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 253 records · Page 14Linked to original sources
PubMed1996

[Psychological stress and neuronal plasticity. An expanded model of the stress reaction process as the basis for understand central nervous system adaptation processes].

A short survey on results and theories in psychosomatic and neurobiologic stress research is presented. Based on a comprehensive definition of the stress-reaction process, the biological and psychological consequences are described which are elicited by either controllable or uncontrollable stress. We conclude that controllable stress triggers the stabilization and facilitation of neuronal networks involved in the generation of appropriate patterns of appraisal and coping, whereas uncontrollable stress favours the extinction of inappropriate patterns and the reorganisation of neuronal connections underlying certain inappropriate behaviors. Both, controllable an uncontrollable stress-reaction-processes are therefore essential prerequisites of, and inherent challenges to, the development and adaptation of an individual in an ever changing external world but may also lead to psychodevelopmental failures and psychosomatic diseases.

Adaptation, Psychological↗
PubMed1992

Neuronal plasticity as an adaptive property of the central nervous system.

This short review presents examples of plasticity in the brains of vertebrates including man. The basic ability of the nervous system to make functionally relevant adaptations to functional challenges of various kinds during development and adulthood is called plasticity. Enucleation of the eyes or lesioning of the lateral geniculate body during development lead to the generation of a new architectonic area within the nonhuman primate and human primary visual cortex. The enucleation of one eye in rats at various postnatal stages causes profound plastic changes in the callosal system of the visual cortex. The central representation of the periphery in the adult cerebral cortex (somatotopy) can also be altered by adaptive processes. Naturally occurring nerve cell death during pre- and early postnatal development can be manipulated by impairing normal development of neuro-transmission. These findings argue for an important role of transmitter receptors in brain plasticity. The number of receptors shows, for most brain regions and receptor types, an overshoot of growth during ontogeny. After lesions have damaged the adult geniculo-cortical and septo-hippocampal systems, receptors can exhibit plastic changes such as upregulation of the number of binding sites (visual cortex) and modifications in the coupling of receptors, transducer proteins (G-proteins) and second messengers (hippocampus).

Aging↗
PubMed1987

The septo-hippocampal pathway in patients suffering from senile dementia of Alzheimer's type. Evidence for neuronal plasticity?

In 7 cases of senile dementia of Alzheimer's type (SDAT) and in 7 age-matched controls, nerve cells of the medial septal nuclei (area CH1) and of the vertical limb of the diagonal band of Broca (area CH2) of the right hemisphere were counted in Cresyl-fast-violet-stained serial sections. The granular cells of the ipsilateral fascia dentata were Golgi-stained and dendritic spine density was quantified in 10-micron segments. There was a significant loss of neurons in areas CH1 and CH2 in SDAT cases compared to controls. The spine density of the granular cell dendrites was significantly reduced in the distal parts of the dendrites. In the most proximal part, where cholinergic septal fibers form synapses, the spine density was not significantly different between the two groups. We assume that collateral sprouting of undamaged inputs occurs maintaining a constant number of spines in the proximal segments despite the loss of source neurons within CH1 and CH2.

Aged↗
PubMed2000

Calcium signaling in the ER: its role in neuronal plasticity and neurodegenerative disorders.

Endoplasmic reticulum (ER) is a multifaceted organelle that regulates protein synthesis and trafficking, cellular responses to stress, and intracellular Ca2+ levels. In neurons, it is distributed between the cellular compartments that regulate plasticity and survival, which include axons, dendrites, growth cones and synaptic terminals. Intriguing communication networks between ER, mitochondria and plasma membrane are being revealed that provide mechanisms for the precise regulation of temporal and spatial aspects of Ca2+ signaling. Alterations in Ca2+ homeostasis in ER contribute to neuronal apoptosis and excitotoxicity, and are being linked to the pathogenesis of several different neurodegenerative disorders, including Alzheimer's disease and stroke.

Animals↗
PubMed2002

Participation of CaMKII in neuronal plasticity and memory formation.

1. The unique biochemical properties of Ca(2+)/calmodulin (CaM)-dependent protein kinase II have made this enzyme one of the paradigmatic models of the forever searched "memory molecule." 2. In particular, the central participation of CaMKII as a sensor of the Ca(2+) signals generated by activation of NMDA receptors after the induction of long-term plastic changes, has encouraged the use of pharmacological, genetic, biochemical, and imaging tools to unveil the role of this kinase in the acquisition, consolidation, and expression of different types of memories. 3. Here we review some of the more exciting discoveries related to the mechanisms involved in CaMKII activation and synaptic plasticity.

Animals↗
PubMed2003

Melatonin regulates neuronal plasticity in the hippocampus.

The influence of melatonin on hippocampal evoked potentials initiated by low- and high-frequency electrical stimulations and by two pulses applied in rapid succession was investigated. In confirmation of our previous studies, melatonin attenuated the population spike triggered by low-frequency stimulation (0.03 Hz). High-frequency stimulation (HFS; 100 Hz for 1 sec, three times every 10 sec), which in control slices permanently facilitated neuronal excitability (347% +/- 32%), was also able to amplify the melatonin-depressed potential (467.8% +/- 59.6%). Because melatonin is a hydrophobic molecule, it was dissolved and applied in ethanol. Ethanol (0.4%) by itself reduced the magnitude of HFS-induced potentiation (233.5% +/- 16.8%). The slices stimulated with two pulses separated with a delay longer than 15 msec demonstrated a facilitation of the response to the second stimuli (paired-pulse facilitation; PPF). The influence of melatonin (100 microM) on PPF was biphasic: Shortly after addition of melatonin, PPF was briefly (5-10 min) reversed to paired-pulse inhibition (PPI), which gradually returned to a stable PPF. Ethanol (0.4%) applied without melatonin exerted only a marginal, facilitatory effect on PPF. The delay between two successively applied pulses, shorter than 13 msec, resulted in attenuation of the response to the second stimuli (PPI). Melatonin (100 microM) reversed the attenuation of the second potential within 15-20 min following its application. Ethanol applied by itself at the concentration of 0.4% temporarily (5-10 min), but significantly, depressed the second potential. These results demonstrate the ability of melatonin to modulate specific forms of plasticity in hippocampal pyramidal neurons.

Animals↗
PubMed2006

Long term recordings with microelectrode arrays: studies of transcription-dependent neuronal plasticity and axonal regeneration.

Substrate integrated microelectrode arrays (MEAs) offer an alternative to classical electrophysiological methods like the patch clamp technique for recording the electrical activity from cells and tissue of neuronal or cardiac origin. Since its introduction 30 years ago, this technology has made possible the repeated simultaneous recording from multiple sites in a non-invasive manner. The MEA technology can be applied to any electrogenic cells or tissue (i.e., central and peripheral neurons, heart cells, and muscle cells), either as cultures or acute cell or slice preparations. The combination of culture techniques and MEAs offers the possibility to monitor the activity of a designed specimen over extended periods of time, up to several months. Furthermore, recording the electrical activity of distributed regions of a preparation yields information on spatial effects that might go undetected with other recording methods. Development, plasticity, and regeneration are examples of applications that could especially benefit from long term monitoring of neuronal activity, as they concern processes that develop over extended periods of time. Here we highlight recent MEA studies on signal regulation of neuronal network behavior and axonal regeneration. We illustrate the use of MEAs to study long term potentiation (LTP) and summarize the advantages of MEA technology over traditional electrophysiological methods for studies aimed at understanding the transcription-dependent late phase of plasticity.

Animals↗
PubMed1992

The hypoglossal-facial anastomosis as model of neuronal plasticity in the rat.

Hypoglossal-facial cross anastomosis (HFA) causes regeneration with change of function, as the axotomized hypoglossal motoneurons sprout into the facial plexus and reinnervate the mimic musculature. Following HFA, hypoglossal-hypoglossal single anastomosis (HHA) and resection of 8-10 mm peripheral hypoglossal nerve in 190 female adult Wistar rats, we compared the axon reactions in the hypoglossal nucleus during 1) regeneration with change of function, 2) regeneration with restoration of original function and 3) degeneration of the nucleus. Following postoperative survival times of 1-16 weeks we estimated the volume of the hypoglossal nucleus and counted the number of hypoglossal neurons with the physical disector on both sides of the brainstem. Additional sections of the same animals were reacted with anti-synaptophysin, anti-GFAP and the isolectin Griffonia simplicifolia I-B4 (GSA I-B4) as cytochemical markers for presynaptic boutons, activated astroglia and microglia. After HHA and HFA all hypoglossal neurons survive and the volume of the hypoglossal nucleus remains constant. Resection of the hypoglossal nerve leads to the loss of one third of the hypoglossal neurons and of one third of the volume of the hypoglossal nucleus within 16 weeks post operation. Hypoglossal-facial anastomosis and hypoglossal-hypoglossal anastomosis differ in postoperative swelling of the hypoglossal nucleus, microglia and astroglia activation and the duration of synaptic stripping. All differences are limited to the acute growth phase during regeneration. It is concluded that hypoglossal-facial anastomosis provides more stimulation and facilitates faster recovery of the hypoglossal nucleus than does hypoglossal-hypoglossal anastomosis.

Anastomosis, Surgical↗
PubMed1992

Evidence for a substrate of neuronal plasticity based on pre- and postsynaptic neurotensin-dopamine receptor interactions in the neostriatum.

The major mechanism underlying the neuroleptic action of the tridecapeptide neurotensin (NT) appears to be an interaction with dopamine receptor mechanisms based on biochemical binding and behavioral experiments. In vivo microdialysis was used in conscious rats to investigate the effects of local perfusion with NT on the sensitivity of striatal dopamine D1 and D2 receptors for their selective agonists by monitoring extracellular dopamine, 3,4-dihydroxyphenylacetic acid, homovanilic acid, and gamma-aminobutyric acid levels in the awake unrestrained male rat. Perfusion with NT (10 nM) counteracted the inhibitory effects of the dopamine D2 agonist pergolide (500 nM) on extracellular levels of dopamine and gamma-aminobutyric acid. In contrast, NT (10 mM) significantly enhanced the reduction of extracellular striatal levels of dopamine after perfusion with the D1 agonist SKF 38393 (5 microM), and this combined treatment also resulted in a significant increase in the extracellular striatal levels of gamma-aminobutyric acid. These results provide in vivo evidence that NT regulates central dopamine transmission by reducing pre-and postsynaptic dopamine D2 and enhancing D1 receptor sensitivity possibly through an antagonistic NT receptor-D2 receptor interaction. This heteroregulation has the potential to substantially increase the plasticity within the dopamine synapse.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2005

Effect of N-methyl-d-aspartate receptor blockade on neuronal plasticity and gastrointestinal transit delay induced by ischemia/reperfusion in rats.

Intestinal ischemia impairs gastrointestinal motility. The aims of this study were to investigate the effect of intestinal ischemia on gastrointestinal transit and on the expression of enteric transmitters in the rat, and whether the glutamate N-methyl-d-aspartate receptors influence these effects. Ischemia (1 h), induced by occluding the superior mesenteric artery, was followed by 0 or 24 h of reperfusion. Normal and sham-operated rats served as controls. Serosal blood flow was measured with laser Doppler flow meter. Gastrointestinal transit was measured as time of appearance of a marker in fecal pellets. Immunohistochemistry was used to evaluate the number of neurons immunoreactive for neuronal nitric oxide synthase (NOS) or vasoactive intestinal polypeptide and the density of substance P immunoreactive fibers in the myenteric plexus. The N-methyl-d-aspartate receptors antagonist, (+)-5-methyl-10,11-dihydro-5HT-[a,b] cyclohepten-5,10-imine (MK-801) (1 mg/kg i.v.) or the NOS inhibitor, N-nitro-l-arginine (10 mg/kg i.v.) was administered prior to ischemia. Serosal blood flow was decreased by 70% during ischemia, but it was not altered in sham-operated rats. Gastrointestinal transit was significantly prolonged in ischemic/reperfused rats compared with controls. There was a significant increase in the number of vasoactive intestinal polypeptide and neuronal nitric oxide synthase immunoreactive neurons, and a marked decrease of substance P immunoreactive fibers in ischemia followed by 24 h of reperfusion animals compared with controls. These alterations were not observed in ischemia without reperfusion. A significant delay of gastrointestinal transit and increase of vasoactive intestinal polypeptide neurons were also observed in sham-operated rats. The changes in transmitter expression and gastrointestinal transit in ischemic/reperfused rats were prevented by pre-treatment with the NOS inhibitor, N-nitro-l-arginine or the N-methyl-d-aspartate receptors antagonist, MK-801. This study suggests an involvement of the glutamatergic system and its interaction with nitric oxide in intestinal ischemia/reperfusion. Ischemia/reperfusion might induce local release of glutamate that activates N-methyl-d-aspartate receptors leading to increased production of nitric oxide and adaptive changes in enteric transmitters that might contribute to gastrointestinal dysmotility.

Analysis of Variance↗
PubMed2002

Neuronal plasticity of interrelated cerebellar and cortical networks.

The comprehension of the cerebellar physiology is rapidly changing in particular because of the demonstration of the cerebellar importance on cognition. In the present paper, recent data on cerebro cerebellar interactions is reviewed, particularly focusing on cerebellar influences over the neurophysiology of primary motor and primary sensory cortices. The cerebellar role in implicit learning and in sensory data processing is analysed and discussed. It is proposed that the cerebellum could control cortical plastic changes by modulating cortical excitability in a discrete topographic manner and that this mechanism could induce the coupling between significant sensory inputs and definite motor outputs considered as the neurobiological substrate for implicit learning.

Afferent Pathways↗
PubMed2006

Transcriptional profiling of brain-derived-neurotrophic factor-induced neuronal plasticity: a novel role for nociceptin in hippocampal neurite outgrowth.

Brain derived neurotrophic factor (BDNF) exhibits a sequence of actions on neurons ranging from acute enhancement of transmission to long-term promotion of neurite outgrowth and synaptogenesis associated with learning and memory. The manifold effects of BDNF on neuronal modifications may be mediated by genomic alterations. We previously found that BDNF treatment acutely increases transcription of the synaptic vesicle protein Rab3A, required for trophin-induced synaptic plasticity, as well as the peptide VGF, which increases during learning. To elucidate comprehensive transcriptional programs associated with short- and long-term BDNF exposure, we now examine mRNA abundance and complexity using Affymetrix GeneChips in cultured hippocampal neurons. Consistent with the modulation of synaptic plasticity, BDNF treatment (3-6 h) induced mRNAs encoding the synapse-associated proteins synaptojanin 2, neuronal pentraxin 1, septin 9, and ryanodine receptor 2. BDNF also induced expression of mRNAs encoding neuropeptides (6-12 h), including prepronociceptin, neuropeptide Y, and secretogranin. To determine whether these neuropeptides induced by BDNF mediate neuronal development, we examined their effects on hippocampal neurons. The four mature peptides derived from post-translational processing of the ppNociceptin propeptide induced the expression of several immediate early genes in hippocampal cultures, indicating neuronal activation. To examine the significance of activation, the effects of nociceptin (orphanin FQ) and nocistatin on neurite outgrowth were examined. Quantitative morphometric analysis revealed that nociceptin significantly increased both average neurite length and average number of neurites per neuron, while nocistatin had no effect on these parameters. These results reveal a novel role for nociceptin and suggest that these neuropeptide systems may contribute to the regulation of neuronal function by BDNF.

Animals↗
PubMed2004

[Functional neuronal plasticity].

INTRODUCTION: Thanks to the contributions made by neuroscientific research and the clinical evidence regarding the functional recovery of the central nervous system in the different motor, cognitive, linguistic and sensory spheres, we now know more about how the brain is built and its modifications. This recovery is possible due to the plasticity of the brain, its capacity to reorganise itself and to modify functions in order to adapt to both external and internal changes. This capacity is inherent to brain cells and allows cortical circuits to be repaired, integrates other cortical areas to carry out modified functions and responds to different disorders. It depends on genetic, neuronal and neurochemical factors and its limits can be manipulated through clinical and pharmacological intervention. DEVELOPMENT: The brain's capacity to adapt itself to changes is crucial in the development of the nervous system and has important repercussions on learning. The neuroanatomical, neurochemical and functional changes that take place during the reorganisation made possible by plasticity will facilitate the recovery acquisition of the functions involved (adaptive plasticity) and may hinder the development of others (maladaptive plasticity). This variability of the possible responses is related to the chronology of the lesion, the site that is affected, the state of the substrata that can take on the function and the type of function that is altered. The mechanisms responsible for facilitating this plasticity are different at any given time (fast and late plasticity), depending on the function that is altered, with expansion of the somatotopic representations in the motor cortex adjacent to the damage, interhemispherical transfer of language or crossed plasticity in the auditory or visual function. The neuropsychological pathology can appear linked to the lesion or secondary to a maladaptive plasticity. CONCLUSIONS: Advancing in our knowledge of the intrinsic mechanisms of brain plasticity and synaptic regulation will lead us to understand the recovery of damaged or lost functions in the brains of children with special needs, and thus allow us to implement favourable clinical and pharmacological interventions.

Central Nervous System↗
PubMed2003

Evidence for cell autonomous AP1 function in regulation of Drosophila motor-neuron plasticity.

BACKGROUND: The transcription factor AP1 mediates long-term plasticity in vertebrate and invertebrate central nervous systems. Recent studies of activity-induced synaptic change indicate that AP1 can function upstream of CREB to regulate both CREB-dependent enhancement of synaptic strength as well as CREB-independent increase in bouton number at the Drosophila neuromuscular junction (NMJ). However, it is not clear from this study if AP1 functions autonomously in motor neurons to directly modulate plasticity. RESULTS: Here, we show that Fos and Jun, the two components of AP1, are abundantly expressed in motor neurons. We further combine immunohistochemical and electrophysiological analyses with use of a collection of enhancers that tightly restrict AP1 transgene expression within the nervous system to show that AP1 induction or inhibition in, but not outside of, motor neurons is necessary and sufficient for its modulation of NMJ size and strength. CONCLUSION: By arguing against the possibility that AP1 effects at the NMJ occur via a polysynaptic mechanism, these observations support a model in which AP1 directly modulates NMJ plasticity processes through a cell autonomous pathway in the motor neuron. The approach described here may serve as a useful experimental paradigm for analyzing cell autonomy of genes found to influence structure and function of Drosophila motor neurons.

Animals↗
PubMed1999

[Neuronal plasticity exemplified by the somatosensory system].

The mammalian brain is capable of a substantial functional reorganization, manifesting on a cortical somatotopical and on a behavioral level. Possible mechanisms are reviewed based on the work by others and ourselves on somatosensory reorganization in humans. The somatosensory system is characterized by divergent projections from the periphery to the cerebral cortex. Changes in synaptic weights allow for reorganization of sensory processing: On one side, limb amputation will result in a representational "invasion" of the differentiated cortex from neighboring regions with concomitant perceptual changes. On the other side, sensorimotor training can increase the representational cortical zone of a limb. Plastic changes can be temporary or persistent. Modulating factors like pain and certain drugs seem to induce a permissive state in the cortex resulting in enhanced reorganization. Thus, specific physical training combined with pharmacoceutical modulation holds promise to improve functional recovery after brain lesions.

Afferent Pathways↗
PubMed1992

Modulation of gamma-actin and alpha 1-tubulin expression by corticosterone during neuronal plasticity in the hippocampus.

Evidence is given for altered gene expression of gamma-actin in the hippocampus in response to entorhinal cortex lesion (ECL). Time course analysis reveals a progressive repression of gamma-actin expression between 4 and 14 days post-lesion, coinciding with the early and middle phases of the hippocampal reinnervation process. RNA prevalence returns to near control values at 30 days post-lesion. Corticosterone administration, which is known to impair the reinnervation process in ECL rats, prevents the lesion-induced reduction in gamma-actin expression and blocks the induction of alpha 1-tubulin in the deafferented hippocampus. The timing of response of gamma-actin to ECL and its modulation by glucocorticoid administration support suggestions that gamma-actin has an important role to play in neuronal cytoarchitecture remodelling during hippocampal reinnervation.

Actins↗
PubMed2005

Synaptic remodeling induced by gonadal hormones: neuronal plasticity as a mediator of neuroendocrine and behavioral responses to steroids.

During recent decades, it has become a generally accepted view that structural neuroplasticity is remarkably involved in the functional adaptation of the CNS. Thus, cellular morphology in the brain is in continuous transition throughout the life span, as a response to environmental stimuli. The effects of the environment on neuroplasticity are mediated by, to some extent, the changing levels of circulating gonadal steroid hormones. Today, it is clear that the function of gonadal steroids in the brain extends beyond simply regulating reproductive and/or neuroendocrine events. In addition, or even more importantly, gonadal steroids participate in the shaping of the developing brain, while their actions during adult life are implicated in higher brain functions such as cognition, mood and memory. A large body of evidence indicates that gonadal steroid-induced functional changes are accompanied by alterations in neuron and synapse numbers, as well as in dendritic and synaptic morphology. These structural modifications are believed to serve as a morphological basis for changes in behavior and cellular activity. Due to their growing functional and clinical significance, the specificity, timeframe, as well as the molecular and cellular mechanisms of hormone-induced neuroplasticity have become the focus of many studies. In this review, we briefly summarize current knowledge and the most significant recent discoveries from our laboratories on estrogen- and dehydroepiandrosterone-induced synaptic remodeling in the hypothalamus and hippocampus, two important brain areas heavily involved in autonomic and cognitive operations, respectively.

Animals↗