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Results for “Neuronal Plasticity”

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At least 397 records · Page 22Linked to original sources

PubMed2004

Acute social defeat reduces neurotrophin expression in brain cortical and subcortical areas in mice.

Acute social defeat in mice activates the hypothalamic-pituitary-adrenal axis (HPA) and induces long-term behavioral changes, including exaggerated fear responses and inhibition of territorial behavior. Stress-induced hormonal and neurotransmitter release may contribute to disruption of expression of genes important for cell survival, neuronal plasticity, and neuronal remodeling. Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor associated with structural cellular changes that occur during nervous system development and contributes to neural plasticity in the adult brain. In rats, acute (1-2 h) restraint stress transiently reduces BDNF mRNA expression in the hippocampus, a region important in the memory and in HPA regulation; restraint stress also decreases BDNF expression in the basolateral amygdala (BLA), a region important for fear consolidation and emotional memory. We hypothesized that a brief (10 min) exposure to intense social stress, a more naturalistic stressor than restraint stress, would also reduce BDNF mRNA in the hippocampus and BLA of mice. In the present study, we examined the time course of expression of BDNF mRNA expression in the hippocampus and amygdala, as well as other subcortical and cortical brain regions, following acute social stress. In situ hybridization analysis for BDNF mRNA expression showed that there was a significant decrease in BDNF mRNA expression in all regions studied in mice 24 h after social defeat when compared to control (naive) mice (P<0.05). These findings support our hypothesis that BDNF mRNA levels are reduced by social stress, and may have implications for brain plasticity and behavioral changes following social stress.

Animals↗

PubMed1994

Plasticity of hippocampal and motor cortical pyramidal neurons induced by self-stimulation experience.

The self-stimulation (SS) induced neuronal plasticity was observed in CA3 hippocampal and layer V motor cortical pyramidal neurons. SS experience was allowed daily for a total of 1 hour for 10 days through four bipolar electrodes implanted bilaterally in lateral hypothalamus (LH) and substantia nigra-ventral tegmental area (SN-VTA) in adult male Wistar rats. Examination of pyramidal neurons stained by rapid Golgi technique was made in a total of 1,600 neurons out of 80 rats consisting of 4 groups. The dendritic intersections were quantified upto 200 and 120 microns radial distances in apical and basal dendrites respectively. The CA3 hippocampal and layer V motor cortical pyramidal neurons of SS group revealed significant increase (P < 0.001, two-way ANOVA) in dendritic intersections in both apical and basal dendrites, compared to normal control (NC), sham control (SH) and experimenter-administered (EA) group of animals. These results demonstrate that SS experience promotes increase in dendritic length in hippocampal and motor cortical pyramidal neurons.

Animals↗

PubMedDate not supplied

Plasticity of neuronal response properties in adult cat striate cortex.

We have utilized an associative conditioning paradigm to induce changes in the receptive field (RF) properties of neurons in the adult cat striate cortex. During conditioning, the presentation of particular visual stimuli were repeatedly paired with the iontophoretic application of either GABA or glutamate to control postsynaptic firing rates. Similar paradigms have been used in kitten visual cortex to alter RF properties (Fregnac et al., 1988, 1992; Greuel et al., 1988; Shulz & Fregnac, 1992). Roughly half of the cells that were subjected to conditioning with stimuli differing in orientation were found to have orientation tuning curves that were significantly altered. In general, the modification in orientation tuning was not accompanied by a shift in preferred orientation, but rather, responsiveness to stimuli at or near the positively reinforced orientation was increased relative to controls, and responsiveness to stimuli at or near the negatively reinforced orientation was decreased relative to controls. A similar proportion of cells that were subjected to conditioning with stimuli differing in spatial phase were found to have spatial-phase tuning curves that were significantly modified. Conditioning stimuli typically differed by 90 deg in spatial phase, but modifications in spatial-phase angle were generally 30-40 deg. An interesting phenomenon we encountered was that during conditioning, cells often developed a modulated response to counterphased grating stimuli presented at the null spatial phase. We present an example of a simple cell for which the shift in preferred spatial phase measured with counterphased grating stimuli was comparable to the shift in spatial phase computed from a one-dimensional Gabor fit of the space-time RF profile. One of ten cells tested had a significant change in direction selectivity following associative conditioning. The specific and predictable modifications of RF properties induced by our associative conditioning procedure demonstrate the ability of mature visual cortical neurons to alter their integrative properties. Our results lend further support to models of synaptic plasticity where temporal correlations between presynaptic and postsynaptic activity levels control the efficiency of transmission at existing synapses, and to the idea that the mature visual cortex is, in some sense, dynamically organized.

Animals↗

PubMed2002

Introduction to olfactory neuroepithelium.

Among the five senses, the sense of smell (olfaction) is the most sensitive and emotional window on the outside world (Stern and Marx, 1999). The olfactory system recognizes and discriminates myriad odorants of diverse molecular structures. What makes the olfactory system so specific and sensitive? OE harboring the olfactory receptor neurons (ORNs) also has an another unusual characteristic ability that fascinates scientists. Neurogenesis in this tissue continues throughout lifetime. This unique character provides an elegant model to study neurogenesis and neuronal plasticity, since neuronal birth, differentiation, survival, axon pathfinding, target recognition, synapse formation, and cell death can be examined in the mature OE. This special issue of Microscopic Research and Technique presents the recent developments in this exciting field of neuroscience, "structure and function of olfactory neuroepithelium."

Cell Death↗

PubMed2004

Histopathologic changes induced by the microtubule-stabilizing agent Taxol in the rat hippocampus in vivo.

Microtubules and their associated proteins play a prominent role in neuronal morphology, axonal transport, neuronal plasticity, and neuronal degeneration. It has been proposed that microtubule damage is sufficient to induce neuronal death. In this regard, the microtubule-stabilizing agent Taxol could be a useful tool to reproduce some aspects of neurodegenerative diseases associated with disturbances of the cytoskeleton and alterations in axonal transport. Although differential effects of Taxol on neuronal viability have been found in vitro, Taxol toxicity in the central nervous system remains to be addressed. We studied the effects of Taxol on neuronal morphology and viability as well as changes in microtubule-associated proteins MAP2 and tau in rat hippocampus. Our results show that Taxol induces dose-dependent neuronal death accompanied by the loss of MAP2 and the presence of dystrophic neurites. Interestingly paired helical filament (PHF)-1 immunoreactivity, which is associated with a phosphorylated epitope of tau proteins, was induced in the damaged hippocampus. Our results suggest that microtubule dynamics have a role in maintenance of neuronal morphology and survival in vivo, and that modifications in microtubule dynamics, may alter the content and neuronal distribution of MAP2 and promote alterations in the phosphorylation state of tau.

Animals↗

PubMedDate not supplied

Variation of the input resistance and membrane potential of a neuron in trace formation.

Trace changes in electrical activity, input resistance (Rinp), and membrane potential (MP) of brain neurons are studied in the mollusk Limnaea stagnalis for intracellular stimulation with a sinusoidal threshold current with a frequency of 0.1 Hz during 20 min. Some neurons are shown to exhibit an effect of facilitation, a rise in the level of activity being attending by an increase in Rinp and depolarization. Other neurons displayed lowered activity with a decrease of Rinp and hyperpolarization. The selectivity of the Rinp variations relative to the parameters of the stimuli (maximum changes at the frequency of the current used) suggests that it is precisely trace changes of Rinp which lie at the basis of the neuronal plasticity in "learning." Some neurons in this series of experiments did not alter their electrical response, Rinp, or MP for stimulation. The possible reason for the non-uniform reaction of different neurons to identical stimulation is discussed.

Animals↗

PubMed2001

Neurosteroids in learning and memory processes.

The discovery that neurosteroids could be synthesized de novo in the brain independent from the periphery and display neuronal actions led to great enthusiasm for the study of their physiological role. Pharmacological studies suggest that neurosteroids may be involved in several physiological processes, such as learning and memory. This chapter summarizes the effects of the administration of neurosteroids on learning and memory capabilities in rodents and in models of amnesia. We address the central mechanisms involved in mediating the modulation of learning and memory processes by neurosteroids. In this regard, the neurosteroid-modulated neurotransmitter systems, such as gamma-aminobutyric acid type A, N-methyl-D-aspartate, and cholinergic and sigma opioid systems, appear to be potential targets for the rapid memory alteration actions of neurosteroids. Moreover, given that some neurosteroids affect neuronal plasticity, this neuronal change could be involved in the long-term modulation of learning and memory processes. To understand the role of endogeneous neurosteroids in learning and memory processes, we present some physiological studies in rodents and humans. However, the latter do not successfully prove a role of endogenous neurosteroids in age-related memory impairments. Finally, we discuss the relative implication of a given neurosteroid vs its metabolites. For this question, a new approach using the quantitative determination of traces of neurosteroids by mass spectrometry seems to have potential for examining the role of each neurosteroid in discrete brain areas in learning and memory alterations, as observed during aging.

Animals↗

PubMed1996

Classical conditioning with electrical stimulation of cerebellum as both conditioned and unconditioned stimulus.

Stimulating electrodes were implanted in rabbit cerebellum, providing an electrical conditioned stimulus (CS) activating cortical parallel fibers and thence Purkinje and other cells, and an electrical unconditioned stimulus (US) activating underlying white matter and eliciting unconditioned responses. Paired CS-US presentations led to the development of conditioned responses, which showed extinction following CS-alone trials and reacquisition with significant savings on reinstatement of paired trials. Increased local excitability as a result of paired training (but not following unpaired stimulus presentations) was observed in cerebellar cortex, as manifested in substantial decreases in CS threshold for response elicitation in all subjects. This preparation offers a model for the study of plastic neuronal interactions within cerebellar networks critically involved in associative learning.

Animals↗

PubMed1993

Ketamine administration during waking increases delta EEG intensity in rat sleep.

Ketamine is known to increase the metabolic rate of limbic brain structures. We exploited this action to test a hypothesis of the homeostatic model of delta sleep: that an increase in the waking metabolic rate of plastic neuronal systems would increase delta electroencephalographic (EEG) intensity in subsequent nonrapid-eye-movement (NREM) sleep. In separate experiments, we gave intraperitoneal injections of ketamine to Sprague-Dawley rats of either 15, 25, or 50 mg/kg (0.055, 0.091, 0.18 mmol/kg) three times, at approximately hourly intervals, during the dark (waking) period; the last dose was given 4 to 5 hours before onset of the light (sleep) period. After ketamine, both NREM duration and delta EEG intensity (amplitude and incidence) increased significantly over control (saline injections) levels. The magnitude of this increase places it among the largest pharmacologically induced stimulations of delta sleep yet observed. The interpretation of this effect is complicated by the fact that ketamine produces widespread metabolic changes throughout the brain and it also acts on several receptor classes. However, since ketamine's major action is noncompetitive blockade of the cation channel gated by the N-methyl-D-aspartate receptor, our data join recent observations that suggest that excitatory amino acid receptor systems are involved in sleep regulation.

Animals↗

PubMed1996

A columnar model of somatosensory reorganizational plasticity based on Hebbian and non-Hebbian learning rules.

Topographical and functional aspects of neuronal plasticity were studied in the primary somatosensory cortex of adult rats in acute electrophysiological experiments. Under these experimental conditions, we observed short-term reversible reorganization induced by intracortical microstimulation or by an associative pairing of peripheral tactile stimulation. Both types of stimulation generate large-scale and reversible changes of the representational topography and of single cell functional properties. We present a model to simulate the spatial and functional reorganizational aspects of this type of short-term and reversible plasticity. The columnar structure of the network architecture is described and discussed from a biological point of view. The simulated architecture contains three main levels of information processing. The first one is a sensor array corresponding to the sensory surface of the hind paw. The second level, a pre-cortical relay cell array, represents the thalamo-cortical projection with different levels of excitatory and inhibitory relay cells and inhibitory nuclei. The array of cortical columns, the third level, represents stellate, double bouquet, basket and pyramidal cell interactions. The dynamics of the network are ruled by two integro-differential equations of the lateral-inhibition type. In order to implement neuronal plasticity, synaptic weight parameters in those equations are variables. The learning rules are motivated by the original concept of Hebb, but include a combination of both Hebbian and non-Hebbian rules, which modifies different intra- and inter-columnar interactions. We discuss the implications of neuronal plasticity from a behavioral point of view in terms of information processing and computational resources.

Animals↗

PubMed2006

Increased hippocampal mRNA expression of neuronal synaptic plasticity related genes in mice chronically exposed to toluene at a low-level human occupational-exposure.

Although neurological symptoms in individuals exposed to toluene both inside and outside the homes have been reported well, the chronic effects of low-level toluene-exposure on the hippocampal expression of neuronal synaptic plasticity related genes have not been studied in vivo. In the present study, to understand the possible adult hippocampal neurobiological responses of mice chronic exposure to toluene at a low-level human occupational-exposure, we exposed 10-week-old C3H/HeN female mice to 50 ppm toluene or filtered air for 6 h a day, on 5-consecutive days of a week for 6 and 12 weeks, in a whole-body exposure chamber. Then, by a quantitative real-time PCR method, we investigated the hippocampal mRNA-expression of several genes, functions of which are necessary to maintain the homeostasis of neuronal synaptic plasticity. We observed that chronic exposure of mice to 50 ppm toluene for a longer period (12 weeks) caused a significant up-regulation of NMDA receptor subunit 2B (NMDA NR2B) expression associated with a simultaneous induction of CaMKIV, CREB-1, and FosB/DeltaFosB in the same hippocampal tissues. Our data indicate that the in vivo transcriptional up-regulation of these genes in the adult hippocampus of our experimental mouse model following the chronic exposure to toluene may be an NMDA-receptor related neuroprotective mechanism of gene expression.

Animals↗

PubMedDate not supplied

Enriched environment, nitric oxide production and synaptic plasticity prevent the aging-dependent impairment of spatial cognition.

In rodents, neuronal plasticity decreases and spatial learning and working memory deficits increase upon aging. Several authors have shown that rats reared in enriched environments have better cognitive performance in association with increased neuronal plasticity than animals reared in standard environments. We hypothesized that enriched environment could preserve animals from the age-associated neurological impairments, mainly through NO-dependent mechanisms of induction of neuronal plasticity. We present evidence that 27 months old rats from an enriched environment show a better performance in spatial working memory than standard reared rats of the same age. Both mtNOS and cytosolic nNOS activities were found significantly increased (73% and 155%, respectively) in female rats from enriched environment as compared with control animals kept in a standard environment. The enzymatic activity of complex I was 80% increased in rats from enriched environment as compared with control rats. We conclude that an extensively enriched environment prevents old rats from the aging-associated impairment of spatial cognition, synaptic plasticity and nitric oxide production.

Aging↗

PubMed2002

Neuroendocrine plasticity in GnRH release during rat estrous cycle: correlation with molecular markers of synaptic remodeling.

Morphological changes in the gonadotropin releasing hormone (GnRH) neurons in the preoptic area (POA) and their terminals in the median eminence-arcuate (ME-ARC) region are reported to occur during ovarian cycle that may be involved in the GnRH release into the portal blood during preovulatory surge. However, the neuronal substrates participating in altered GnRH neuronal plasticity are poorly understood. The present study was designed to determine whether morphological changes occurring in the GnRH neuron cell bodies in the POA and their terminals in the ME-ARC region of hypothalamus with pulsatile GnRH release in cycling female rats are associated with expression of intrinsic determinants of neuronal plasticity. The plasticity markers studied are polysialylated neural cell adhesion molecule (PSA-NCAM), high molecular weight isoforms of NCAM, growth associated protein (GAP-43), glial fibrillary acidic protein (GFAP) and synaptophysin. Regularly cycling female rats were sacrificed at diestrous, i.e., when GnRH release is low, and at proestrous, i.e., when preovulatory GnRH surge occurs, using perfusion fixation method for immunohistochemical staining of GnRH cells. GnRH cell bodies and their terminals from the POA and ME-ARC region respectively, were localized using immunohistochemical technique in proestrous and diestrous phase of estrous cycle and our results showed a marked increase in the GnRH nerve terminals length and immunoreactivity in the ME-ARC region from proestrous phase rats as compared to diestrous rats. Immunoblot analyses of the POA and ME-ARC region of the hypothalamus revealed a significant increase in the content of PSA-NCAM, NCAM-180, NCAM-140, GAP-43 and synaptophysin from proestrous phase rats as compared to diestrous phase rats. The ME-ARC region showed more pronounced increase in the protein expression of these markers of neuronal plasticity as compared to the POA, whereas, hippocampal region did not show any significant change in the content of these markers showing specificity of the changes to the GnRH system. GFAP content was significantly decreased in the POA with a marginal increase in the GFAP level from the ME-ARC region. These results demonstrate the involvement of synaptic proteins in the dynamic plasticity of the ME-ARC region of hypothalamus, allowing GnRH nerve terminals to release the neurohormone into the pituitary portal blood on the day of proestrous.

Animals↗

PubMed1988

Synaptic and neuronal-glial plasticity in the adult oxytocinergic system in response to physiological stimuli.

Magnocellular oxytocinergic neurons in the hypothalamus offer a striking example of a mammalian neuronal system whose basic architecture and synaptic circuitry can be reversibly modified in adulthood. During parturition, lactation and prolonged osmotic stimulation, glial coverage of oxytocinergic neurons markedly diminishes and their surfaces are left in extensive juxtaposition; concurrently, there is formation of new synapses, which are predominantly GABAergic and which couple two or more oxytocinergic neurons simultaneously. These structural changes do not permanently modify the anatomy of the system since upon cessation of stimulation, neuronal juxtapositions and shared synapses disappear, to reappear upon new stimulation. At present, we can only speculate about the cellular mechanisms and factors responsible for these reversible neuroanatomical changes. However, oxytocin itself appears to be of primary importance since it can induce similar anatomical changes when chronically infused into the third ventricle.

Animals↗

PubMed1993

[New views on pathogenesis and treatment of pain caused by nerve injury].

The article focuses on the pathophysiology of pain as a result of injury to the peripheral or central nervous system. The nervous system is dynamic, and nerve injury leads to long-lasting changes in the nociceptive neurons. Plasticity in the neuronal systems regulating nociception is important in explaining clinical features associated with nerve injury pain. To treat nerve injury pain more effectively, measures should be taken to both prevent and reverse the functional neuronal changes and plasticity caused by nerve injury.

Central Nervous System↗

PubMed2005

Delayed treatment with monoclonal antibody IN-1 1 week after stroke results in recovery of function and corticorubral plasticity in adult rats.

Neuronal death due to ischemic stroke results in permanent deficits in sensory, language, and motor functions. The growth-restrictive environment of the adult central nervous system (CNS) is an obstacle to functional recovery after stroke and other CNS injuries. In this regard, Nogo-A is a potent neurite growth-inhibitory protein known to restrict neuronal plasticity in adults. Previously, we have found that treatment with monoclonal antibody (mAb) IN-1 to neutralize Nogo-A immediately after stroke enhanced motor cortico-efferent plasticity and recovery of skilled forelimb function in rats. However, immediate treatment for stroke is often not clinically feasible. Thus, the present study was undertaken to determine whether cortico-efferent plasticity and functional recovery would occur if treatment with mAb IN-1 was delayed 1 week after stroke. Adult rats were trained on a forelimb-reaching task, and the middle cerebral artery was occluded to induce focal cerebral ischemia to the forelimb sensorimotor cortex. After 1 week, animals received mAb IN-1 treatment, control antibody, or no treatment, and were tested for 9 more weeks. To assess cortico-efferent plasticity, the sensorimotor cortex opposite the stroke lesion was injected with an anterograde neuroanatomical tracer. Behavioral analysis demonstrated a recovery of skilled forelimb function, and anatomical studies revealed neuroplasticity at the level of the red nucleus in animals treated with mAb IN-1, thus demonstrating the efficacy of this treatment even if administered 1 week after stroke.

Animals↗

PubMed1999

Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same.

During learning and development, neural circuitry is refined, in part, through changes in the number and strength of synapses. Most studies of long-term changes in synaptic strength have concentrated on Hebbian mechanisms, where these changes occur in a synapse-specific manner. While Hebbian mechanisms are important for modifying neuronal circuitry selectively, they might not be sufficient because they tend to destabilize the activity of neuronal networks. Recently, several forms of homeostatic plasticity that stabilize the properties of neural circuits have been identified. These include mechanisms that regulate neuronal excitability, stabilize total synaptic strength, and influence the rate and extent of synapse formation. These forms of homeostatic plasticity are likely to go 'hand-in-glove' with Hebbian mechanisms to allow experience to modify the properties of neuronal networks selectively.

Animals↗

PubMed2003

Calcium dynamics are altered in cortical neurons lacking the calmodulin-binding protein RC3.

RC3 is a neuronal calmodulin-binding protein and protein kinase C substrate that is thought to play an important regulatory role in synaptic transmission and neuronal plasticity. Two molecules known to regulate synaptic transmission and neuronal plasticity are Ca(2+) and calmodulin, and proposed mechanisms of RC3 action involve both molecules. However, physiological evidence for a role of RC3 in neuronal Ca(2+) dynamics is limited. In the current study we utilized cultured cortical neurons obtained from RC3 knockout (RC3-/-) and wildtype mice (RC3+/+) and fura-2-based microscopic Ca(2+) imaging to investigate a role for RC3 in neuronal Ca(2+) dynamics. Immunocytochemical characterization showed that the RC3-/- cultures lack RC3 immunoreactivity, whereas cultures prepared from wildtype mice showed RC3 immunoreactivity at all ages studied. RC3+/+ and RC3-/- cultures were indistinguishable with respect to neuron density, neuronal morphology, the formation of extensive neuritic networks and the presence of glial fibrillary acidic protein (GFAP)-positive astrocytes and gamma-aminobutyric acid (GABA)ergic neurons. However, the absence of RC3 in the RC3-/- neurons was found to alter neuronal Ca(2+) dynamics including baseline Ca(2+) levels measured under normal physiological conditions or after blockade of synaptic transmission, spontaneous intracellular Ca(2+) oscillations generated by network synaptic activity, and Ca(2+) responses elicited by exogenous application of N-methyl-D-aspartate (NMDA) or class I metabotropic glutamate receptor agonists. Thus, significant changes in Ca(2+) dynamics occur in cortical neurons when RC3 is absent and these changes do not involve changes in gross neuronal morphology or neuronal maturation. These data provide direct physiological evidence for a regulatory role of RC3 in neuronal Ca(2+) dynamics.

Animals↗