PubMed Health⌕ Search

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 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↗
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↗
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↗
PubMed1993

Calcium and neuronal plasticity.

The proposed involvement of free intracellular calcium concentration ([Ca]i) in neuronal plasticity is examined. While it is generally believed that a rise of [Ca]i is necessary for the triggering of long-term modification of synaptic connections, there are many unresolved issues related to this dogma; it is not entirely clear what is the source of the elevated calcium, how much of a calcium rise is sufficient to produce the synaptic potentiation, where and for how long, and what are the relevant chemical consequences of the transient rise of [Ca]i. It is generally believed that the dendritic spine is the locus of synaptic modification, yet little evidence exists to support this view. High resolution calcium imaging studies may contribute to the clarification of some key issues in the field of neuronal plasticity.

Animals↗
PubMed1995

Mechanisms of neuronal plasticity as analyzed at the single cell level.

This chapter has highlighted how correlates of neuronal plasticity such as electrophysiological responsiveness and changes in gene expression may be examined in defined CNS regions as well as in single cells. The ability to simultaneously measure the mRNA levels for hundreds of different genes, to clone novel genes, and to characterize the physiology and morphology of the cell promises to provide insight into molecular mechanisms of plasticity. The importance of understanding how one gene product changes relative to another (coordinated changes) as well as subcellular distribution of mRNAs cannot be overstated. It is only through an analysis of both the molecular and cellular processes associated with plasticity that a thorough understanding of the mechanisms of neuronal plasticity can be gained.

Animals↗
PubMed1995

Neurotrophins and neuronal plasticity.

There is increasing evidence that neurotrophins (NTs) are involved in processes of neuronal plasticity besides their well-established actions in regulating the survival, differentiation, and maintenance of functions of specific populations of neurons. Nerve growth factor, brain-derived neurotrophic factor, NT-4/5, and corresponding antibodies dramatically modify the development of the visual cortex. Although the neuronal elements involved have not yet been identified, complementary studies of other systems have demonstrated that NT synthesis is rapidly regulated by neuronal activity and that NTs are released in an activity-dependent manner from neuronal dendrites. These data, together with the observation that NTs enhance transmitter release from neurons that express the corresponding signal-transducing Trk receptors, suggest a role for NTs as selective retrograde messengers that regulate synaptic efficacy.

Animals↗
PubMed1978

Identification of pyramidal cells as the critical elements in hippocampal neuronal plasticity during learning.

The activity of single neurons recorded from rabbit hippocampus during classical conditioning of the nictitating membrane reflex was studied. All cells were first categorized according to their responses after fornix stimulation--i.i., antidromic activation, orthodromic activation, or no activation. The majority of cells that were antidromically activated--pyramidal cells--showed a highly positive correlation between the pattern of unit discharge and the topography of the nicititating membrane response within trial periods. Units that were orthodromically driven by fornix stimulation tended to inhibit during the presentation of trial stimuli, whereas most non-activated cells maintained low spontaneous levels of activity at all times. Thus, the major output neurons of the hippocampus appear to be the neuroanatomical substrate for the large and rapidly developing neuronal plasticity induced by this classical conditioning paradigm.

Action Potentials↗
PubMed1993

Neuronal plasticity induced by self-stimulation rewarding experience in rats--a study on alteration in dendritic branching in pyramidal neurons of hippocampus and motor cortex.

Self-stimulation rewarding experience promoted structural changes in pyramidal neurons of the CA3 region of the hippocampus and the Vth layer of the motor cortex in adult male Wistar rats. Self-stimulation experience was allowed for 1 h daily for a duration of 10 days through bipolar electrodes placed bilaterally in lateral hypothalamus and substantia nigra--ventral tegmental area. At the end of 10 days, rats were sacrificed, and rapid Golgi examination of the CA3 hippocampal and layer V pyramidal neurons of the motor cortex was made for a grand total of 1600 neurons from 80 rats divided into 4 groups. The neurons of the self-stimulation experienced (SS) group revealed a significant (ANOVA, F-test) increase in dendritic branching in the perisomatic domains. Such changes were not observed in neurons of sham control (SH), experimenter administered stimulation (EA) and normal control (NC) groups. SS animals also showed a significant increase in the thickness of lacunosum and radiatum laminae of CA3 neurons of the hippocampus. Our results reveal that both limbic and neocortical neurons undergo changes in dendritic branching patterns due to self-stimulation rewarding experience. It is tempting to hypothesize that neuronal plasticity is the result of motivation and learning experienced by rats which underwent self-stimulation.

Animals↗
PubMed1993

Toward understanding of the molecular basis of loss of neuronal plasticity in ageing.

Although there are several lines of evidence which suggest that neuronal plasticity decreases in some regions of both the central and peripheral nervous systems as well as in neuroendocrine tissues during development and ageing, the molecular mechanisms underlying loss of plasticity are largely unknown. To explore this question, we examined changes in expression profiles of neuronal growth-associated proteins (nGAPs) during ageing as well as the molecular regulatory mechanisms of their induction by nerve growth factor (NGF). SCG10, one of the nGAPs, is expressed in subsets of central neurons which maintain a high degree of plasticity in the adult, and is induced after neuronal deafferentation. This is a basis for analysing if SCG10 is involved in the remodelling of adult neurons during reactive synaptogenesis in diseased brains as well as in normal ageing. Studies of the induction of SCG10 by NGF in PC12 cells suggest that transcriptional inducible element(s) are present, at least in part, in the upstream region of the SCG10 gene. These studies of the regulation of nGAPs in ageing brains and neuroendocrine cells may yield new insights on reactivating neurites of partially degenerated neurons in the ageing brain.

Aged↗
PubMed1994

Activity-dependent and hormonal regulation of neurotrophin mRNA levels in the brain--implications for neuronal plasticity.

The neurotrophins exhibit neurotrophic effects on specific, partially overlapping populations of neurons both in the peripheral and the central nervous system (CNS). In the periphery, they are synthesized by a variety of nonneuronal cells, and their synthesis seems to be independent of the neuronal input. In contrast, in the CNS all neurotrophins are expressed under physiological conditions primarily by neurons. The production of NGF and BDNF is controlled by neuronal activity: up-regulation by glutamate and acetylcholine, down-regulation by gamma-aminobutyric acid. In contrast, NT-3 regulation is independent of neuronal activity, but it is up-regulated by thyroid hormones and BDNF. The latter observation suggests that NT-3 might be controlled indirectly by neuronal activity via BDNF. In peripheral nonneuronal tissues, glucocorticoid hormones down-regulate NGF mRNA levels both in vitro and in vivo. In contrast, in the CNS, neuronal production of NGF is enhanced by glucocorticoids. The rapid regulation of NGF and BDNF by subtle physiological stimuli together with the recent demonstration that the neurotrophins release neurotransmitters such as acetylcholine opens up interesting perspectives for the function of neurotrophins as mediators of neuronal plasticity.

Animals↗
PubMed1978

Extrinsic control of intrinsic neuronal plasticity: an hypothesis from work on simple systems.

All advanced nervous systems use plastic properties of neurons for learning, remembering and achieving other information processing feats. Recent findings on a variety of relatively simple nervous systems or reduced parts of more complex ones suggest the notion that, in addition to having neurons with intrinsically plastic properties, nervous systems also have mechanisms for controlling the development, expression, and maintenance of changes in their inherently malleable neurons. This hypothesis has important implications for understanding both the brain's learning machinery and also aspects of nervous system organization not obviously related to learning.

Afferent Pathways↗
PubMed1994

Expression of basic-helix-loop-helix transcription factor ME2 during brain development and in the regions of neuronal plasticity in the adult brain.

We report the isolation of a cDNA encoding the mouse class A bHLH transcription factor ME2 and the analysis of its expression. ME2 is expressed in the cerebral cortex, Purkinje and granule cell layers of the cerebellum, olfactory neuroepithelium, pyramidal cells of hippocampal layers CA1-CA4, and in the granular cells of the dentate gyrus. The specific expression of ME2 during development and in the regions of neuronal plasticity in the adult brain suggest that ME2 may have a regulatory function in developmental processes as well as during neuronal plasticity.

Amino Acid Sequence↗
PubMed1994

Gonadal steroids and neuronal plasticity. Studies in the adult rat hypothalamus.

In this chapter, recent studies on gonadal steroid-induced neural plasticity in the adult rat hypothalamus have been described. Neurons in the VMN and DMN are capable of rapid, reversible structural alterations in response to a changing hormonal environment. Given the importance of the VMN in mediating lordosis in female rats, the present studies suggest that hormonally induced morphological changes in the VMN may be necessary for the manifestation of lordosis. This possibility is supported by the 5,7-DHT studies which indicate that the induction of dendritic spines on VMN neurons may somehow decrease the threshold of E needed to elicit lordosis. Moreover, the sex differences in hormonal requirements for lordosis in 5,7-DHT-treated rats are probably the result of organizational effects of gonadal steroids. Our data support the idea that activational effects can only be superimposed on existing brain circuitry to a certain degree. Finally, the neuronal plasticity seen in the hypothalamus may be an important physiological mechanism by which gonadal steroid feedback mediates reproductive and behavioral function.

Animals↗
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↗
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↗