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Results for “Neuronal Plasticity”

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PubMed2004

Calcium signal-dependent plasticity of neuronal excitability developed postnatally.

Neuronal plasticity and its development were investigated at pyramidal neurons in the cortical slices of rats. The threshold and probability of firing spikes were measured by using whole-cell recording to assess neuronal excitability. Postsynaptic high frequency activity (HFA) at the pyramidal neurons, evoked by 20 trains (250-ms interval) of five depolarization-pulses (1 ms) at 100 Hz, persistently lowered the threshold and increased the probability of firing spikes. After long-term enhancement of neuronal excitability by HFA was stable, another HFA induced further enhancement. Infusing 1 mM 1,2-bis(2-aminophenoxy)-ethane-N, N,N',N'-tetraacetic acid or 100 microM CaMKII(281-301) into the recording neurons prevented HFA-induced long-term enhancement of neuronal excitability. The infusion of 40 microM calcineurin autoinhibitory peptide enhanced neuronal excitability, which occluded HFA effect. HFA-induced long-term enhancement of intrinsic excitability expressed at most pyramidal neurons after postnatal day (PND) 14, but not at those before PND 9. Our results show a new type of neuronal plasticity induced by physiological activity at cortical neurons, which requires calcium-dependent protein phosphorylation and develops during postnatal period. An upregulation of intrinsic excitability at cortical neurons facilitates their activity and broadens signal codes; consequently, their computational ability is upgraded.

Action Potentials↗

PubMed2005

Functional magnetic resonance imaging and multiple sclerosis: the evidence for neuronal plasticity.

Blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) has emerged as a powerful technique to visualize the localization of cerebral activity in both healthy and diseased brains. BOLD fMRI has been used to assess brain function in a variety of diseases, including multiple sclerosis (MS), and has shown that altered patterns of connectivity are used to recruit more widespread eloquent brain networks engaged in tasks relating to motor activity, sensory and cognitive function, and memory when compared to normal controls. This review will examine the evidence that functional reorganization is a consequence of demyelination and tissue loss in MS that may serve as an adaptive response to limit clinical disability. It remains unclear whether cerebral plasticity is a marker of permanent functional restructuring or a short-term compensatory response to injury. Long-term longitudinal studies that correlate fMRI activity with other MRI markers of disease burden and activity, as well as with clinical measures of disease activity and progression, are badly needed to determine fMRI's relevance to clinical practice and its place as a surrogate outcome measure in MS.

Brain↗

PubMed1995

Protein phosphorylation in neuronal plasticity and gene expression.

Protein kinases and phosphatases are intimately involved in several forms of synaptic plasticity. They play a critical role in the initiation of long-term potentiation and long-term depression, as well as in the induction of genes that permit long-term expression of altered synaptic states. Recent findings demonstrate a central role for the cAMP signaling pathway in the persistent phase of long-term potentiation. Genetic approaches have established that the transcription factor CREB is essential for long-term memory.

Animals↗

PubMed1981

Neuronal plasticity: how changes in dendritic architecture can affect the spread of postsynaptic potentials.

Calculations from a theoretical model are presented which illustrate the electrophysiological changes that can result from alterations in dendritic branching. Much evidence has implicated modifications in dendritic architecture with learning, aging and certain neural pathologies. It is found that both the peak amplitude and the half-width of a time-varying postsynaptic potential generated by a previously established synapse can be affected by dendritic changes distal to the input. For the examples considered in this paper peak amplitude is decreased if distal branching occurs, whereas half-width is increased.

Animals↗

PubMed1993

[3H]phorbol ester binding sites and neuronal plasticity in the hippocampus following entorhinal cortex lesions.

Entorhinal cortex lesioning (ECL) produces a loss of more than 80% of the synapses in the outer molecular layer of the hippocampus. However, the loss of synapses is transient. Beginning a few days after denervation, new synapses are formed, virtually replacing the lost inputs within 2 months. Synaptic remodelling induced by ECL is associated with specific modifications of neurotransmitters, hormones and growth factors. Particularly, protein kinase C (PKC) plays important functional roles in receptor-mediated transmembrane signal transduction. PKC is also involved in various aspects of synaptic plasticity, such as cellular growth and differentiation. To investigate further the potential roles of PKC in synaptic plasticity observed in the ECL model, [3H]phorbol 12,13-dibutyrate ([3H]PDBu) binding, a putative marker of PKC, was examined at different times post-lesion. [3H]PDBu binding sites transiently decreased bilaterally at 2 and 8 days post-lesion (20%) in different laminae and sub-fields of the rostral hippocampus but returned to control values at 14 and 30 days post-lesion. In caudal portion of the hippocampus, [3H]PDBu binding was also decreased at 2 days post-lesion but only on the contralateral side. Interestingly, [3H]PDBu binding sites in the cortex increased by up to 30% in the contralateral side while no significant change was observed in the ipsilateral side at any time post-lesion. It is known that PKC can be regulated by different systems following alterations of neuronal and glial activity. We suggest that these could be involved in the response of PKC and [3H]PDBu binding sites following ECL. Moreover, PKC seemed to be modified in different brain areas in neuronal inputs from the entorhinal cortex and the subsequent reinnervation process.

Acetylcholinesterase↗

PubMed2000

Neuronal plasticity and stressor toxicity during aging.

Brain aging, Alzheimer disease and stroke share common elements of deficits in calcium regulation, declines in mitochondrial function, increases in generation of reactive oxygen species (ROS), accumulated damage from ROS and immune system dysfunction. The problem is to distinguish less significant side reactions, such as gray hair, from aspects of aging that contribute to disease. Toward establishing cause and effect relationships, a neuron cell culture system is described that allows comparisons with age under uniform environmental conditions. This neuron culture model indicates that susceptibility to death by apoptosis and consequences of the inflammatory response from beta-amyloid are age-related and an inherent characteristic of the neurons. Further mechanistic investigations are possible. New therapeutic approaches are suggested that combine inhibition of calcium overloads (calcium channel blockers), reduced ROS damage (melatonin, N-acetyl-cysteine), and bolstered mitochondrial function and energy generation (creatine). Together with newly demonstrated capabilities for adult and aged neuron regeneration and multiplication, i.e. plasticity, these approaches offer new hope toward reversing age-related decrements and damage from neurodegenerative disease.

Aging↗

PubMed1994

Neuronal plasticity and pre-emptive analgesia: implications for the management of postoperative pain.

Prevention of injury-induced functional alterations in the central nervous system by pre-emptive analgesia or other techniques is a fascinating working hypothesis based on substantial scientific evidence. Although experimental data may provide a rationale for this concept, translation into clinical practice has led to some debate, especially about interpretation of results from studies in postoperative patients (Katz et al. 1992a, 1993; Dahl et al 1992a, 1993b; Dahl & Kehlet 1993a). This may partly be due to a difference in experimental versus clinical benefits from pre-emptive analgesia and furthermore, clinicians may ask if preoperative administration of morphine or other opioids is really a "novel approach" (Katz 1993) to the management of postoperative pain. Thus, administration of opioids for premedication, and during induction and maintenance of general anaesthesia has been common clinical practice for decades. In spite of this practice, patients have suffered from unacceptable postoperative pain. Several critical elements must be addressed before the concept can be applied into clinical practice. Thus, the idea originates from experimental studies, often with anaesthetized or decerebrated animals, and with nociceptive stimuli which did not involve severe ongoing tissue damage. The various types of noxious stimuli (C-fiber stimulation, heat-, chemical-, inflammatory- and neuronal lesions) may differ from the surgical injury, and the time-scale of the experiments, and the profiles of analgesic effects and efficacy may differ from the clinical situation. In a study of patients undergoing gynaecological laparotomy, increased sensitivity to noxious electrical stimulation of the sural nerve was observed postoperatively, with a corresponding trend in the nociceptive flexion reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

PubMedDate not supplied

The effects of antibodies against proteins of the s100 group on neuron plasticity in sensitized and non-sensitized snails.

The effects of antibodies to a total fraction of s100 proteins and protein s100b on the activity of defensive behavior command neurons LP11 and RP11 were studied in common snails, using non-sensitized animals and animals which had acquired nociceptive sensitization. In non-sensitized snails, application of antibodies against s100 or s100b (0.1 mg/ml) induced membrane depolarization, increased membrane permeability, and suppressed slow excitatory postsynaptic potentials in the responses of neurons to sensory stimulation. Acquisition of sensitization in snails in the presence of antibodies to s100 or s100b (0.1 mg/ml) led to significantly less marked facilitation of synaptic transmission and smaller increases in neuron membrane excitability than in cells of control sensitized animals. The difference in synaptic facilitation in the neurons of control sensitized snails and neurons in sensitized snails given antibody was comparable with the magnitude of synaptic depression due to antibody in non-sensitized animals. At a dose of 0.01 mg/ml, antibody had no effect on these measures of neuron activity. It is suggested that s100 proteins, particularly s100b, are involved in the mechanisms regulating excitability, the membrane potential, and synaptic transmission in command neurons in untrained snails, as well as in the mechanism of plasticity of the electrogenic membranes of nerve cells during the acquisition of nociceptive sensitization.

Action Potentials↗

PubMed1991

[Hemisphere dominance of cortical speech processing and its dynamics in the course of aphasia therapy. A psychophysiologic contribution to the discussion of the neuronal plasticity hypothesis].

Examinations of aphasic patients by using cognitive tasks were based on the hypothesis that semantically evoked potentials correlate to the processing of information in the cortical areas of Broca and Wernicke. Some of the examined right-handed patients with ischemic lesions of the left hemisphere produced characteristic potentials in the right temporal lobe, and not in the dominant left lobe as was expected. These case histories suggest that in these patients speech processing moved into the subdominant hemisphere as a result of compensation after cerebral damage by using the faculty of neuroplasticity. Furthermore an extended classification of aphasias is presented, illustrated by a three-parameter model.

Aged↗

PubMed1998

Fibromyalgia and headache. Failure of serotonergic analgesia and N-methyl-D-aspartate-mediated neuronal plasticity: their common clues.

A defect in serotonergic analgesia and a hyperalgesic state are proposed as features common to headache and fibromyalgia. The benefit to both migraine and fibromyalgia from inhibiting ionotropic N-methyl-D-aspartate receptor activity implies that redundant hyperalgesia-related neuroplastic changes are crucial for severe or chronic migraine and primary fibromyalgia. The fact that migraine and primary fibromyalgia share some pivotal set-up of serotonergic and excitatory amino acid systems led us to analyse epidemiological data supporting the hypothesis that analgesic disruption and a consequent hyperalgesic state are mechanisms of both migraine and fibromyalgia. Beyond demonstrating the comorbidity between migraine and primary fibromyalgia, the data suggest that migraine may represent a risk factor for fibromyalgia.

Analgesics↗

PubMed1986

Abnormal arborizations of Purkinje cell dendrites in Creutzfeldt-Jakob disease: a manifestation of neuronal plasticity?

A case is presented of the ataxic variety of Creutzfeldt-Jakob disease with particular reference to the cerebellar cortex. The main features were loss of granule cells, subtotal in the vermis, severe in the lateral lobes, mild to moderate loss of Purkinje cells and preservation of tangential and basket fibres. The Purkinje cell dendrites showed malorientation and hypertrophy of the primary and secondary branches, the so-called "antler" or "staghorn" deformity. These findings indicate that remodelling of the dendritic tree may start early in the course of the disease even in adults, the total length of history in this case being eight months. They do not throw any additional light on the pathogenesis of the dendritic abnormalities, in particular on the controversy whether they are a non-specific response of the Purkinje cell to a variety of noxious agents or a reaction to partial deafferentation. The authors favour the latter hypothesis.

Brain↗

PubMed2007

Neuronal plasticity and neuroregeneration in the skin -- the role of inflammation.

The skin develops probably the densest and most complex innervation of all mammalian organs, consisting of sensory and autonomic nerves loaded with a plethora of neuropeptides and neurotransmitters. Skin innervation, as well as the expression patterns of neurotrophins and their receptors, is subject to dramatic changes during not only morphogenesis but also adult tissue remodeling under physiological or inflammatory conditions. Bilateral neuroimmune interactions are the basis of adaptive responses to tissue remodeling (such as hair cycling), psycho-emotional stress or skin inflammation. Dermatitis and hair loss may be exacerbated by stress-induced neurogenic inflammation. In addition, selected inflammatory skin diseases are associated with increased innervation. Finally, inflammatory cytokines influence the cutaneous expression of neurotrophins, as well as neurotrophin-induced neurite outgrowth following axotomy. Here, we review key studies on bilateral neuroimmune interactions in the skin under both healthy and disease conditions to provide a basis for future research on the role of inflammation in peripheral nerve regeneration.

Animals↗

PubMed2005

Neuronal plasticity in persistent perennial allergic rhinitis.

OBJECTIVE: Persistent perennial allergic rhinitis belongs to the most frequent diseases in occupational and environmental medicine. Because the innervation may play a role in the pathogenesis of the disease, the present study analyzed nasal mucosal nerve profiles. METHODS: Neuropeptide-containing nerve fibers were examined using immunohistochemistry and related to eosinophil and mast cell numbers. RESULTS: In contrast to constant numbers of mast cells, there was a significant increase in the number of eosinophils. Immunohistochemistry for calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP), and neuropeptide tyrosine (NPY) revealed abundant staining of mucosal nerves. Semiquantitative assessment of nerve fiber neuropeptide density demonstrated a significant increase of VIP-positive fibers in rhinitis tissues. CONCLUSIONS: The present data indicate a differential regulation of neuropeptide-containing nerve fibers with increased numbers of VIPergic fibers suggesting a modulatory role of the upper airway innervation in perennial allergic rhinitis.

Adolescent↗

PubMed1994

Inverse patterns of myelination and GAP-43 expression in the adult CNS: neurite growth inhibitors as regulators of neuronal plasticity?

In the central nervous system (CNS) myelin is present not only in white matter, but also in varying amounts in many gray matter areas. In addition to the function of electrical insulation of axons, myelin and oligodendrocytes contain molecules that are powerful inhibitors of neurite growth. Nevertheless plastic changes involving sprouting of nerve terminals occur in several brain regions of adult animals after partial lesions. In this study we have tried to correlate the plastic potential of CNS regions with the degree of their myelination. The expression of the growth-associated protein GAP-43 was used as an indicator of the potential for plastic changes, and a histological myelin stain was used to assess myelination. We have found that myelination and GAP-43 expression have strikingly inverse expression patterns in the majority of CNS gray matter areas. Densely myelinated regions, that is, most brainstem nuclei, the tegmentum, and the inferior colliculus, are low in GAP-43. In contrast, unmyelinated or lightly myelinated areas, such as the substantia gelatinosa of the spinal cord, the nucleus of the solitary tract, or the septum, express high levels of GAP-43. Areas known to show lesion-induced sprouting are typically high in GAP-43 and only lightly myelinated. During postnatal development the myelination pattern precedes the GAP-43 pattern, a sequence that is consistent with a role of myelin and the associated neurite growth inhibitors in modifying GAP-43 expression. Our results support the hypothesis that myelin-associated neurite growth inhibitors are involved in regulating the stability of neural connections.

Animals↗

PubMed2005

[Endogenous cannabinoid system. Effect on neuronal plasticity and pain memory].

AIM: The aim of this study was to evaluate the role of the endogenous cannabinoid system in controlling neuroplasticity. METHODS: The pain threshold for electrical stimuli was determined in transgenic mice lacking the cannabinoid receptor type 1 (CB1(-/-)) and in the corresponding respective wild-type animals. Electrophysiological experiments were performed in prepared brain slices to test the effect of endogenous and exogenous cannabinoids on synaptic transmission and long-term potentiation (LTP) in the amygdala. RESULTS: The pain threshold was nearly identical in both groups for the first pain induction; however, with repeated pain induction it decreased to a significantly greater extent in the CB1(-/-) mice than in the wild-type animals. Synoptic transmission and the inducibility of LTP were not influenced by the acute pharmacological blockade of CB1 receptors, but inhibited by the CB1 agonist WIN55,212-2. CONCLUSION: The endogenous cannabinoid system is involved in the control of neuroplasticity as part of pain processing . Cannabinoids prevent the formation of LTP in the amygdala via activation of CB1 receptors. Synoptic transmission and the inducibility of LTP were not influenced by the acute pharmacological blockade of CB1 receptors, but inhibited by the CB1 agonist Win55,212-2.

Cannabinoids↗

PubMed2004

Psychomotor stimulants and neuronal plasticity.

Considerable evidence suggests that neuroadaptations leading to addiction involve the same glutamate-dependent cellular mechanisms that enable learning and memory. Long-term potentiation (LTP) and long-term depression (LTD) have therefore become an important focus of addiction research. This article reviews: (1) basic mechanisms underlying LTP and LTD, (2) the properties of LTP and LTD in ventral tegmental area, nucleus accumbens, dorsal striatum and prefrontal cortex, (3) studies demonstrating that psychomotor stimulants influence LTP or LTD in these brain regions. In addition, we discuss our recent work on cellular mechanisms by which dopamine may influence LTP and LTD. Based on evidence that AMPA receptors are inserted into synapses during LTP and removed during LTD, we investigated the effects of D1 receptor stimulation on AMPA receptor trafficking using primary cultures prepared from nucleus accumbens and prefrontal cortex. Our results suggest that activation of the D1 receptor-protein kinase A signaling pathway leads to externalization of AMPA receptors and promotes LTP. This provides a mechanism to explain facilitation of reward-related learning by dopamine. When this mechanism is activated in an unregulated manner by psychostimulants, maladaptive forms of neuroplasticity may occur that contribute to the transition from casual to compulsive drug use.

Animals↗

PubMed2001

Neuronal plasticity and formation of new synaptic contacts follow pyramidal lesions and neutralization of Nogo-A: a light and electron microscopic study in the pontine nuclei of adult rats.

Regeneration and compensatory sprouting are limited after lesions in the mature mammalian central nervous system in contrast to the developing central nervous system (CNS). After neutralization of the growth inhibitor Nogo-A, however, massive sprouting and rearrangements of fiber connections occurred after unilateral pyramidal tract lesions in adult rats: Corticofugal fibers from the lesioned side crossed the midline of the brainstem and innervated the contralateral basilar pontine nuclei. To determine whether these newly sprouted fibers formed synaptic contacts, we analyzed the corticofugal fibers in the basilar pontine nuclei contralateral to the lesion by light and electron microscopy 2 weeks after pyramidotomy and treatment with the Nogo-A-inhibiting monoclonal antibody IN-1 (mAb IN-1). The mAb IN-1, but not a control antibody, led to structural changes in the basilar pons ipsilateral and contralateral to the lesion site. Fibers sprouted across the pontine midline and terminated topographically. They established asymmetric synaptic contacts with the characteristics of normal corticopontine terminals. These results show that adult CNS fibers are able to sprout and to form new synaptic contacts after a lesion when a growth-permissive microenvironment is provided.

Animals↗

PubMed2000

Ras-related and MAPK signalling in neuronal plasticity and memory formation.

Ras-related guanosine triphosphatases (GTPases) couple receptor activity to a number of intracellular signalling events culminating in the control of cell morphology and gene transcription. In culture cells, the best-understood Ras-dependent signalling pathway involves the mitogen-activated protein kinase/extracellular-regulated kinase (MAPK/ERK) cascade. A growing body of evidence has recently been accumulating to suggest a crucial role of Ras and MAPK signalling in neuronal functions connected to synaptic plasticity. In the present review article we discuss the experimental basis supporting the notion that the Ras/MAPK pathway interacts with other synaptic mechanisms to regulate invertebrate and vertebrate behavioural responses such as those implicated in learning and memory processes.

Animals↗