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Results for “Neuronal Plasticity”

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PubMed1997

Mechanisms controlling neuronal plasticity in somatosensory cortex.

gamma-Aminobutyric acid containing neurons in the somatosensory cortex are the major controlling element determining receptive field size and location. This control of the excitability of cortical neurons can be modulated by activity arising in the basal forebrain. A hypothesis is developed stating that both cholinergic and gamma-aminobutyric acid containing projections from the basal forebrain play important roles in the production of a state in cortex permitting neuronal plasticity to occur. This proposed mechanism involving a simultaneous reduction of inhibition and increased release of acetylcholine allows sensory signals to induce long-term changes in the location and responsiveness of cutaneous receptive fields, thereby changing the somatotopic organization of primary somatosensory cortex.

Acetylcholine↗
PubMed1978

Identification of pyramidal cells as the critical elements in hippocampal neuronal plasticity during learning.

The activity of single neurons recorded from rabbit hippocampus during classical conditioning of the nictitating membrane reflex was studied. All cells were first categorized according to their responses after fornix stimulation--i.i., antidromic activation, orthodromic activation, or no activation. The majority of cells that were antidromically activated--pyramidal cells--showed a highly positive correlation between the pattern of unit discharge and the topography of the nicititating membrane response within trial periods. Units that were orthodromically driven by fornix stimulation tended to inhibit during the presentation of trial stimuli, whereas most non-activated cells maintained low spontaneous levels of activity at all times. Thus, the major output neurons of the hippocampus appear to be the neuroanatomical substrate for the large and rapidly developing neuronal plasticity induced by this classical conditioning paradigm.

Action Potentials↗
PubMed2003

[Research strategy for understanding neuronal plasticity and degeneration].

After the disclosure of human genomic information in 2003, the new era of post-genomic research will be in full bloom in the field of neuroscience, brain science as well as in neuropsychiatry. In this paper, the authors discussed possible strategies for understanding neuronal plasticity and neuronal degeneration in the post-genomic research paradigm. Five presentations are discussed in the following orders; 1) pharmacogenomics and epigenetics, 2) neuronal stem cell differentiation and transplantation into brain tissue, 3) Elucidation of the mechanism of neuro-protection and neurogenesis, 4) mechanisms of protein processing, especially importance of regulated intramembranous proteolysis, and 5) simulation analysis of signal transduction pathways. All of these newly developing strategies will be of increasing importance in the research in neuropsychiatry.

Nerve Degeneration↗
PubMed2003

Neuronal plasticity in thalamocortical networks during sleep and waking oscillations.

Spontaneous brain oscillations during states of vigilance are associated with neuronal plasticity due to rhythmic spike bursts and spike trains fired by thalamic and neocortical neurons during low-frequency rhythms that characterize slow-wave sleep and fast rhythms occurring during waking and REM sleep. Intracellular recordings from thalamic and related cortical neurons in vivo demonstrate that, during natural slow-wave sleep oscillations or their experimental models, both thalamic and cortical neurons progressively enhance their responsiveness. This potentiation lasts for several minutes after the end of oscillatory periods. Cortical neurons display self-sustained activity, similar to responses evoked during previous epochs of stimulation, despite the fact that thalamic neurons remain under a powerful hyperpolarizing pressure. These data suggest that, far from being a quiescent state during which the cortex and subcortical structures are globally inhibited, slow-wave sleep may consolidate memory traces acquired during wakefulness in corticothalamic networks. Similar phenomena occur as a consequence of fast oscillations during brain-activated states.

Animals↗
PubMed2006

Molecular mechanism of neuronal plasticity: induction and maintenance of long-term potentiation in the hippocampus.

Recent studies have demonstrated that activation of enzymes can be observed in living cells in response to stimulation with neurotransmitters, hormones, growth factors, and so forth. Thus, the activation of enzymes was shown to be closely related to the dynamic states of various cell functions. The development of new experimental methodologies has enabled researchers to study the molecular basis of neuronal plasticity in living cells. In 1973, Bliss and his associates identified the phenomena of long-term potentiation (LTP). Since it was thought to be a model for neuronal plasticity such as learning and memory, its molecular mechanism has been extensively investigated. The mechanism was found to involve a signal transduction cascade that includes release of glutamate, activation of the NMDA glutamate receptors, Ca(2+) entry, and activations of Ca(2+)/calmodulin-dependent protein kinases (CaM kinases) II and IV and mitogen-activated protein kinase (MAPK). Consequently, AMPA glutamate receptors were activated by phosphorylation by CaM kinase II, resulting in an increase of Ca(2+) entry into postsynaptic neurons. Furthermore, activation of CaM kinase IV and MAPK increased phosphorylation of CREB (cyclic AMP response element binding protein) and expression of c-Fos by stimulation of gene expression. These results suggest that LTP induction and maintenance would be models of short- and long-term memory, respectively.

Animals↗
PubMed2005

Antidepressants and prolonged stress in rats modulate CAM-L1, laminin, and pCREB, implicated in neuronal plasticity.

Previously, we reported an ability of NE to promote processes of plasticity in neuroblastoma cells, as observed by morphological changes such as an elongated granule-rich cell body and neuritegenesis, in addition to a progressive decrease in the pluripotent marker Oct4 and an increase in the growth cone marker GAP-43. This was accompanied by the induction of three plasticity genes forming a functional cluster, the cell adhesion molecule L1 (CAM-L1), laminin, and CREB, all involved in neuronal plasticity and neurite outgrowth. In the present study, we hypothesized that the regulation of CAM-L1, laminin, and CREB/pCREB by NE could mediate processes of plasticity in the mode of action of antidepressants, as well as in the long-term effects of stress, in rats, given the association of both with NE alterations and neuronal plasticity. In the first experiment, rats were chronically administered with antidepressants (21 days). In the second experiment, rats were exposed to chronic stress and examined 4 months later, a model shown to exhibit behavioral indices of stress. We found brain region-specific alterations in mRNA and protein levels of CAM-L1, laminin, and pCREB in rats chronically treated with the noradrenergic antidepressant desipramine and, to a lesser extent, in those treated with fluoxetine. Stressed rats presented a decrease in CAM-L1, laminin, and pCREB, specifically in brain areas implicated in stress. Our findings suggest that noradrenergic-regulated plasticity genes such as CAM-L1, laminin, and CREB play an important role both in stress and in the treatment of depression.

Animals↗
PubMed2004

Slow-wave sleep: serotonin, neuronal plasticity, and seizures.

This article starts by enumerating several data that vindicate Michel Jouvet's hypothesis regarding serotonin as a factor promoting slow-wave sleep. The core of the article is devoted to the description of neuronal bases underlying sleep oscillations, with emphasis on the cortically generated slow oscillation (0.5-1 Hz) that groups both low-frequency (spindles and delta) and high-frequency (beta/gamma) rhythms. The low-frequency rhythms are generated by the synchronous firing of cortical neurons during the depolarizing phase of the slow oscillation, which impacts on the thalamic circuitry to generate spindles and clock-like delta potentials. The fast activity is voltage-dependent and occurs during the depolarization component of the slow cortical oscillation. This coalescence of brain rhythms, discovered in intracellular studies of neocortical and thalamic neurons, is now supported by EEG studies during human sleep. The rich spontaneous activity of neocortical neurons during slow-wave sleep is associated with neuronal plasticity that may play a role in consolidating memory traces acquired during the state of waking. Surprisingly, neuronal plasticity, usually regarded as a beneficial phenomenon implicated in memory and learning, could develop during slow-wave sleep into self-sustained paroxysmal discharges, similar to spike-wave complexes that appear in some epileptic syndromes.

Animals↗
PubMed1996

Trimethyltin-induced plastic neuronal changes in rat hippocampus are accompanied by astrocytic trophic activity.

Partial deafferentation of the hippocampus due to trimethyltin (TMT) intoxication has been reported to induce plastic rearrangements of neuronal elements but the factors that direct these responses are unknown. To assess the possible involvement of nerve growth factor (NGF) in the phenomenon we evaluated the presumable changes in the expression pattern of NGF immunoreactivity (NGF-IR) in rat hippocampus 21 days after administration of TMT (8 mg/kg, i.p.) when reactive changes are fully developed. Immunolabelling for TrkA known to mediate biological effects of NGF and for GFAP to identify astroglial cells as a one of presumed source of postinjury produced factors was carried out on adjacent sections to establish the relation between expression of these proteins. In control hippocampus NGF-IR and TrkA-IR were localized in neurons and/or neuropil. After exposure to TMT remarkable non-neuronal expression of both proteins was observed. The distribution pattern of NGF, TrkA and GFAP overlapped suggesting that reactive astrocytes may not only produce NGF but also may become responsive to this neurotrophin. Zones of extensive NGF and TrkA astroglial expression corresponded to areas of axonal-dendritic rearrangements reported earlier. The data suggest that astroglia-derived trophic activity may be involved in neuronal plastic events associated with treatment with TMT.

Animals↗
PubMed1993

Neuronal plasticity induced by self-stimulation rewarding experience in rats--a study on alteration in dendritic branching in pyramidal neurons of hippocampus and motor cortex.

Self-stimulation rewarding experience promoted structural changes in pyramidal neurons of the CA3 region of the hippocampus and the Vth layer of the motor cortex in adult male Wistar rats. Self-stimulation experience was allowed for 1 h daily for a duration of 10 days through bipolar electrodes placed bilaterally in lateral hypothalamus and substantia nigra--ventral tegmental area. At the end of 10 days, rats were sacrificed, and rapid Golgi examination of the CA3 hippocampal and layer V pyramidal neurons of the motor cortex was made for a grand total of 1600 neurons from 80 rats divided into 4 groups. The neurons of the self-stimulation experienced (SS) group revealed a significant (ANOVA, F-test) increase in dendritic branching in the perisomatic domains. Such changes were not observed in neurons of sham control (SH), experimenter administered stimulation (EA) and normal control (NC) groups. SS animals also showed a significant increase in the thickness of lacunosum and radiatum laminae of CA3 neurons of the hippocampus. Our results reveal that both limbic and neocortical neurons undergo changes in dendritic branching patterns due to self-stimulation rewarding experience. It is tempting to hypothesize that neuronal plasticity is the result of motivation and learning experienced by rats which underwent self-stimulation.

Animals↗
PubMed1995

Models of neuronal plasticity and repair in the enteric nervous system: a review.

In the Fifties we developed an experimental model of neuronal plasticity in adulthood, involving the intestinal myenteric plexus. Causing an incomplete stenosis of the gut, the thickness of the wall and the diameter of the lumen underwent a massive increase on the oral side of the obstruction. The myenteric neurons innervating such hypertrophic and hyperplastic smooth muscle became hypertrophic and increased their number per ganglion, in absence of mitoses. Therefore we hypothesized the existence of a reserve pool of morphologically undifferentiated elements within the plexus, undergoing differentiation under conditions of functional hyperactivity. Some recent experiments suggest once again the existence in adulthood of a reserve pool of potential neurons. In fact, we put in evidence a subpopulation of NADPH-diaphorase positive myenteric neurons, very small in size orally to the stenosis and even smaller in the control gut. Following experimental ablation of the myenteric plexus in an intestinal segment and induction of hypertrophy in its smooth muscle layers, we found a two-five-fold increase in neuronal density along mesenteric nerves. This increase is probably due to the recruitment of cells, not readily identifiable as neurons, along mesenteric nerves in an attempt to reinnervate the damaged ileum. Moreover, it is demonstrated that hypertrophic smooth muscle cells may induce neuronal differentiation of transplanted PC12 cells. Finally, we explain the decreased total number of myenteric neurons in advanced age with the exhaustion of this reserve pool: in fact, NADPH-diaphorase positive small neurons in the myenteric plexus of old rats could not be found.

Animals↗
PubMed1993

Toward understanding of the molecular basis of loss of neuronal plasticity in ageing.

Although there are several lines of evidence which suggest that neuronal plasticity decreases in some regions of both the central and peripheral nervous systems as well as in neuroendocrine tissues during development and ageing, the molecular mechanisms underlying loss of plasticity are largely unknown. To explore this question, we examined changes in expression profiles of neuronal growth-associated proteins (nGAPs) during ageing as well as the molecular regulatory mechanisms of their induction by nerve growth factor (NGF). SCG10, one of the nGAPs, is expressed in subsets of central neurons which maintain a high degree of plasticity in the adult, and is induced after neuronal deafferentation. This is a basis for analysing if SCG10 is involved in the remodelling of adult neurons during reactive synaptogenesis in diseased brains as well as in normal ageing. Studies of the induction of SCG10 by NGF in PC12 cells suggest that transcriptional inducible element(s) are present, at least in part, in the upstream region of the SCG10 gene. These studies of the regulation of nGAPs in ageing brains and neuroendocrine cells may yield new insights on reactivating neurites of partially degenerated neurons in the ageing brain.

Aged↗
PubMed2006

Role of delayed nonsynaptic neuronal plasticity in long-term associative memory.

BACKGROUND: It is now well established that persistent nonsynaptic neuronal plasticity occurs after learning and, like synaptic plasticity, it can be the substrate for long-term memory. What still remains unclear, though, is how nonsynaptic plasticity contributes to the altered neural network properties on which memory depends. Understanding how nonsynaptic plasticity is translated into modified network and behavioral output therefore represents an important objective of current learning and memory research. RESULTS: By using behavioral single-trial classical conditioning together with electrophysiological analysis and calcium imaging, we have explored the cellular mechanisms by which experience-induced nonsynaptic electrical changes in a neuronal soma remote from the synaptic region are translated into synaptic and circuit level effects. We show that after single-trial food-reward conditioning in the snail Lymnaea stagnalis, identified modulatory neurons that are extrinsic to the feeding network become persistently depolarized between 16 and 24 hr after training. This is delayed with respect to early memory formation but concomitant with the establishment and duration of long-term memory. The persistent nonsynaptic change is extrinsic to and maintained independently of synaptic effects occurring within the network directly responsible for the generation of feeding. Artificial membrane potential manipulation and calcium-imaging experiments suggest a novel mechanism whereby the somal depolarization of an extrinsic neuron recruits command-like intrinsic neurons of the circuit underlying the learned behavior. CONCLUSIONS: We show that nonsynaptic plasticity in an extrinsic modulatory neuron encodes information that enables the expression of long-term associative memory, and we describe how this information can be translated into modified network and behavioral output.

Animals↗
PubMed1994

Activity-dependent and hormonal regulation of neurotrophin mRNA levels in the brain--implications for neuronal plasticity.

The neurotrophins exhibit neurotrophic effects on specific, partially overlapping populations of neurons both in the peripheral and the central nervous system (CNS). In the periphery, they are synthesized by a variety of nonneuronal cells, and their synthesis seems to be independent of the neuronal input. In contrast, in the CNS all neurotrophins are expressed under physiological conditions primarily by neurons. The production of NGF and BDNF is controlled by neuronal activity: up-regulation by glutamate and acetylcholine, down-regulation by gamma-aminobutyric acid. In contrast, NT-3 regulation is independent of neuronal activity, but it is up-regulated by thyroid hormones and BDNF. The latter observation suggests that NT-3 might be controlled indirectly by neuronal activity via BDNF. In peripheral nonneuronal tissues, glucocorticoid hormones down-regulate NGF mRNA levels both in vitro and in vivo. In contrast, in the CNS, neuronal production of NGF is enhanced by glucocorticoids. The rapid regulation of NGF and BDNF by subtle physiological stimuli together with the recent demonstration that the neurotrophins release neurotransmitters such as acetylcholine opens up interesting perspectives for the function of neurotrophins as mediators of neuronal plasticity.

Animals↗
PubMed1978

Extrinsic control of intrinsic neuronal plasticity: an hypothesis from work on simple systems.

All advanced nervous systems use plastic properties of neurons for learning, remembering and achieving other information processing feats. Recent findings on a variety of relatively simple nervous systems or reduced parts of more complex ones suggest the notion that, in addition to having neurons with intrinsically plastic properties, nervous systems also have mechanisms for controlling the development, expression, and maintenance of changes in their inherently malleable neurons. This hypothesis has important implications for understanding both the brain's learning machinery and also aspects of nervous system organization not obviously related to learning.

Afferent Pathways↗
PubMed1994

Expression of basic-helix-loop-helix transcription factor ME2 during brain development and in the regions of neuronal plasticity in the adult brain.

We report the isolation of a cDNA encoding the mouse class A bHLH transcription factor ME2 and the analysis of its expression. ME2 is expressed in the cerebral cortex, Purkinje and granule cell layers of the cerebellum, olfactory neuroepithelium, pyramidal cells of hippocampal layers CA1-CA4, and in the granular cells of the dentate gyrus. The specific expression of ME2 during development and in the regions of neuronal plasticity in the adult brain suggest that ME2 may have a regulatory function in developmental processes as well as during neuronal plasticity.

Amino Acid Sequence↗
PubMed1997

Learning transfer and neuronal plasticity in humans trained in tactile discrimination.

Adult humans were unilaterally trained in a tactile discrimination task of sequentially applied multi-finger stimuli. Magnetic source imaging (MSI) was performed before and after the training to evaluate use-dependent neuronal plasticity. All subjects showed fast improvements in performance and complete transfer of the learned task. MSI recordings revealed an unilateral decrease in current dipole strength in the somatosensory system contralateral to the trained hand. Attenuation of sensory evoked fields and a complete learning transfer indicate learning in associative and secondary cortices rather than perceptual plasticity operating on neuronal populations involved in early sensory processing. This findings are discussed with respect to an equivalent animal model and to learning specificity and generalization.

Adult↗
PubMed1994

Gonadal steroids and neuronal plasticity. Studies in the adult rat hypothalamus.

In this chapter, recent studies on gonadal steroid-induced neural plasticity in the adult rat hypothalamus have been described. Neurons in the VMN and DMN are capable of rapid, reversible structural alterations in response to a changing hormonal environment. Given the importance of the VMN in mediating lordosis in female rats, the present studies suggest that hormonally induced morphological changes in the VMN may be necessary for the manifestation of lordosis. This possibility is supported by the 5,7-DHT studies which indicate that the induction of dendritic spines on VMN neurons may somehow decrease the threshold of E needed to elicit lordosis. Moreover, the sex differences in hormonal requirements for lordosis in 5,7-DHT-treated rats are probably the result of organizational effects of gonadal steroids. Our data support the idea that activational effects can only be superimposed on existing brain circuitry to a certain degree. Finally, the neuronal plasticity seen in the hypothalamus may be an important physiological mechanism by which gonadal steroid feedback mediates reproductive and behavioral function.

Animals↗
PubMed2005

Adenylate cyclase-mediated forms of neuronal plasticity in hippocampal area CA1 are reduced with aging.

Beta-adrenergic receptors and the cyclic AMP signaling pathway play an important role in neuronal plasticity and in learning and memory and are known to change with aging. We examined the effects of beta-adrenergic stimulation paired with 5-Hz low frequency stimulation (LFS) of Schaffer collateral-commissural afferents on population spike amplitude in area CA1 of hippocampal slices from young (3 mo) and aged (22 mo) Fischer 344 rats. Application of the beta-adrenergic agonist isoproterenol (1 microM) for 10 min followed immediately by 3 min LFS produced long-lasting potentiation in young hippocampi, but the magnitude of potentiation in aged rats was significantly attenuated and was not long-lasting. In slices prepared from young rats, long-term potentiation (LTP) induced by this protocol occludes subsequent attempts to produce conventional high frequency stimulation-induced LTP, and vice versa, suggesting that these two forms of potentiation share one or more molecular mechanisms. Age-related differences in response to LFS alone were not observed, but significant differences in response to beta-adrenergic stimulation were apparent. Similarly, significant age-related differences in response to direct activation of adenylate cyclase with forskolin (10 microM) were observed. In both age groups, this enhancement produced by isoproterenol or forskolin is only transient, returning to baseline within 60 or 90 min, respectively. Taken together, these studies of adenylate cyclase-mediated forms of potentiation in area CA1 suggest that there is an age-related defect, either upstream or downstream of adenylate cyclase activation, in this important signaling system. Such changes may contribute to the compromised performance on memory tasks that is often observed with normal aging.

Adenylyl Cyclases↗