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Results for “Neuronal Plasticity”

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At least 235 records · Page 13Linked to original sources
PubMed2003

Neuronal plasticity in relation to nociception and healing of rat achilles tendon.

Nerve regeneration and the occurrence of three neuropeptides; i.e. substance P (SP), calcitonin gene related peptide (CGRP) and galanin (GAL), were studied during healing of tendon rupture in the rat by semi-quantitative immunohistochemistry. The neuronal findings were related to nociception as assessed by hindpaw withdrawal latencies at thermal and mechanical tests. Experimental rupture of rat Achilles tendon--normally devoid of nerves--elicited extensive nerve ingrowth into the rupture site in the early phase of healing followed by almost complete fiber disappearance (weeks 12-16). The ingrowth of SP and CGRP positive fibers, seen already at weeks 1-2, was associated with increased nociception. Subsequently, the occurrence of GAL positive fibers at weeks 4-6 was associated with decreased nociception. An even stronger relationship to nociception during healing was observed when the rate of change in neuropeptide expression instead of the expression in absolute terms was considered, according to the "cascade" formula of SP(')+CGRP(')-GAL(').It may prove that the observed temporal occurrence of different neuropeptides reflects a role of the peripheral nervous system in regulating synchronously nociception and healing.

Achilles Tendon↗
PubMedDate not supplied

Excitatory amino acids and neuronal plasticity: modulation of AMPA receptors as a novel substrate for the action of nootropic drugs.

The nootropic drug, aniracetam, behaves as a positive modulator of AMPA-sensitive glutamate receptors in a variety of systems, including intact brain tissue, amphibian oocytes injected with rat brain mRNA, and cultured neurons. In electrophysiological studies, aniracetam both increases the peak amplitude and reduces the rate of decay of the ion current generated by AMPA or quisqualate. In cultured neurons, aniracetam (as well as oxiracetam and piracetam) enhances the stimulation of 45Ca2+ influx produced by AMPA but not that produced by kainate or NMDA. In addition, aniracetam (as other nootropic drugs) increases the maximal density of low affinity binding sites for [3H]AMPA in crude synaptic membranes. Positive modulation of AMPA receptors by aniracetam provides a novel molecular substrate which explains the clinical efficacy of nootropic drugs as memory and cognition enhancers.

Amino Acids↗
PubMed1998

[Developmental neuronal plasticity and its importance in the recovery and function of neural tissue].

Plasticity is understand as a natural ability of the nervous tissue to respond to intrinsic and extrinsic stimuli by means of functional or structural changes. All its manifestations, including the developmental changes and processes of recovery are controlled by general genetic programs. One of the major research goals in the field of neuroplasticity is to design a strategy for the activation of the functional recovery. Enough evidence has shown that the internal environment of the nervous tissue is one of the decisive factors which determine the degree of both the developmental and regenerative plasticity. To improve capacity for the recovery it is therefore necessary to activate these intrinsic neuroplastic mechanisms. One alternative is the method of implantation of the embryonal nerve cells suspension into the site of neuronal lesion. The grafted cells can either replace the lost cells or they might become a source of stimulating factors which may activate the process of recovery. In the model of the intrahippocampal pathways interruption (experimental partial elimination of granule cells in the dorsal blade of the dentate gyrus), the subsequent implantation of embryonal neurons of the same origin into the site of lesion can partly restore the structural pattern of the gyrus dentatus and probably preserve some of the afferent connections. However, the outgrow of efferent fibers probably remains limited to the grafted tissue.

Animals↗
PubMed2002

A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning.

We have investigated a potential mechanism by which a diet, similar in composition to the typical diet of most industrialized western societies rich in saturated fat and refined sugar (HFS), can influence brain structure and function via regulation of neurotrophins. We show that animals that learn a spatial memory task faster have more brain-derived neurotrophic factor (BDNF) mRNA and protein in the hippocampus. Two months on the HFS diet were sufficient to reduce hippocampal level of BDNF and spatial learning performance. Consequent to the action of BDNF on synaptic function, downstream effectors for the action of BDNF on synaptic plasticity were reduced proportionally to BDNF levels, in the hippocampus of rats maintained on the HFS diet between 2 and 24 months. In particular, animals maintained on the HFS diet showed a decrease in levels of: (i) synapsin I mRNA and protein (total and phosphorylated), important for neurotransmitter release; (ii) cyclic AMP-response element-binding protein (CREB) mRNA and protein (total and phosphorylated); CREB is required for various forms of memory and is under regulatory control of BDNF; (iii) growth-associated protein 43 mRNA, important for neurite outgrowth, neurotransmitter release, and learning and memory. Diet-related changes were specific for the hippocampus consequent to its role in memory formation, and did not involve neurotrophin-3, another member of the neurotrophin family. Our results indicate that a popularly consumed diet can influence crucial aspects of neuronal and behavioral plasticity associated with the function of BDNF.

Animals↗
PubMed2003

Apoptosis in the mechanisms of neuronal plasticity in the developing visual system.

Visual experience during early postnatal life is essential for normal development of synaptic connections in the visual system. In fact, altered visual experiences such as monocular deprivation (MD) or abnormal visual stimulation (e.g. strabismus, anisometropia) during this period disrupt the physiologic organization of the visual pathway, leading to loss of visual responses in cortical neurons and reduction in visual acuity of the affected eye, so that it becomes amblyopic. The authors review the main functional and morphologic changes induced by altered visual experiences in the developing visual system and focus on the recent discovery that MD induces apoptotic cell death in the lateral geniculate nucleus of newborn rats. Particular attention is given to the authors' studies documenting that, during development, MD leads retinal terminals to release excessive glutamate in the lateral geniculate nucleus where it elevates nitric oxide and causes DNA fragmentation. The latter event is known to activate poly-(ADP-ribose) polymerase, which in turn may trigger apoptosis. Better understanding of the mechanisms underlying the morphologic changes induced by altered visual experiences during development may open new venues for studying novel neuroprotective strategies for amblyopia and, more generally, for the treatment of ophthalmic diseases associated with neuronal apoptosis.

Amblyopia↗
PubMed1991

Postnatal neuronal plasticity of the pyramidal cells of CA1 area of the hippocampus as a reaction to neurotoxic damage.

Kainic acid (KA) was injected into both lateral ventricles of the brain of adult laboratory rats with the aim of verifying whether damage to afferent fibres in the hippocampal CA1 area would also be reflected in changes in the dendritic arborization of the neurones after maturation of these structures was completed. A significant proportion of the afferent fibres ending in area CA1 comes from CA3-4. The neurodegenerative effect of KA on the neurones in CA3-4 thus leads to marked reconstruction of the dendritic network of the pyramidal cells in the CA1 area. In the CA1 area of the experimental animals, there are fewer segments in the proximal part of the basal dendrites and in the lateral branches of the apical dendrites. The total number of segments in the apical dendrites is smaller and the higher order segments are likewise reduced. In the experimental group, the segments of both the basal and the apical dendrites are shorter. In the experimental animals, dendritic spine density in the lateral preterminal branches, the distal part of the apical shaft, the terminal segments of the lateral branches and the apical preterminal branches are smaller than in the controls, whereas in the segments proximal to the soma of the pyramidal cells it is greater. It can be seen from the results that area CA1 of the hippocampus is endowed, even in adulthood, not only with high functional plasticity, but also with surprisingly high morphological plasticity.

Animals↗
PubMed1993

Laryngeal muscle and motor neuron plasticity in Xenopus laevis: testicular masculinization of a developing neuromuscular system.

In Xenopus laevis, the sexual differentiation of the neuromuscular system responsible for courtship song is controlled by testicular androgen secretion. To explore the sensitivity of this system to androgenic stimulation, male and female frogs were gonadectomized and given testis transplants at seven different developmental stages between the end of metamorphosis and adulthood, grown to sexual maturity, and the laryngeal muscle fibers and motor axons were counted. Muscle fiber and axon numbers in males were not affected by the testicular transplant at any stage. In females, testicular transplants at all developmental stages increased muscle fiber numbers in adulthood. Values attained were, however, significantly less than those of adult intact or testis-transplanted males. Testis transplantation increased laryngeal axon numbers in females to levels equivalent to those of intact males; this effect was obtained at every stage of postmetamorphic development including adulthood. To further explore androgen regulation in adults, males and females were gonadectomized and implanted with silicone tubes containing testosterone propionate for 1.5-3 years and laryngeal muscle fibers and axon numbers compared to those of gonadectomized or sham-operated adult controls. Neither treatment with exogenous androgen nor gonadectomy had any effect on laryngeal muscle fiber or axon number in either males or females; values did not differ from those of sham-operated controls. We conclude that testicular secretions can induce laryngeal muscle fiber and axon addition in females throughout postmetamorphic life. This degree of plasticity, exhibited after the period when adult values are normally attained, stands in contrast to the effects of administration of synthetic androgen and suggests that the degree of plasticity in adult females may be underestimated if exogenous hormones rather than testicular transplants are provided.

Animals↗
PubMed1996

GAP-43: putting constraints on neuronal plasticity.

The brain must balance the need for synaptic precision with the ability to generate and change connectivity patterns in response to environmental stimuli. GAP-43 is a phosphoprotein associated with the cytosolic surface of the membrane, and is one of the most abundant among the small subset of total cellular proteins transported to the growth cone. It appears to play an unusual role amplifying signals from the microenvironment. One of the several ways to perform this task involves interaction of GAP-43 with the G protein transduction cascade. In mice rendered GAP-43 null by homologous recombination, some nerves manifest aberrant growth at decision points, such as the optic chiasm. Thus, GAP-43 may work via modulation of signaling cascades, rather than autonomously causing growth, and could serve to keep plasticity within constraints needed to generate and maintain accurate synaptic wiring.

Animals↗