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Results for “Neuronal Plasticity”

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At least 19 recordsLinked to original sources
PubMed1991

Concanavalin A: a tool to investigate neuronal plasticity.

Neuronal plasticity is the ability of neurons to alter their cellular properties in response to changes in their environment. These changes are typically triggered by the binding of specific ligands, such as neurotransmitters, growth factors or other neuromodulators, to receptors on the neuronal membrane surface. Since the extracellular domains of many of these receptors are glycosylated, they can also be bound by lectins--proteins with high affinity binding sites for polysaccharides. Different lectins have different affinities for various sugar residues. This feature has made lectins useful in the investigation of the regional localization and relative mobility of different classes of glycosylated membrane receptors, and in the subsequent purification of the receptors. This article reviews some of the different kinds of neuronal plasticity produced by the plant lectin concanavalin A (Con A), such as enhancement of neurite outgrowth, modulation of neurotransmitter responses, and alteration in the specificity and strength of synaptic connections.

Amino Acid Sequence↗
PubMed2002

[Introduction to neuronal plasticity].

Neuronal plasticity is observed throughout animal kingdom. It underlies processes of functional restoration after brain injury or peripheral deafferentation and it also makes learning and memory possible. The paper reviews briefly the conditions which, according to Hebb's rule, are required for neuronal plasticity to occur. It stresses the importance of convergence of signals, coincidence and repetition. The roles of NMDA receptors and neuromodulators are described. The paper reviews current concepts and data concerning anatomical changes that accompany plasticity of cortical representations.

Animals↗
PubMed2003

The relationship between neuronal plasticity and serotonergic neurons in the brainstem of SIDS victims.

BACKGROUND: The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its cause is still unknown. Recently, the medullary serotonergic network deficiency theory has been proposed and an association between SIDS and neuronal plasticity has also been suggested. The growth-associated phosphoprotein 43 (GAP43) is a marker of synaptic plasticity and is critical for normal development of the serotonergic innervation. Therefore, the characteristics of GAP43-positive elements and their association with serotonergic neurons were here investigated in the brainstem of SIDS victims. MATERIALS AND METHODS: The materials of this study included 26 cases of SIDS and 12 control cases. The brainstem material was collected and the immunohistochemistry of GAP43 and tryptophan hydroxylase (TrypH) carried out. The density of GAP43-positive neurons and dendrites and of TrypH-positive neurons were measured quantitatively. Nonparametric analyses of GAP43 between SIDS and non-SIDS and correlation analyses between GAP43 and TrypH were performed. RESULTS: No significant difference in GAP43-associated findings was found between SIDS and non-SIDS nor any significant correlation between GAP43-associated findings and TrypH-positive neurons. CONCLUSIONS: The results of this study were not in agreement with the association of GAP43 with SIDS and with serotonergic innervation in SIDS.

Brain Stem↗
PubMed1995

Spontaneous calcium transients regulate neuronal plasticity in developing neurons.

Calcium ions play critical roles in neuronal differentiation. We have recorded transient, repeated elevations of calcium in embryonic Xenopus spinal neurons over periods of 1 h in vitro and in vivo, confocally imaging fluo 3-loaded cells at 5 s intervals. Calcium spikes and calcium waves are found both in neurons in culture and in the intact spinal cord. Spikes rise rapidly to approximately 400% of baseline fluorescence and have a double exponential decay, whereas waves rise slowly to approximately 200% of baseline fluorescence and decay slowly as well. Imaging of fura 2-loaded neurons indicates that intracellular calcium increases from 50 to 500 nM during spikes. Both spikes and waves are abolished by removal of extracellular calcium. Developmentally, the incidence and frequency of spikes decrease, whereas the incidence and frequency of waves are constant. Spikes are generated by spontaneous calcium-dependent action potentials and also utilize intracellular calcium stores. Waves are produced by a mechanism that does not involve classic voltage-dependent calcium channels. Spikes are required for expression of the transmitter GABA and for potassium channel modulation. Waves in growth cones are likely to regulate neurite extension. The results demonstrate the roles of a novel signaling system in regulating neuronal plasticity, that operates on a time scale 10(4) times slower than that of action potentials.

Animals↗
PubMed1991

Role of the growth-associated protein B-50/GAP-43 in neuronal plasticity.

The neuronal phosphoprotein B-50/GAP-43 has been implicated in neuritogenesis during developmental stages of the nervous system and in regenerative processes and neuronal plasticity in the adult. The protein appears to be a member of a family of acidic substrates of protein kinase C (PKC) that bind calmodulin at low calcium concentrations. Two of these substrates, B-50 and neurogranin, share the primary sequence coding for the phospho- and calmodulin-binding sites and might exert similar functions in axonal and dendritic processes, respectively. In the adult brain, B-50 is exclusively located at the presynaptic membrane. During neuritogenesis in cell culture, the protein is translocated to the growth cones, i.e., into the filopodia. In view of many positive correlations between B-50 expression and neurite outgrowth and the specific localization of B-50, a role in growth cone function has been proposed. Its phosphorylation state may regulate the local intracellular free calmodulin and calcium concentrations or vice versa. Both views link the B-50 protein to processes of signal transduction and transmitter release.

Amino Acid Sequence↗
PubMed2000

Synaptic vesicle proteins and neuronal plasticity in adrenergic neurons.

The neurons in the superior cervical ganglion are active in plasticity and re-modelling in order to adapt to requirements. However, so far, only a few studies dealing with synaptic vesicle related proteins during adaptive processes have been published. In the present paper, changes in content and expression of the synaptic vesicle related proteins in the neurons after decentralization (cutting the cervical sympathetic trunk) or axotomy (cutting the internal and external carotid nerves) were studied. Immunofluorescence studies were carried out using antibodies and antisera against integral membrane proteins, vesicle associated proteins, NPY, and the enzymes TH and PNMT. For colocalization studies, the sections were simultaneously double labelled. Confocal laser scanning microscopy was used for colocalization studies as well as for semi-quantification analysis, using the computer software. Westen blot analysis, in situ 3'-end DNA labelling, and in situ hybridization were also employed. After decentralization of the ganglia several of the synaptic vesicle proteins (synaptotagmin I, synaptophysin, SNAP-25, CLC and GAP-43) were increased in the iris nerve terminal network, but with different time patterns, while TH-immunoreactivity had clearly decreased. In the ganglia, these proteins had decreased at 1 day after decentralization, probably due to degeneration of the pre-ganglionic nerve fibres and terminals. At later intervals, these proteins, except SNAP-25, had increased in the nerve fibre bundles and re-appeared in nerve fibres outlining the principal neurons.

Animals↗
PubMed1993

Neuronal plasticity and function.

Neuronal plasticity is a key issue in neuroscience. It is defined as the capability of the neuron to adapt to a changing internal or external environment, to previous experience or to trauma. It appears that during all phases of the individual life span in the nervous system, changes take place that relate to development, degeneration, and regeneration. Growth cones are a focus of neuronal plasticity, and current views emphasize the importance of local intracellular [Ca2+] to the control of their function. Hence, outgrowth of neurites from neurons in culture may be manipulated by drugs that affect intracellular Ca2+ homeostasis. In the adult nervous system, much research deals with synaptic plasticity, especially with the activity-dependent changes seen after long-term potentation of hippocampal synapses. As in the growth cone, such changes involve Ca(2+)-dependent pre- and postsynaptic processes, among which is the activation of protein kinase C. During aging, Ca2+ homeostasis may be slightly disturbed over a long period of time that could result in loss of function seen after a short, toxic high level of intracellular [Ca2+]. In this respect, the beneficial effects of chronic treatment with the L-channel Ca(2+)-blocker nimodipine on sensorimotor function of aged rats is discussed.

Adult↗
PubMedDate not supplied

Molecular mechanisms of neuronal plasticity during learning: the role of secondary messengers.

We present published data along with our own results concerning the role of second messengers and their intracellular receptors in molecular mechanisms associated with the plasticity of neurons during learning. The participation of cyclic 3',5'-adenosine monophosphate, cyclic 3',5'-guanosine monophosphate, calcium, calmodulin, and also the metabolic products of inositol phospholipids, inositol-1,4,5-triphosphate, diacylglycerol and the protein kinase C activated by it, arachidonic acid, and the products of its lipoxygenase oxidation during the regulation of neuronal plasticity over the course of prolonged potentiation, sensitization, habituation, and classical associative training are discussed.

Animals↗
PubMed1999

Rat motor neuron plasticity induced by dorsal rhizotomy.

The control of peripheral structural plasticity of motor neurons by primary sensory neurons was studied in rat extensor digitorum longus (EDL) muscle. Polyinnervation of muscle fibers, sprouting and the motor neuron peripheral field size following L4 dorsal root cutting were evaluated using three different approaches: intracellular recording of end plate potentials, histochemical demonstration of sprouting and polyinnervation and in vivo recording of nerve-evoked twitch. Nodal sprouting was found in rhizotomized rats but not in controls and consistently muscle polyinnervation appeared. The muscle portion innervated by L3 ventral root was relatively reduced and that innervated by L5 was relatively enlarged: a trend to caudal shift of muscle innervation arose in rhizotomized rats. A control of motor neuron plasticity by primary sensory neurons is suggested.

Animals↗
PubMed2001

Neuronal plasticity and signal transduction in nociceptive neurons: implications for the initiation and maintenance of pathological pain.

Pathological pain, consisting of tissue injury-induced inflammatory and nerve injury-induced neuropathic pain, is an expression of neuronal plasticity. One component of this is that the afferent input generated by injury and intense noxious stimuli triggers an increased excitability of nociceptive neurons in the spinal cord. This central sensitization is an activity-dependent functional plasticity that results from activation of different intracellular kinase cascades leading to the phosphorylation of key membrane receptors and channels, increasing synaptic efficacy. Central sensitization is both induced and maintained in a transcription-independent manner. Several different intracellular signal transduction cascades converge on MAPK (mitogen-activated protein kinase), activation of which appears to be a master switch or gate for the regulation of central sensitization. In addition to posttranslational regulation, the MAPK pathway may also regulate long-term pain hypersensitivity, via transcriptional regulation of key gene products. Pharmacological intervention targeted specifically at the signal transduction pathways in nociceptive neurons may provide, therefore, new therapeutic opportunities for pathological pain.

Animals↗
PubMed1998

Dynamic regulation of RGS2 suggests a novel mechanism in G-protein signaling and neuronal plasticity.

Long-term neuronal plasticity is known to be dependent on rapid de novo synthesis of mRNA and protein, and recent studies provide insight into the molecules involved in this response. Here, we demonstrate that mRNA encoding a member of the regulator of G-protein signaling (RGS) family, RGS2, is rapidly induced in neurons of the hippocampus, cortex, and striatum in response to stimuli that evoke plasticity. Although several members of the RGS family are expressed in brain with discrete neuronal localizations, RGS2 appears unique in that its expression is dynamically responsive to neuronal activity. In biochemical assays, RGS2 stimulates the GTPase activity of the alpha subunit of Gq and Gi1. The effect on Gi1 was observed only after reconstitution of the protein in phospholipid vesicles containing M2 muscarinic acetylcholine receptors. RGS2 also inhibits both Gq- and Gi-dependent responses in transfected cells. These studies suggest a novel mechanism linking neuronal activity and signal transduction.

Animals↗
PubMed1997

Amygdalar lesions block discriminative avoidance learning and cingulothalamic training-induced neuronal plasticity in rabbits.

Learning to fear dangerous situations requires the participation of neurons of the amygdala. Here it is shown that amygdalar neurons are also involved in learning to avoid dangerous situations. Amygdalar lesions severely impaired the acquisition of acoustically cued, discriminative instrumental avoidance behavior of rabbits. In addition, the development of anterior cingulate cortical and medial dorsal thalamic training-induced neuronal plasticity in the early stages of behavioral acquisition was blocked in rabbits with lesions. The development of training-induced neuronal plasticity in the medial dorsal and anterior thalamic nuclei in late stages of behavioral acquisition was also blocked in rabbits with lesions. These results indicate that the integrity of the amygdala is essential for the establishment of both early and late training-induced cingulothalamic neuronal plasticity. It is hypothesized that amygdalar training-induced neuronal plasticity in the initial trials of conditioning represents a substrate of learned fear, essential for the early and late cingulothalamic plasticity that is involved in mediation of acquisition of the instrumental avoidance response.

Amygdala↗
PubMed2002

Molecular mechanisms of CaMKII activation in neuronal plasticity.

Calcium/calmodulin-dependent protein kinase II (CaMKII) is thought to be a critical mediator of neuronal plasticity that links transiently triggered Ca(2+) signals to persistent changes in neuronal physiology. In one of its roles, CaMKII is an essential player in the N-methyl-D-aspartate receptor-mediated increase in conductance at glutamatergic synapses, a process described as long-term potentiation, which serves as a common model for neuronal plasticity and memory. Recent studies have used genetic, biochemical, live cell imaging and mathematical modeling approaches to investigate neuronal CaMKII and have led to a model of the molecular steps of CaMKII translocation and activation that can explain its role in neuronal plasticity.

Animals↗
PubMed1998

Regulation of neuronal plasticity in the central nervous system by phosphorylation and dephosphorylation.

Neuronal plasticity can be defined as adaptive changes in structure and function of the nervous system, an obvious example of which is the capacity to remember and learn. Long-term potentiation and long-term depression are the experimental models of memory in the central nervous system (CNS), and have been frequently utilized for the analysis of the molecular mechanisms of memory formation. Extensive studies have demonstrated that various kinases and phosphatases regulate neuronal plasticity by phosphorylating and dephosphorylating proteins essential to the basic processes of adaptive changes in the CNS. These proteins include receptors, ion channels, synaptic vesicle proteins, and nuclear proteins. Multifunctional kinases (cAMP-dependent protein kinase, Ca2+/phospholipid-dependent protein kinase, and Ca2+/calmodulin-dependent protein kinases) and phosphatases (calcineurin, protein phosphatases 1, and 2A) that specifically modulate the phosphorylation status of neuronal-signaling proteins have been shown to be required for neuronal plasticity. In general, kinases are involved in upregulation of the activity of target substrates, and phosphatases downregulate them. Although this rule is applicable in most of the cases studied, there are also a number of exceptions. A variety of regulation mechanisms via phosphorylation and dephosphorylation mediated by multiple kinases and phosphatases are discussed.

Animals↗
PubMed2006

alpha-Tocopherol affects neuronal plasticity in adult rat dentate gyrus: the possible role of PKCdelta.

Hippocampus dentate gyrus (DG) is characterized by neuronal plasticity processes in adulthood, and polysialylation of NCAM promotes neuronal plasticity. In previous investigations we found that alpha-tocopherol increased the PSA-NCAM-positive granule cell number in adult rat DG, suggesting that alpha-tocopherol may enhance neuronal plasticity. To verify this hypothesis, in the present study, structural remodeling in adult rat DG was investigated under alpha-tocopherol supplementation conditions. PSA-NCAM expression was evaluated by Western blotting, evaluation of PSA-NCAM-positive granule cell density, and morphometric analysis of PSA-NCAM-positive processes. In addition, the optical density of synaptophysin immunoreactivity and the synaptic profile density, examined by electron microscopy, were evaluated. Moreover, considering that PSA-NCAM expression has been found to be related to PKCdelta activity and alpha-tocopherol has been shown to inhibit PKC activity in vitro, Western blotting and immunohistochemistry followed by densitometry were used to analyze PKC. Our results demonstrated that an increase in PSA-NCAM expression and optical density of DG molecular layer synaptophysin immunoreactivity occurred in alpha-tocopherol-treated rats. Electron microscopy analysis showed that the increase in synaptophysin expression was related to an increase in synaptic profile density. In addition, Western blotting revealed a decrease in phospho-PKC Pan and phospho-PKCdelta, demonstrating that alpha-tocopherol is also able to inhibit PKC activity in vivo. Likewise, immunoreactivity for the active form of PKCdelta was lower in alpha-tocopherol-treated rats than in controls, while no changes were found in PKCdelta expression. These results demonstrate that alpha-tocopherol is an exogenous factor affecting neuronal plasticity in adult rat DG, possibly through PKCdelta inhibition.

Animals↗
PubMed2004

BDNF and 5-HT: a dynamic duo in age-related neuronal plasticity and neurodegenerative disorders.

Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are known to regulate synaptic plasticity, neurogenesis and neuronal survival in the adult brain. These two signals co-regulate one another such that 5-HT stimulates the expression of BDNF, and BDNF enhances the growth and survival of 5-HT neurons. Impaired 5-HT and BDNF signaling is central to depression and anxiety disorders, but could also play important roles in the pathogenesis of several age-related disorders, including insulin resistance syndrome, Alzheimer's disease and Huntington's disease. Enhancement of BDNF signaling may be a key mechanism whereby cognitive stimulation, exercise, dietary restriction and antidepressant drugs preserve brain function during aging. Behavioral and pharmacological manipulations that enhance 5-HT and BDNF signaling could help promote healthy brain aging.

Adaptation, Physiological↗
PubMed2004

Central neuronal plasticity, low back pain and spinal manipulative therapy.

OBJECTIVE: Recent experimental evidence demonstrating neuronal/synaptic plasticity and, in particular, long-term potentiation (LTP) and long-term depression (LTD) in spinal neurons is reviewed. The implications of these studies for possible mechanistic explanations of low back pain and its remediation by spinal manipulative therapy (SMT) are explored. Brief descriptions of LTP and LTD and elaboration of the key roles of calcium, glutamate, and glutamate receptors in LTP/LTD are provided as separate appendices. DATA SOURCES: The referenced articles regarding LTP/LTD in spinal cord neurons and neuronal plasticity, in general, were identified from accumulated review of the neuroscience literature. Publications cited from chiropractic sources relevant to central neuronal plasticity and LTP/LTD were identified using the Index to Chiropractic Literature and informal review. STUDY SELECTION: Experimental studies examining LTP/LTD mechanisms in spinal neurons and more general references useful as an introduction to central neuronal plasticity and LTP/LTD are included.Data Extraction Experimental evidence presented in this review has been previously published and illustrates neuronal plasticity from an animal model for low back pain. DATA SYNTHESIS: Both in vitro and in vivo evidence identifying LTP and LTD in dorsal horn nociceptive neurons is reviewed. Of special interest are studies showing LTP in response to intense noxious stimulation and reports that Adelta-mechanosensitive afferent activation can reverse an existing LTP condition in dorsal horn neurons. CONCLUSIONS: The potential involvement of LTP in low back pain is discussed and a role for LTD in spinal manipulative therapy is proposed. The need for future studies is identified in the areas of spatial and temporal changes in symptomatology post-SMT of the low back; combining, sequencing, and comparing several therapeutic approaches; and demonstrating LTD in spinal cord neurons post-SMT-like stimulation.

Animals↗