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PubMedDate not supplied

[Cortical plasticity and restoration of neurologic functions: an update on this topic].

INTRODUCTION: Neuroplasticity is a natural property of the nervous system to change its function and to reorganize due to a lesion or environmental changes. We review some of the main experimental and clinical experiences on cortical sensorimotor plasticity related to central nervous system (CNS) lesions. DEVELOPMENT: In the last 10 years increasing interest in neuronal plasticity has been prompted by several important discoveries. Long term potentiation and depression have been described as basic synaptic mechanism mediating functional recovery after CNS lesions, modulated by the up-down regulation of inhibitory-excitatory activity related to GABA, acetylcholine and glutamate between other neurotransmitters. In humans there are evidences from functional reorganization in the affected hemisphere in patients with hemispheric lesions, and the activation of homologues areas in the contralateral healthy hemisphere. Significative changes in the topography of cortical somatosensory and motor maps have been demonstrated using non invasive mapping techniques as multichannel EEG, evoked potential, transcranial magnetic stimulation, functional magnetic resonance imaging and positron emission tomography. Axonal and dendritic sprouting take place in animal models of brain lesions; but effective neural regeneration in the CNS does not seem to be a plausible mechanism for functional restoring. CONCLUSIONS: Plastic changes after CNS lesions make it possible the restoration of neurological functions in a high number of patients. It is important now to understand which changes are related to the clinical improvement of patients, and what might be done to promote or facilitate this changes and to inhibit maladaptive phenomena, for the design of rationale therapeutics strategies with modulatory influence on this process.

Amputation, Surgical↗

PubMed1991

Neurosciences research in space: future directions.

Future research in the neurosciences can best be understood in the context of NASA's life sciences goals in the near term (1990-95), mid term (1995-2000), and long term (2000 and beyond). Since NASA is planning short-duration Spacelab and International Microgravity Laboratory (IML) flights for many years to come, the acute effects of exposure to microgravity will continue to be of experimental and operational interest in the near term. To this end, major new areas of research will be devoted to ground-based studies of preflight adaptation trainers and their efficacy in preventing or reducing the incidence of space motion sickness. In addition, an extensive series of studies of the vestibular system will be conducted inflight on the IML-1 mission The IML-2 mission will emphasize behavior and performance, biological rhythms, and further vestibular studies. In the mid-term period, Spacelab missions will employ new technology such as magnetic recording techniques in order to evaluate changes in the processing of sensory and motor inputs at the brainstem and cortical level during exposure to microgravity. Two Space Life Sciences (SLS) missions planned for the mid to late 1990's, SLS-4 and SLS-5, will utilize an onboard centrifuge facility that will enable investigators to study the effects of partial gravity on sensory and motor function. In the long term (2000 and beyond), Space Station Freedom and long-duration missions will provide opportunities to explore new options in the neurosciences, such as sensory substitution and augmentation, through the use of physical sensors to provide three-dimensional tactile-visual, tactile-auditory and tactile-somatosensory inputs. The use of this technology will be extremely important in the area of robotic telepresence. Finally, Space Station Freedom and proposed LifeSat missions will provide neuroscientists the opportunity to study the effects of partial gravity and microgravity on neuronal plasticity.

Centrifugation↗

PubMed2004

Overexpression of CREB reduces CRE-mediated transcription: behavioral and cellular analyses in transgenic mice.

The CREB transcription factor mediates neuronal plasticity in many systems, but the relationship between CREB levels and CRE-mediated transcription in individual neurons in vivo is unclear. In FVB/N nontransgenic mice, we observed that Purkinje cells showed low basal levels of Ser(133)-phosphorylated CREB protein yet displayed strong CRE-directed transcription. Transgenic mice overexpressing CREB in Purkinje cells and dentate gyrus granule cells showed a decreased CRE-lacZ signal in the same cells, indicating repression of ATF/CREB family function. Dentate region long-term potentiation was not altered by these changes in CREB expression. CREB transgenic mice demonstrated an inability to perform the rotarod task, without signs of overt ataxia. Our results demonstrate that the level of phosphorylated CREB protein is not a reliable indicator of CRE-mediated function. Furthermore, we conclude that CRE-mediated transcription may be linked to only a subset of cerebellum-mediated motor behaviors and may not be universally required for long-lasting synaptic potentiation.

Activating Transcription Factors↗

PubMed2006

Plasticity of secretory neurons in the supraoptic and paraventricular nuclei of the hypothalamus on exposure to light.

Light and electron microscopic methods were used to analyze changes in secretory neurons in the supraoptic (SON) and paraventricular (PVN) nuclei in the hypothalamus in 100 adult male rats at time points from the first minutes to 180 days after 48 hours of full-time exposure to bright light. At the early time points after exposure, the cellular formulae of the SON and PVN shifted towards functionally active neurons with minimal quantities of secretory granules, large nuclei and nucleoli, low RNA contents, small numbers of rough endoplasmic reticulum cisterns, vacuoles, and lysosomes in the perikarya. The number of cells depositing secretion was greater than in controls at 24 h in the SON and PVN and at 10 days in the SON. Normalization of the cellular formula and the structural organization of the protein-synthesizing apparatus of PVN neurons occurred at 10-30 days, with normalization in the SON at 30-180 days. These data provide evidence that the range of plasticity of neurons in the PVN on exposure to full-time bright light was more significant than that in the SON.

Adaptation, Physiological↗

PubMed2005

Rapid WAVE dynamics in dendritic spines of cultured hippocampal neurons is mediated by actin polymerization.

The Wiskott-Aldrich syndrome protein family Verprolin-homologous protein (WAVE) complex has been proposed to link Rho GTPase activity with actin polymerization but its role in neuronal plasticity has never been documented. We now examined the presence, distribution and dynamics of WAVE3 in cultured hippocampal neurons. WAVE3 was localized to dendritic spines via its N-terminal domain. Green fluorescent protein (GFP)-tagged WAVE3 clusters demonstrate an F-actin-dependent high rate of local motility. Constitutive Rac activation translocates WAVE3 (via the N-terminus), to the leading edge of lamellipodia. Also, spinogenesis is associated with actin-based motility of the WAVE3 protein. Brain specific WAVE1 showed similar localization and effects on spine density. Cytoplasmic fragile X mental retardation protein interacting protein (CYFIP) and non-catalytic region of tyrosine kinase adaptor protein 1 (NCK-1), proteins that are assumed to complex with WAVE, have a somewhat similar cellular distribution and motility. We propose that the WAVE complex is a downstream effector of the Rac signaling cascade, localized to sites of novel synaptic contacts by means of its N-terminal domain, to guide local actin polymerization needed for morphological plasticity of neurons.

2-Amino-5-phosphonovalerate↗

PubMedDate not supplied

Age-related decrease in sympathetic sprouting is primarily due to decreased target receptivity: implications for understanding brain aging.

Aging of the nervous system is characterized by reduced anatomical plasticity. The cause of this decreased plasticity is not known because it is usually not possible to distinguish between extrinsic and intrinsic factors that affect neuronal growth. One example of age-related reduced neuronal plasticity that is amendable to such analysis is the growth of sympathetic axons into the rat hippocampal formation following septal denervation. This sprouting response can be elicited throughout the lifespan of the rat but is drastically reduced in aged animals. The age-related reduction in ingrowth could theoretically be due to decreased receptivity of the target (reduced trophic support or increased inhibition of growth), decreased responsivity of the sympathetic neurons or a combination of both factors. In order to test the relative contributions of the age of the target tissue and the age of the sympathetic neurons to the reduced growth observed in aged animals, superior cervical ganglia were transplanted from young animals into old animals (y/o) and from old animals into young animals (o/y) as well as autologously within the same animals (y/y and o/o). The extent of sympathetic ingrowth and the survival of transplanted neurons were assessed with fluorescence histochemical methods. The extent of ingrowth was significantly greater in young hosts compared with old hosts regardless of the age of the donor. In addition, the survival of transplanted neurons was greater in younger hosts than in aged hosts regardless of donor age. These results indicate that sympathetic ingrowth is reduced in aging primarily because of decreased receptivity of the hippocampal target tissue.

Adrenergic Fibers↗

PubMed1989

N-methyl-D-aspartate receptor plasticity in kindling: quantitative and qualitative alterations in the N-methyl-D-aspartate receptor-channel complex.

Kindling is an animal model of epilepsy and neuronal plasticity produced by periodic electrical stimulation of the brain. Electrophysiologic studies indicate that this phenomenon is associated with increased participation of N-methyl-D-aspartate (NMDA) receptors in excitatory synaptic transmission. Biochemical studies suggest that a change intrinsic to the NMDA receptor-channel complex may contribute to the increase in NMDA receptor-mediated synaptic transmission. We tested this idea by measuring the binding of 3-[(+)-2-(carboxypiperazin-4-yl)][1,2-3H]propyl-1-phosphonic acid ([3H]CPP), [3H]glycine, and tritiated N-[(1-thienyl)cyclohexyl]piperidine [( 3H]TCP) to rat hippocampal membranes. In this preparation these ligands are selective for the NMDA receptor, the strychnine-insensitive glycine receptor, and the NMDA receptor-gated ion channel, respectively. Kindling increased the density of CPP, glycine, and TCP binding sites in hippocampal membranes by 47%, 42%, and 25%, respectively. No significant changes were detected in the affinity of these binding sites. Surprisingly, alterations in the glycine binding site were detected in animals sacrificed 1 month but not 1 day after the final kindling stimulation. Thus, delayed upregulation of the NMDA receptor-channel complex may be one molecular mechanism that maintains the long-lasting hyperexcitability of hippocampal neurons in kindled animals.

Animals↗

PubMed1994

Pathophysiology of binocular vision and amblyopia.

This article focuses on three important issues that have received much attention during the past year. The first is sensitive periods for amblyopia. Recent physiological studies suggest a surprising degree of neural plasticity in the adult visual cortex. A review of the literature suggests that at least some human amblyopes retain cortical plasticity into adulthood. The second issue is new methods of treatment for amblyopia. Certain neurotransmitters have been implicated in neuronal plasticity. Based on this finding, a potentially promising new method for treating amblyopia, levodopa, is being tested in adults and children with amblyopia. Unfortunately the early results provide more questions than answers. The third topic is neural mechanisms of amblyopia. In primates and humans, the weight of evidence suggests that the neural effects of strabismus and anisometropia are expressed primarily in the cortex. These cortical effects are expressed in a loss of cortical neurons and in alterations in the contrast sensitivity and range of preferred spatial frequencies of the neurons dominated by the amblyopic eye. The relationship between these physiological effects and psychophysical performance is reviewed.

Amblyopia↗

PubMed1990

Post-ischemic synaptic plasticity in the rat hippocampus after long-term survival: histochemical and autoradiographic study.

The hippocampus provides a suitable area in the brain for the analysis of neuronal plasticity after application of a selective lesioning technique. Using histochemistry and autoradiography, we studied synaptic reorganization in the rat hippocampus with selective CA1 pyramidal cell lesioning caused by transient forebrain ischemia after long-term survival. An autoradiographic study was performed on second messenger systems ([3H]inositol 1,4,5-trisphosphate, [3H]forskolin and [3H]phorbol 12,13-dibutyrate binding). One-hundred days after ischemia, depletion of CA1 pyramidal cells and marked shrinkage of the CA1 subfield was noted in spite of unaltered thickness of the CA3 band and of the dentate molecular layers. Although neuronal density in the CA3 region of animals killed seven days after ischemia was not different from the normal group, 78% of animals showed neuronal loss of 30-50% in the stratum pyramidale of the CA3b 100 days after recirculation. Sixty-seven per cent of animals exhibited supragranular mossy fiber sprouting in the dentate gyrus. However, CA3 neuronal loss did not correlate with mossy fiber sprouting. Succinic dehydrogenase was depleted in the CA1 100 days after ischemia, and animals with CA3 damage showed a reduction of succinic dehydrogenase activity in the CA3. In contrast to the unaltered acetylcholinesterase in the animals killed seven days after ischemia, high density bands of acetylcholinesterase activity in the stratum pyramidale of the CA1 were found to be broadened 100 days after ischemia. In the CA1 subfield, subnormal activity of [3H]phorbol 12,13-dibutyrate and [3H]forskolin binding were observed in spite of the depleted [3H]inositol 1,4,5-triphosphate binding. [3H]Forskolin binding in the hilus had increased by 62% 100 days after ischemia, although binding in the stratum lucidum of the CA3 and in the stratum moleculare of the dentate gyrus was unaltered. However, no visible supragranular increase in [3H]forskolin binding was observed. These results indicate that long-term survival after CA1 pyramidal cell depletion caused by transient forebrain ischemia induced the modulation of neuronal activity and synaptic rearrangements in the whole hippocampal formation.

Acetylcholinesterase↗

PubMed2003

The effect of brain-derived neurotrophic factor on neuritogenesis and synaptic plasticity in Aplysia neurons and the hippocampal cell line HiB5.

Brain-derived neurotrophic factor (BDNF) plays a key role in the differentiation and neuritogenesis of developing neurons, and in the synaptic plasticity of mature neurons, in the mammalian nervous system. BDNF binds to the receptor tyrosine kinase TrkB and transmits neurotrophic signals by activating neuron-specific tyrosine phosphorylation pathways. However, the neurotrophic function of BDNF in Aplysia neurons is poorly understood. We examined the specific effect of BDNF on neurite outgrowth and synaptic plasticity in cultured Aplysia neurons and a multipotent rat hippocampal stem cell line (HiB5). Our study indicates that mammalian BDNF has no significant effect on the neuritogenesis, neurotransmitter release, excitability, and synaptic plasticity of cultured Aplysia neurons in our experimental conditions. In contrast, BDNF in combination with platelet-derived growth factor (PDGF) increases the length of the neurites and the number of spine-like structures in cells of HiB5.

Animals↗

PubMed2006

Plasticity from muscle to brain.

Recognition that the entire central nervous system (CNS) is highly plastic, and that it changes continually throughout life, is a relatively new development. Until very recently, neuroscience has been dominated by the belief that the nervous system is hardwired and changes at only a few selected sites and by only a few mechanisms. Thus, it is particularly remarkable that Sir John Eccles, almost from the start of his long career nearly 80 years ago, focused repeatedly and productively on plasticity of many different kinds and in many different locations. He began with muscles, exploring their developmental plasticity and the functional effects of the level of motor unit activity and of cross-reinnervation. He moved into the spinal cord to study the effects of axotomy on motoneuron properties and the immediate and persistent functional effects of repetitive afferent stimulation. In work that combined these two areas, Eccles explored the influences of motoneurons and their muscle fibers on one another. He studied extensively simple spinal reflexes, especially stretch reflexes, exploring plasticity in these reflex pathways during development and in response to experimental manipulations of activity and innervation. In subsequent decades, Eccles focused on plasticity at central synapses in hippocampus, cerebellum, and neocortex. His endeavors extended from the plasticity associated with CNS lesions to the mechanisms responsible for the most complex and as yet mysterious products of neuronal plasticity, the substrates underlying learning and memory. At multiple levels, Eccles' work anticipated and helped shape present-day hypotheses and experiments. He provided novel observations that introduced new problems, and he produced insights that continue to be the foundation of ongoing basic and clinical research. This article reviews Eccles' experimental and theoretical contributions and their relationships to current endeavors and concepts. It emphasizes aspects of his contributions that are less well known at present and yet are directly relevant to contemporary issues.

Animals↗

PubMed2006

Characterization and plasticity of the double synapse spines in the barrel cortex of the mouse.

The somatosensory barrel cortex of rodents and its afferent pathway from the facial vibrissae is a very useful model for studying neuronal plasticity. Dendritic spines are the most labile elements of synaptic circuitry and the most likely substrate of experience-dependent alterations in neuronal circuits in cerebral cortex. We characterized morphologically and numerically a specific population of spines, i.e. double synapse spines, which have two different inputs--one excitatory and the other inhibitory, in the B2 barrel of mouse somatosensory cortex. We also described changes in morphology of double synapse spines induced by classical conditioning in which stimulation of vibrissae was paired with a tail shock. The analysis was carried out by means of serial EM micrograph reconstruction. We showed that double spines account for about 10% of all analyzed spines. The morphology of a typical double synapse spine is similar to the morphology of single synapse spine and both consist of two parts--a large head and a narrow, long neck. Excitatory synapses are preferentially located on the head of double synapse spines and inhibitory synapses are usually located on the neck of these spines. The length of the double synapse spine neck decreases and the cross-section area of the spine neck increases significantly as a result of sensory conditioning.

Animals↗

PubMed1995

[Ryanodine receptors in the central nervous system].

Ryanodine receptor (RyR) is a calcium release channel protein on the intracellular Ca(2+)-store. While inositol 1,4,5-trisphosphate receptor (IP3R), another intracellular calcium release channel protein, is mainly found in non-muscle cells, such as neurons and hepatocytes, and smooth muscles, RyR is the Ca(2+)-release channel protein in skeletal and cardiac muscles. At least three genetically distinct isoforms of RyR are identified: isoform proteins Ryr1, Ryr2, and Ryr3 expressed by ryr1, ryr2 and ryr3, respectively. In the central nervous system where IP3R is much more abundant than RyR, the main isoform of RyR is Ryr2, which is specific to the cardiac ventricular muscle. Recently, ryr3 was detected in specific regions of the brain. In this paper, the heterogeneous distribution and localization of RyR isoforms in the brain are summarized. The discussion extends into their putative functions, especially potential involvement in neuronal plasticity.

Animals↗

PubMed2001

Characterization of Fyn-mediated tyrosine phosphorylation sites on GluR epsilon 2 (NR2B) subunit of the N-methyl-D-aspartate receptor.

The N-methyl-d-aspartate (NMDA) receptors play critical roles in synaptic plasticity, neuronal development, and excitotoxicity. Tyrosine phosphorylation of NMDA receptors by Src-family tyrosine kinases such as Fyn is implicated in synaptic plasticity. To precisely address the roles of NMDA receptor tyrosine phosphorylation, we identified Fyn-mediated phosphorylation sites on the GluR epsilon 2 (NR2B) subunit of NMDA receptors. Seven out of 25 tyrosine residues in the C-terminal cytoplasmic region of GluR epsilon 2 were phosphorylated by Fyn in vitro. Of these 7 residues, Tyr-1252, Tyr-1336, and Tyr-1472 in GluR epsilon 2 were phosphorylated in human embryonic kidney fibroblasts when co-expressed with active Fyn, and Tyr-1472 was the major phosphorylation site in this system. We then generated rabbit polyclonal antibodies specific to Tyr-1472-phosphorylated GluR epsilon 2 and showed that Tyr-1472 of GluR epsilon 2 was indeed phosphorylated in murine brain using the antibodies. Importantly, Tyr-1472 phosphorylation was greatly reduced in fyn mutant mice. Moreover, Tyr-1472 phosphorylation became evident when hippocampal long term potentiation started to be observed, and its magnitude became larger in murine brain. Finally, Tyr-1472 phosphorylation was significantly enhanced after induction of long term potentiation in the hippocampal CA1 region. These data suggest that Tyr-1472 phosphorylation of GluR epsilon 2 is important for synaptic plasticity.

Animals↗

PubMed1996

Different localizations of growth-associated protein (GAP-43) in mechanoreceptors and free nerve endings of adult rat periodontal ligament, dental pulp and skin.

Distributions of growth-associated protein-43 (GAP-43) in the periodontal ligament and dental pulp of adult rats were studied by light and electron microscopy. The mature periodontal ligament and dental pulp contained numerous GAP-43-positive neural elements, comprising periodontal Ruffini endings and thin nerve fibers, but expression patterns differed among the kinds of nerves. In the periodontal ligament of rat molars, immunoelectron microscopy revealed that GAP-43 like immunoreactivity in the Ruffini ending, an essential mechanoreceptor, was confined to the Schwann sheaths around the axon terminals and was not in the axon terminals themselves, unlike free endings that revealed axonal GAP-43. However, the lamellar Schwann cells associated with the cutaneous receptors did not exhibit any GAP-43 like immunoreactivity though they were intensely reactive for low affinity nerve growth factor receptor (p75-NGFR), a marker for lamellar Schwann cells in mechanoreceptors. The characteristically uniform expression of GAP-43 in the Schwann lamellae that surround the Ruffini mechanoreceptors of rat molar ligament suggests that Schwann cells are involved in the GAP-43 mediated plasticity of these receptors. On the other hand, the pulpal nerves were filled with the reaction products in their axonal spaces, suggesting the potential for neuronal plasticity during normal function and after tooth injury.

Animals↗

PubMed1996

Membrane depolarization induces calcium-dependent secretion of tissue plasminogen activator.

Tissue plasminogen activator (tPA), a serine protease that converts inactive plasminogen to active plasmin, is produced in the rat and mouse hippocampus and participates in neuronal plasticity. To help define the role of tPA in the nervous system, we have analyzed the regulation of its expression in the neuronal cell line PC12. In control cultures, tPA activity is exclusively cell-associated, and no activity is measurable in the culture medium. When the cells are treated with depolarizing agents, such as KCI, tPA activity becomes detectable in the medium. The increased secreted tPA activity is not accompanied by an increase in tPA mRNA levels, and it is not blocked by protein synthesis inhibitors. In contrast, tPA release is abolished by Ca2+ channel blockers, suggesting that chemically induced membrane depolarization stimulates the secretion of preformed enzyme. Moreover, KCI has a similar effect in vivo when administered to the murine brain via an osmotic pump: tPA activity increases along the CA2-CA3 regions and dentate gyrus of the hippocampal formation. These results demonstrate a neuronal activity-dependent secretory mechanism that can rapidly increase the amount of tPA in neuronal tissue.

Animals↗

PubMed2000

Antidepressant treatment and neural plasticity.

The use of psychopharmacologic agents in children is complicated by several factors. One important neurobiologic consideration is the relationship of the effect of the medication to ongoing brain development. Although available data are inadequate to address this issue directly, a review of ancillary data suggests that there are theoretical reasons to exercise prudence in prescribing psychopharmacologic agents. For example, the effects of serotonin on neuronal plasticity suggest that agents that can alter serotonergic function may alter neuronal wiring. Although this can occur in any brain, it may be of particular importance in a developing nervous system. The consequences of these induced changes are not clear. Animal studies on the effect of long-term antidepressant administration in immature pups may begin to answer some of the clinical concerns of these observations.

Animals↗

PubMed1991

[Pathophysiologic regulatory mechanisms in chronic schizophrenia].

Two collectives of chronic schizophrenics were psychometrically rated by means of the BPRS and of Gebhardt's primary AMP-scales. Their scores of coexistent Positive and Negative Symptomatology were correlated with equivalents of catecholergic levels of tone as represented by plasma tyrosine concentration in its role as the catecholergic precursor. Levels of catecholergic tone state- and time-dependently correlated directly with Positive and inversely with Negative Symptomatology. Opposite ends of catecholergic tone from supra- to subnormal ranges ran parallel to a psychometric continuum from predominant Positive to predominant Negative Symptomatology, to a diagnostic continuum from "paranoid" to "disorganised/hebephrenic", and to a global metabolic continuum from under- to overweight. Findings did not support the hypothesis on psychotogenic dopaminergic supersensitivity. Postulated was a primary psychotogenic process of denervation or/and degeneration of a specific 'trigger system', and supersensitivity-induced neuronal damage was conjectured the biological substrate of Negative Symptomatology. A pathophysiological hypothesis put forth, corresponded with Cannon's Rules within the frame of functional neuronal plasticity.

Adult↗