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Results for “Neuronal Plasticity”

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At least 307 records · Page 17Linked to original sources
PubMed1978

Neuronal plasticity in primate telencephalon: anomalous projections induced by prenatal removal of frontal cortex.

When the dorsolateral prefrontal cortex in one hemisphere of a rhesus monkey is resected 6 weeks before birth and the fetus survives to postnatal ages, neurons of the corresponding cortex in the intact hemisphere issue a greatly expanded projection to the contralateral caudate nucleus in addition to a normal projection to the ipsilateral caudate. The enhancement of the crossed prefronto-caudate pathway after prenatal neurosurgery provides direct evidence for lesion-induced neuronal rearrangement in the primate telencephalon.

Animals↗
PubMed2005

Apnea, glial apoptosis and neuronal plasticity in the arousal pathway of victims of SIDS.

Of 27,000 infants whose sleep-wake characteristics were studied under the age of 6 months, 38 died unexpectedly 2-12 weeks after the sleep recording in a pediatric sleep laboratory. Of these infants, 26 died of sudden infant death syndrome (SIDS), and 12 of definitely identified causes. The frequency and duration of sleep apneas were analysed. Sleep recordings and brainstem histopathology were studied to elucidate the possible relationship between sleep apnea and neuropathological changes within the arousal system. Immunohistochemical analyses were conducted using tryptophan hydroxylase (TrypH), a serotonin synthesizing enzyme, and growth-associated phosphoprotein 43 (GAP43), a marker of synaptic plasticity. The terminal-deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method was used for apoptosis. The pathological and physiological data were correlated for each infant. In the SIDS victims, statistically significant positive correlations were seen between the number of TrypH-positive neurons in the dorsal raphe nucleus of the midbrain and the duration of central apneas (p = 0.03), between the number of TUNEL-positive glial cells in the pedunculopontine tegmental nucleus (PPTN) and the average number of spines in GAP43-positive neurons in the PPTN (p = 0.04). These findings in the dorsal raphe nucleus of the midbrain and PPTN, that play important roles in the arousal pathway suggest a possible link between changes in arousal and SIDS.

Apoptosis↗
PubMed1977

[Modeling of neuronal plasticity by studies of spatio-temporal behavior of neural structures].

In order to point out spatio-temporal filtering of nervous structures after previous studies of their spatial behaviour, we have built a new model of cell according to synaptic and membrane plasticity (it agrees with properties of integration, memory and synaptic fatigue). This model, intended to be produced in many units, is made with integrated circuits in "thick film" technology.

Action Potentials↗
PubMed1997

Neurosteroids in the Hippocampus: Neuronal Plasticity and Memory.

The hippocampus, which is critically involved in learning and memory processes, is known to be a target for the neuromodulatory actions of steroid hormones produced by the adrenal glands and gonads. Much of the work of B.S. McEwen and collaborators has focused on the role of glucocorticosteroids and estrogen in modulating hippocampal plasticity and functions. In addition to hormones derived from the endocrine glands, cells in the hippocampus may be exposed to locally synthesized neurosteroids, including pregnenolone, dehydroepiandrosterone and their sulfated esters as well as progesterone and its reduced metabolites. In contrast to hormones derived from the circulation, neurosteroids have paracrine and/or autocrine activities. In the hippocampus, they have been shown to have trophic effects on neurons and glial cells and to modulate the activity of a variety of neurotransmitter receptors and ion channels, including type A gamma-aminobutyric acid, N-methyl-D-aspartate and sigma receptors and N- and L-type Ca2+ channels. There is accumulating evidence that some neurosteroids, in particular pregnenolone sulfate, have strong influences on learning and memory processes, most likely by regulating neurotransmission in the hippocampus. However, the hippocampus is not the only target for the mnesic effects of neurosteroids. Associated brain regions, the basal nuclei of the forebrain and the amygdaloid complex, are also involved. Some neurosteroids may thus be beneficial for treating age- or disease-related cognitive impairments.

Journal Article↗
PubMed1981

Neuronal plasticity in the deafferented hypothalamic arcuate nucleus of adult female rats and its enhancement by treatment with estrogen.

The hypothalamic arcuate nucleus (ARCN) was examined ultrastructurally 3 or 21 days after complete deafferentation of the medial basal hypothalamus (MBH) in ovariectomized adult female rats. Axodendritic shaft (SHS) and spine synapses (SPS) were counted in a field of 18,000 mu m2 in the middle part of the ARCN in each brain. The mean numbers of SHS and SPS at 3 or 21 days after deafferentation were reduced to about half of those in intact control animals. When the ARCNs of the ovariectomized MBH-island rats were examined 3 days after treatment with estradiol benzoate (EB, 2 mu g/day), the numbers of SHS and SPS did not differ from those in ovariectomized MBH-island rats without EB treatment. However, EB treatment for 21 days produced a marked increase in the number of both SHS and SPS in the ovariectomized MBH-island females, with the number of SHS in these females being restored to almost 75% of the intact level; the incidence of SPS was also significantly greater than that in the intact control animals. In these EB-treated, ovariectomized MBH-island rats, double synapses (spine-spine and spine-shaft double synapses) were frequently observed. In ovariectomized females without MBH deafferentation, however, estrogen failed to increase the numbers of SHS, SPS, and double synapses, which were almost comparable to those in intact and ovariectomized controls. These results suggest that estrogen has a facilitatory effect on SHS and SPS formation in the deafferented ARCN, presumably stimulating not only axonal sprouting but also dendritic spine formation by intact arcuate neurons in the MBH island.

Afferent Pathways↗
PubMed1980

The parcellation theory and its relation to interspecific variability in brain organization, evolutionary and ontogenetic development, and neuronal plasticity.

Recently discovered neocortical equivalents in anamniotes and certain patterns of interspecific variability in brain organization provide new insights into evolutionary and ontogenetic mechanisms of development. The new data suggest that nervous systems become more complex, not by one system invading another, but by a process of parcellation that involves the selective loss of connections of the newly formed daughter aggregates and subsystems. The parcellation process is reflected in the normal ontogenetic development of the CNS in a given species and can be manipulated, to a certain extent, by deprivation or surgically induced sprouting. The parcellation theory allows certain predictions about the range of variation of a given system at all levels of analysis including the cellular and aggregate levels. For example, the interspecific variability in organization of cortical columns, thalamic nuclei, cortical areas and tectal layers can be explained. The findings, summarized here, suggest that diffuse, undifferentiated systems existed in the beginning of vertebrate evolution and that during the evolution of complex behaviors, and analytical capacities related to these behaviors, a range of patterns of neural systems evolved that relate to these functions. One principle underlying the growth, differentiation and multiplication of neural systems appears to be the process of parcellation as defined by the theory.

Amphibians↗
PubMed2002

[Molecular aspects of antidepressive therapy. Transsynaptic effects on signal transduction, gene expression and neuronal plasticity].

Simple neurotransmitter theories cannot sufficiently explain the mode of action of antidepressant drugs. Molecular pharmacological studies demonstrate that antidepressive treatment initially modulates the neurotransmitter-receptor interaction, subsequently influences signal transduction cascades beyond the synapse and gene transcription mechanisms, and ultimately triggers the expression of specific target genes. Such genes often code for molecules which play an important role in the maintenance of neural and synaptic plasticity. Chronic (but not acute) treatment with antidepressants modulates, for example, the cAMP-second-messenger system and increases the expression of neurotrophic factors. Furthermore, antidepressants promote hippocampal neurogenesis. Stress, an important risk factor for psychiatric disorders, often induces opposite effects. A better understanding of the molecular and cellular effects of stress and therapy with psychotropic drugs will stimulate the development of innovative treatment strategies for which an optimised antidepressant efficacy with a simultaneously improved tolerance is expected.

Antidepressive Agents↗
PubMedDate not supplied

[Network of plastic neurons capable of forming conditioned reflexes ("membrane" model of learning)].

Simple net neuronal model was suggested which was able to form the conditioning due to changes of the neuron excitability. The model was based on the following main concepts: (a) the conditioning formation should result in reduction of the firing threshold in the same neurons where the conditioning and reinforcement stimuli were converged, (b) neuron threshold may have only two possible states: initial and final ones, these were identical for all cells, the threshold may be changed only once from the initial value to the final one, (c) isomorphous relation may be introduced between some pair of arbitrary stimuli and some subset of the net neurons; any two pairs differing at least in one stimulus have unlike subsets of the convergent neurons. Stochastically organized neuronal net was used for analysis of the model. Considerable information capacity of the net gives the opportunity to consider that the conditioning formation is possible on the basis of the nervous cells. The efficienty of the model turn out to be comparable with the well known models where the conditioning formation was due to the modification of the synapses.

Conditioning, Classical↗
PubMed1978

On the question of neuronal plasticity in the mature visual cortex.

In adult cats one eye was surgically immobilized by sectioning the eye muscles, or inverted by 180 degrees rotation, or pattern-deprived by suturing the eyelids for 1-12 weeks. Orientation and direction selectivity of cortical cells and binocularity were preserved; no shift in the ocular dominance distribution toward either eye was found. The visual cortex of adult cats is therefore not susceptible to changes in the content of the visual input.

Age Factors↗
PubMed2006

On neural plasticity, new neurons and the postischemic milieu: an integrated view on experimental rehabilitation.

This review discusses actual and potential contributors to functional improvement after stroke injuries. Topics that will be covered are neuronal re-organization and sprouting, neural stem/progenitor cell activation and neuronal replacement, as well as the neuronal milieu defined by glia, inflammatory cells and blood vessel supply. It is well established that different types of neuronal plasticity ultimately lead to post-stroke recovery. However, an untapped potential which only recently has started to be extensively explored is neuronal replacement through endogenous or exogenous resources. Major experimental efforts are needed to achieve progress in this burgeoning area. The review stresses the importance of applying neurodevelopmental principles as well as performing a characterization of the role of the postischemic milieu when studying adult brain neural stem/progenitor cells. Integrated and multifaceted experimentation, incorporating actual and possible poststroke function modulators, will be necessary in order to determine future strategies that will ultimately enable considerable progress in the field of neurorehabilitation.

Humans↗