darkness. These unique changes in expression highlight the complex response across IEGs to environmental input and suggest a genetic "on/off' signaling mechanism. There were marked differences in the laminar distribution of EGR-1 and Fos proteins between young and adult cats. In young animals, cells in all visual cortical layers showed high levels of EGR-1 and Fos proteins. In adults, immunostaining was largely specific to cells located above and below layer IV and only very faint labeling occurred within layer IV. These differences in laminar distribution between ages are inconsistent with a simple explanation of IEG expression in terms of neural activity level; rather, they suggest a relation between IEG expression and the state of plasticity in visual cortex.

Animals↗

PubMed1999

Amelioration of fornix lesion induced learning deficits by self-stimulation rewarding experience.

Intracranial self-stimulation (ICSS) rewarding experience is known to modulate learning and memory and induce morphological and neurochemical changes in hippocampus. Therefore, we studied the effect of ICSS on the hippocampus-dependent operant and the spatial learning tasks in rats with bilateral electrolytic lesioning of fornix. Bilateral lesioning of fornix induced deficits in acquisition and performance of both the tasks, whereas exposure to 10 days of ICSS experience from ventral tegmental area reversed these behavioural deficits. Hence, we propose that the ICSS experience ameliorates the fornix lesion induced behavioural deficits, by inducing neuronal plasticity in the hippocampus which may act as a compensatory mechanism for the deficits produced by the lesioning of fornix.

Animals↗

PubMed1999

Tolerance develops to the inhibitory effect of orphanin FQ on morphine-induced antinociception in the rat.

Recent studies that intracerebroventricular (i.c.v.) administration of orphanin FQ (OFQ) blocks opioid-induced antinociception in a variety of animal models of pain. In the present study, we sought to investigate the inhibitory effect of OFQ on morphine-induced antinociception using the hot plate test in rats and to examine whether tolerance develops to the anti-opioid effect of the peptide. Microinjection of OFQ (50nmol, i.c.v.) significantly attenuated the antinociceptive effect of morphine without affecting baseline hot plate latencies, suggesting that modification of morphine-induced antinociception can be achieved via activation of the ORL-1 receptor by OFQ with no apparent mu opioid receptor blockade or interference with basal nociceptive responses. Chronic treatment with OFQ (50 nmol/day for 5 days) produced a complete loss of the inhibitory effect of the peptide indicating that tolerance developed to the anti-opioid effect of OFQ. Taken together, these results indicate that neuronal plasticity may occur following chronic use of OFQ as is evident for the other opioid agonists.

Analgesics, Opioid↗

PubMed2005

Distributed neural plasticity for shape learning in the human visual cortex.

Expertise in recognizing objects in cluttered scenes is a critical skill for our interactions in complex environments and is thought to develop with learning. However, the neural implementation of object learning across stages of visual analysis in the human brain remains largely unknown. Using combined psychophysics and functional magnetic resonance imaging (fMRI), we show a link between shape-specific learning in cluttered scenes and distributed neuronal plasticity in the human visual cortex. We report stronger fMRI responses for trained than untrained shapes across early and higher visual areas when observers learned to detect low-salience shapes in noisy backgrounds. However, training with high-salience pop-out targets resulted in lower fMRI responses for trained than untrained shapes in higher occipitotemporal areas. These findings suggest that learning of camouflaged shapes is mediated by increasing neural sensitivity across visual areas to bolster target segmentation and feature integration. In contrast, learning of prominent pop-out shapes is mediated by associations at higher occipitotemporal areas that support sparser coding of the critical features for target recognition. We propose that the human brain learns novel objects in complex scenes by reorganizing shape processing across visual areas, while taking advantage of natural image correlations that determine the distinctiveness of target shapes.

Form Perception↗