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Results for “Neuronal Plasticity”

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At least 73 records · Page 4Linked to original sources

PubMed1994

Absence of maladaptive neuronal plasticity after genitofemoral-ilioinguinal neurectomy.

BACKGROUND: Pain (neuralgia) and paresthesia in the inguinal region after lower abdominal surgery is rare. Historically, treatment consisted of neurolysis, local injections, and administration of various medications. The management of chronic pain syndromes is often coordinated by anesthesiologists. Neurolytic therapy is seldom recommended, on the basis of the theory of maladaptive neuronal plasticity. METHODS: Twenty-three patients underwent genitofemoral neurectomy at our institution between 1981 and 1990. Records were reviewed to determine preoperative symptoms, evaluation, and treatment. Patients were contacted and questioned about current symptoms and disability. RESULTS: All records were reviewed. Sixteen (70%) of the patients were located for long-term follow-up. Patients were symptomatic for an average of 3.3 years and underwent 3.1 operations before referral. Inguinal herniorrhaphy was the most common initial surgery (14 of 16 patients). All patients underwent multidisciplinary evaluation. Fifteen underwent L1-2 paraspinous nerve block, and 13 had total pain relief. Postoperative follow-up ranged from 36 to 144 months. Ten patients reported significant pain relief, and three patients reported slight improvement. Three of the six patients who had persistent neuralgia had significant orchialgia. None of the patients who had significant relief had preoperative testicular pain. CONCLUSIONS: Genitofemoral neurectomy provided long-term relief in 62.5% of patients with genitofemoral neuralgia. Severe testicular pain indicated a less favorable outcome. These data do not support the maladaptive neuronal plasticity theory but do support early referral of some patients for neurectomy.

Adult↗

PubMed1999

[Effect of the cytoskeleton dynamic condition on the neuronal plasticity].

Infringement of the Lymnaea stagnalis cytoskeleton condition affected preservation and repeated development of plastic responses. Stabilising of the microtubules led to a dependence of the development and preservation dynamics of the plastic responses. Stabilising of the microfilaments transformed short-term plastic responses into long-term ones. The findings suggest a key role of reorganisation of the cytoskeleton in neuronal plasticity.

Action Potentials↗

PubMed2005

Persistent sodium current is a target for cAMP-induced neuronal plasticity in a state-setting modulatory interneuron.

We have identified a TTX-resistant low-threshold persistent inward sodium current in the cerebral giant cells (CGCs) of Lymnaea, an important state-setting modulatory cell type of molluscan feeding networks. This current has slow voltage-dependent activation and de-activation kinetics, ultra-slow inactivation kinetics and fast de-inactivation kinetics. It activates at approximately -90 mV, peaks at approximately -30 mV, reverses at approximately +35 mV and does not show full voltage-dependent inactivation even at positive voltage steps. Lithium-sodium replacement experiments indicate that the persistent sodium current makes a significant contribution to the CGC membrane potential. Injection of cyclic adenosine monophosphate (cAMP) into the CGC cell body produces a large increase in the persistent sodium current that lasts for several hours. cAMP injection also leads to increased bursting, a significant decrease in the resistance and a significant depolarization of the soma membrane, indicating that cAMP-dependent mechanisms induce prolonged neuronal plasticity in the CGCs. Our observations provide the first link between cAMP-mediated modulation of a TTX-resistant persistent sodium current and prolonged neuronal plasticity in an identified modulatory cell type that plays an important role in behavioral state setting.

Action Potentials↗

PubMedDate not supplied

[A mathematical model of neuronal plasticity].

A model of the neuron is proposed which is capable of learning with a teacher. The model is based on hypothetic chemical processes which can proceed in a real nerve cell. It is shown that such model having O(N2) elements of the memory is capable of dividing in two classes O(N2) of different input images, where N is the dimensionality of the input vector.

Models, Neurological↗

PubMedDate not supplied

The effects of the dynamic state of the cytoskeleton on neuronal plasticity.

The effects of degrading and stabilizing microtubules and microfilaments on the formation of plastic reactions were studied in isolated nerve cells from the mollusk Lymnaea stagnalis. Degradation of the cytoskeleton affected the performance, retention, and repeated acquisition of plastic reactions. Stabilization of microtubules led to the appearance of a relationship between the dynamics of the development and retention of plastic reactions and the series of stimulation. Stabilization of microfilaments led to transient plastic reaction, along with long-term reactions. These results show that rearrangements of the cytoskeleton have a key role in the processes of neuronal plasticity.

Actin Cytoskeleton↗

PubMed1989

Neuronal plasticity in the adult invertebrate nervous system.

This essay provides a brief overview of neuronal plasticity in adult invertebrate nervous systems. Our discussion focuses on the factors which influence sprouting by adult neurons, i.e., (1) the nature of the neuron itself, (2) axon integrity, (3) the presence of targets, (4) diffusible factors, and (5) ageing. Evidence that the neurites of some adult neurons exhibit a dynamic equilibrium of expansion and retraction is presented, a topic which prompted us to speculate on the significance of such plasticity in altered behavioral states. We conclude with some suggestions as to specific questions that need to be addressed by future studies in this challenging area.

Animals↗

PubMed2002

A dual role for the SDF-1/CXCR4 chemokine receptor system in adult brain: isoform-selective regulation of SDF-1 expression modulates CXCR4-dependent neuronal plasticity and cerebral leukocyte recruitment after focal ischemia.

The chemoattractant stromal cell-derived factor-1 (SDF-1) and its receptor CXC chemokine receptor 4 (CXCR4) are key modulators of immune function. In the developing brain, SDF-1 is crucial for neuronal guidance; however, cerebral functions of SDF-1/CXCR4 in adulthood are unclear. Here, we examine the cellular expression of SDF-1 isoforms and CXCR4 in the brain of mice receiving systemic lipopolysaccharide (LPS) or permanent focal cerebral ischemia. CXCR4 mRNA was constitutively expressed in cortical and hippocampal neurons and ependymal cells. Hippocampal neurons targeted the CXCR4 receptor to their somatodendritic and axonal compartments. In cortex and hippocampus, CXCR4-expressing neurons exhibited an overlapping distribution with neurons expressing SDF-1 transcripts. Although neurons synthesized SDF-1alpha mRNA, the SDF-1beta isoform was selectively expressed by endothelial cells of cerebral microvessels. LPS stimulation dramatically decreased endothelial SDF-1beta mRNA expression throughout the forebrain but did not affect neuronal SDF-1alpha. After focal cerebral ischemia, SDF-1beta expression was selectively increased in endothelial cells of penumbral blood vessels and decreased in endothelial cells of nonlesioned brain areas. In the penumbra, SDF-1beta upregulation was associated with a concomitant infiltration of CXCR4-expressing peripheral blood cells, including macrophages. Neuronal SDF-1alpha was transiently downregulated and neuronal CXCR4 was transiently upregulated in the nonlesioned cerebral cortex in response to ischemia. Although endothelial SDF-1beta may control cerebral infiltration of CXCR4-carrying leukocytes during cerebral ischemia, the neuronal SDF-1alpha/CXCR4 system may contribute to ischemia-induced neuronal plasticity. Thus, the isoform-specific regulation of SDF-1 expression modulates neurotransmission and cerebral infiltration via distinct CXCR4-dependent pathways.

Animals↗

PubMed1989

Neuronal plasticity in the hedgehog supraoptic nucleus during hibernation.

The purpose of the present study was to identify processes of plasticity in the receptive field of neurosecretory neurons of the supraoptic nucleus during hibernation in the hedgehog, in order to correlate them with the increased neurosecretory activity observed in this nucleus during this annual period. Using the Rapid Golgi method, a quantitative study was conducted in the receptive field of bipolar and multipolar neurons (the main components of the nucleus). Results indicate a generalized increase in the following characteristics: (1) number of dendritic spines per millimeter along the dendritic shafts; (2) degree of branching in the dendritic field; and (3) dendritic density around the neuronal soma. These data demonstrate modification of the dendritic field in the supraoptic nucleus during hibernation, a change undoubtedly related to functional conditions. Since the observed changes affect structures such as dendritic spines which are directly related to the arrival of neural afferences, the discussion is centered on the types of stimuli which may be responsible for the observed processes.

Animals↗

PubMed1992

Neuronal plasticity depending on a glycoprotein synthesized in goldfish leptomeninx.

Transcription of a calcium and zinc binding, nervous system-specific cell adhesion glycoprotein, ependymin, in goldfish leptomeninx was significantly enhanced after active avoidance conditioning, followed by enhanced translation and secretion. Inactivation of secreted ependymin by injected antisera interfered with behavioral adaptations. In addition to the site of synthesis in reticular cells of the leptomeninx electronmicroscopic immunochemistry localized the protein to tectal neurons of the superficial plexiform and the periventricular cell layers. Detection of ependymin in cells where it is not synthesized, namely in neurons, suggests a re-uptake during functional activity of the CNS and assigns a pivotal role to the cerebrospinal and interstitial brain fluids for the distribution of protein factors that support axonal growth and neuronal plasticity.

Animals↗

PubMed1995

Differential expression and distinct DNA-binding specificity of ME1a and ME2 suggest a unique role during differentiation and neuronal plasticity.

Class A basic-helix-loop-helix (bHLH) proteins have been referred to as ubiquitous and are believed to have redundant functions. They are involved in the control of several developmental pathways, such as neurogenesis and myogenesis. To rationalize the existence of multiple class A bHLH proteins, we evaluated the differences and similarities between ME1a and ME2, two class A bHLH proteins, highly expressed in differentiating neuronal cells. In situ hybridization analyses reveal that ME1a and ME2 are characterized by distinguishable patterns of expression in areas of the adult mouse brain where neuronal plasticity occurs. Also, DNA-binding assays show that both proteins bind to E-boxes as homodimers and heterodimers, and show differences in their DNA-binding specificities, which suggest selective interactions with different binding sites of target genes. In addition, in vitro DNA-binding assays demonstrate that Id2 forms heterodimers with ME1a and ME2. As a result of these interactions, their DNA-binding activity is abolished. Furthermore, overexpression of Id2 in neuronal cells suppresses ME1a and ME2 transcriptional activity. Based on our data, we hypothesize that ME1a and ME2 may activate gene expression of different target genes and therefore are likely to be differently involved during neurogenesis.

Animals↗

PubMed1998

The relationship between adhesion molecules and neuronal plasticity.

1. It is presently widely assumed that structural reorganization of synaptic architectures subserves the functional gains that define certain neuronal plasticities. 2. While target molecules thought to participate in such morphological dynamics are not well defined, growing evidence suggests a pivotal role for cell adhesion molecules. 3. Herein, brief discussions are presented on (i) the history of how adhesion molecules became implicated in plasticity and memory processes, (ii) the general biology of some of the major classes of such molecules, and (iii) the future of the adhesion molecule/plasticity relationship.

Animals↗

PubMed2005

Exogenous gangliosides, neuronal plasticity and repair, and the neurotrophins.

Gangliosides, a heterogeneous family of glycosphingolipids abundant in the brain, have been shown to affect neuronal plasticity during development, adulthood and aging. This review will examine old and recent evidence that exogenous gangliosides and in particular GM1, the prototype member of this family, exhibit multimodal neurotrophic effects. Since these compounds are a potential therapeutic tool for the treatment of various forms of acute or chronic neurodegenerative diseases, understanding the dynamic interplay of gangliosides and neuronal cells is essential in the effort to cure neurological disorders. Focus will be given to the novel and provocative hypothesis that gangliosides' neuroprotective properties may derive from their ability to mimic endogenous neurotrophic factors.

Gangliosides↗

PubMed1997

Hormonally induced neuronal plasticity in the adult motoneurons.

Sex steroids are known to play a crucial role in reproductive neuroendocrine functions in adulthood. A number of neurons in the neuroendocrine brain contain sex steroid receptors, and are thought to be a key element of functional neural circuits that are regulated by sex steroids. Motoneurons in the spinal nucleus of the bulbocavernosus in adult male rodents are one of the androgen-sensitive neural substrates. In the spinal nucleus of the bulbocavernosus, castration of adult male rats results in a significant decrease in the somatic size and dendritic length of the motoneurons, and in the number and size of chemical and electrical (gap junction) synapses onto these motoneurons. Androgen treatment of castrates reverses these changes. Furthermore, androgen has been reported to be involved in regulation of androgen receptor expression and gene expression of structural proteins such as beta-actin, beta-tubulin and gap junction channels in these motoneurons. The findings suggest that androgen induces morphological and molecular changes in the motoneurons that reflect their neural functions, and may provide evidence for the mechanisms of hormonally induced neuronal plasticity in the motoneurons in adulthood.

Actins↗

PubMed2000

Neuronal plasticity: increasing the gain in pain.

We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.

Animals↗

PubMed1989

Down-regulation of norepinephrine sensitivity after induction of long-term neuronal plasticity (kindling) in the rat dentate gyrus.

Actions of norepinephrine (NE) in the dentate gyrus were examined before and after kindling-induced epilepsy, neuronal plasticity produced by daily high-frequency stimulation. NE, acting on beta 1-receptors, depolarized granule cells, increased input resistance, firing and influx of Ca2+ in response to repetitive stimulation, and elicited long-lasting potentiation of synaptic potentials. In addition, NE acting via alpha 1-receptors, attenuated Ca2+-dependent regenerative potentials. After kindling-induced plasticity, there were marked reductions in all these effects of NE on granule cells, changes likely to influence kindling-induced seizures, protecting against further enhancement of excitability once plasticity is in place.

Action Potentials↗

PubMed2003

Reversible paired helical filament-like phosphorylation of tau is an adaptive process associated with neuronal plasticity in hibernating animals.

Neurofibrillary pathology [paired helical filaments (PHFs)] formed by the microtubule-associated protein tau in a hyperphosphorylated form is a major hallmark of Alzheimer's disease and related disorders. The process of tau phosphorylation, thought to be of critical importance for PHF formation, and its potential link to neurodegeneration, however, is not understood very well, mostly because of the lack of a physiological in vivo model of PHF-like tau phosphorylation. Here we describe the formation of highly phosphorylated tau, containing a number of PHF-like epitopes in torpor during hibernation. PHF-like phosphorylation of tau was not associated with fibril formation and was fully reversible after arousal. Distribution of PHF-like tau followed a consistent pattern, being most intense in the entorhinal cortex, hippocampus, and isocortical areas. Within the hippocampus, a particularly high labeling was seen in CA3 pyramidal cells. Somewhat lesser reactivity was present in CA1 neurons while dentate gyrus granule cells were not reactive. Formation of PHF-like tau in CA3 neurons was paralleled by the regression of synaptic contacts of the mossy fiber system terminating on CA3 apical dendrites. Mossy fiber afferentation was re-established during arousal, concomitantly with the decrease of PHF-like tau in CA3 neurons. These findings implicate an essential link between neuronal plasticity and PHF-like phosphorylation of tau. The repeated formation and degradation of PHF-like tau might, thus, represent a physiological mechanism not necessarily associated with pathological effects. Hibernation will, therefore, be a valuable model to study the regulation of PHF-like tau-phosphorylation and its cell biological sequelae under physiological in vivo conditions.

Adaptation, Physiological↗

PubMed1993

Effects of intracortical infusion of anticholinergic drugs on neuronal plasticity in kitten striate cortex.

During a critical period of postnatal development the mammalian visual cortex is highly susceptible to experience-dependent alterations of neuronal response properties. These modifications are facilitated by the neuromodulators noradrenaline and acetylcholine. To identify the cholinergic mechanisms responsible for this facilitation, muscarinic and nicotinic antagonists were infused into the visual cortex of kittens while the animals were subject to monocular deprivation. Subsequently the ocular dominance of cortical cells was assessed by single-unit recording. Ocular dominance changes were suppressed by scopolamine and pirenzepine but not by gallamine, hexamethonium and mecamylamine. This blocking effect was concentration-dependent, and control experiments revealed that it was not due to suppression of neuronal responses to light. It is concluded from these results that acetylcholine facilitates neuronal plasticity in the visual cortex through mechanisms activated by muscarinic M1 receptors.

Animals↗

PubMed2005

Site-specific phosphorylation of SCG10 in neuronal plasticity: role of Ser73 phosphorylation by N-methyl D-aspartic acid receptor activation in rat hippocampus.

Accumulated evidence suggests that actin and microtubule regulating proteins contribute to neuronal structural dynamics, which subsequently affect neuronal plasticity. SCG10 is a neuronal-specific stathmin protein with microtubule destabilizing activity that is affected by multiple phosphorylation, at least in vitro. SCG10 has four major phosphorylation sites: Ser50 and Ser97 targeted by protein kinase A (PKA), and Ser62 and Ser73 targeted by mitogen-activated protein kinase (MAPK). To explore the potential roles of site-specific phosphorylation in physiological models, we developed phosphorylation site-specific antibodies and examined the SCG10 status in primary cultured hippocampal neurons and tissues. Although SCG10 is concentrated in growth cones and the Golgi apparatus in primary cultured neurons, the phosphorylated form was also detected in both regions, suggesting that MT dynamics within the growth cone may be regulated by protein phosphorylation. In the adult hippocampus, an intense stimulus such as kainate treatment induced a rapid phosphorylation of Ser73 within 15 min that was sustained for at least 60 min. This response was mediated through the N-methyl D-aspartic acid (NMDA) receptor and was ablated by the antagonist MK-801. The MAPK enzyme Erk2 was simultaneously activated along a similar time course to SCG10, suggesting that Erk2 may directly phosphorylate Ser73. These results demonstrate that changes in the phosphorylation status of SCG10 in vivo, dependent upon neural activity and/or plasticity, could affect the microtubule dynamics in neuronal dendrites.

Amino Acid Sequence↗