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 145 records · Page 8Linked to original sources

PubMed1996

Nitric oxide, a neuronal messenger. Its role in the hippocampus neuronal plasticity.

Nitric oxide (NO), a free radical gas, has recently been recognized as an important messenger molecule having a neurotransmitter-like function. Studies on the localization of the enzyme synthesizing NO (NO synthase-NOS) have indicated its presence in almost all parts of the brain with a prevalence in the cerebellum. From recent experimental investigations it is apparent that NO might meet the essential criteria to function as a retrograde messenger for Long-term potentiation in hippocampal cells, a process known to be involved in mammalian learning and memory. However, within the hippocampus NO is present in a few cell types which probably form the local neuronal circuit. Thus NO might function as a paracrine factor rather than a retrograde messenger in the hippocampal neurons.

Animals↗

PubMed2002

Motoneuron and sensory neuron plasticity to varying neuromuscular activity levels.

The size and phenotypic properties of the neural and muscular elements of the neuromuscular unit are matched under normal conditions. When subjected to chronic decreases or increases in neuromuscular activity, however, the adaptations in these properties are much more limited in the neural compared with the muscular elements.

Adaptation, Physiological↗

PubMed1998

Postoperative chronic pain and bladder dysfunction: windup and neuronal plasticity--do we need a more neurological approach in pelvic surgery?

PURPOSE: Cases of combined symptoms of dysfunctional voiding and associated pelvic discomfort are difficult diagnostic and therapeutic challenges. Surgical solutions not uncommonly fail to relieve those symptoms. We determine why these symptoms persist postoperatively. MATERIALS AND METHODS: Four cases of ureteral injury during gynecological laparoscopic procedures for pelvic/menstrual pain are presented. The cases are reviewed for their severity and similarity in presenting symptoms, complications and long-term consequences. RESULTS: In all cases light pain symptoms and/or dysfunctional voiding problems that existed before the initial surgery escalated severely after corrective pelvic surgery. CONCLUSIONS: There are established neurophysiological mechanisms that would explain the observed increase in pain after surgical manipulation of the pelvis. Windup and changes in neuronal plasticity are direct consequences of wounding and/or neural injury to the central nervous system. These principles are important for surgeons to appreciate due to the impact they can have on the outcomes of surgery. Blocking the sensory input into the spinal cord, inherent to every surgical procedure, through use of local anesthetics, that is preemptive anesthesia, before creation of a wound provides the greatest protection against escalation of symptoms. Thorough evaluation of all patients before pelvic surgery is recommended to identify high risk groups (preexisting pain, voiding syndromes).

Adult↗

PubMed1991

Growth-regulated proteins and neuronal plasticity. A commentary.

Growth-regulated proteins (GRPs) of the neuron are synthesized during outgrowth and regeneration at an increased rate and enriched in nerve growth cones. Therefore, they can be used to some degree as markers of neurite growth. However, these proteins are not unique to the growing neuron, and their properties are not known sufficiently to assign them a functional and/or causal role in the mechanisms of outgrowth. During synaptogenesis, GRPs decrease in abundance, and growth cone functions of motility and organelle assembly are being replaced by junctional contact and transmitter release. However, there is a stage during which growth cone and synaptic properties overlap to some degree. We propose that it is this overlap and its continuation that allow for synaptic plasticity in developing and adult nervous systems. We also propose a hypothesis involving (a) trophic factor(s) that might explain the regulation of synaptic sizes and collateral sprouting. Some GRPs, especially GAP43/B50/pp46/F1, are more prominent in adult brain regions of high plasticity, and they undergo change, such as phosphorylation, during long-term potentiation (LTP). Without precise functional knowledge of GRPs, it is impossible to use changes in such proteins to explain the plasticity mechanism. However, changes in these "growth markers" are likely to be an indication of sprouting activity, which would explain well the various phenomena associated with plasticity and learning in the adult. Thus, plasticity and memory may be viewed as a continuation of the developmental process into adulthood.

Animals↗

PubMed2003

Motoneuron and sensory neuron plasticity to varying neuromuscular activity levels.

Case-Control Studies↗

PubMed1990

Tonic 5-HT modulation of spinal dorsal horn neuron activity evoked by both noxious and non-noxious stimuli: a source of neuronal plasticity.

The influence of tonic serotonergic modulation on the responses of spinal dorsal horn neurons to natural peripheral stimulation was examined in physiologically intact, awake, drug-free cats. Systemically administered methysergide (maximum cumulative dose 2 mg/kg) caused significant changes in responses of some dorsal horn neurons to both mildly noxious and non-noxious stimulation. Individual changes provide evidence, in this model, for tonic 5-HT modulation of many aspects of sensory transmission at the level of the spinal cord. Taken together, the changes demonstrate the significant degree of plasticity that exists for some spinal dorsal horn neurons. It is clear that the plasticity of some spinal dorsal horn neurons allows for a much broader response profile than would be apparent under the restricted circumstances of a normal neurophysiologic study. Removal of tonic inhibition on responses to noxious stimuli may be an aspect of neuronal plasticity that functions to provide an immediate change in the way that the nervous system responds to a noxious stimulus.

Action Potentials↗

PubMed1986

[Organization of the nervous system after coagulation of the follicles of mystacial vibrissae in the newborn mouse: an example of neuronal plasticity].

In the mouse the vibrissae and the common fur of the head are a good model of the so called neural plasticity. The characteristics of this model are: the pattern of implantation of the vibrissae at the periphery and that of the arrangement of barrels in the contralateral cortical projection area of vibrissae as well as that of the "barreloïds" in the subcortical vibrissal relays (somato sensory thalamus and trigeminal nuclear complex) are homeomorphic with one another. Each barrel and "barreloïd" receives projections from one vibrissa. Moreover at the level of the cortex these projections are also in register with projections from ipsilateral vibrissae. Head fur hairs project to well defined but entirely distinct areas. Destruction of vibrissae follicles at birth beside preventing barrel and barreloïd formation in the CNS, leads to several morphological changes: degeneration of the primary sensory neurons innervating vibrissae in the trigeminal ganglion, thus degeneration of their central axons and the corresponding terminals in the trigeminal vibrissal relays changes in the distribution of the activity of succinate dehydrogenase in the IVth layer of the cortical vibrissal area and in the corresponding subcortical relays, from the normal discrete (barrel hollow) pattern--corresponding to the clustered vibrissal afferents--to a continuous band, keeping a normal level of activity, excepted in the trigeminal vibrissal relays and a remarkable preservation of cortical thickness but a notable atrophy in the trigeminal vibrissal projection areas. Beside upsetting the anatomy vibrissae follicle destruction causes marked functional changes an outstanding take-over of the deafferented cortical vibrissal area (still identifiable from projections of vibrissae ipsilateral to it) by the head fur hairs this take over exist also in the subcortical vibrissal relays a change in the thalamo-cortical connections. Modifications in the organization of connections are initiated by the loss of the primary sensory neurons innervating vibrissae, in the trigeminal ganglion and results only from early lesions. In mice lesioned when adults the loss of primary sensory neurons is less important and functional take over by the common fur is not observed.

Afferent Pathways↗

PubMed1987

Noradrenaline neuron plasticity in developing rat brain: effects of neonatal 6-hydroxydopamine demonstrated by dopamine-beta-hydroxylase immunocytochemistry.

The present study was conducted to assess the morphological changes produced by neonatal administration of 6-hydroxydopamine (6-OHDA) in the noradrenergic innervation of the developing and adult rat brain. As demonstrated by dopamine-beta-hydroxylase (DBH) immunohistochemistry, the major alterations are the following. First, neocortical and hippocampal noradrenergic innervation is permanently eliminated by the treatment, with lesser effects on other telencephalic structures. These changes appear by postnatal day 5 and are permanent in nature. In adult treated animals, most thalamic nuclei are hyperinnervated by DBH-immunoreactive axons as are the cerebellum and a number of brainstem nuclei. The hyperinnervation of these structures occurs after postnatal day 20, and is extremely specific, with the pattern of organization and distribution of noradrenergic axons in treated animals identical to that of controls. In contrast, the noradrenergic innervation of the hypothalamus is relatively unaffected by 6-OHDA treatment. The principal exception is the development of an anomalous plexus of DBH immunoreactive axons in the lateral hypothalamus. The timing and organization of the changes produced by neonatal 6-OHDA administration are consistent with the hypothesis that noradrenergic neurons, and particularly those of the locus coeruleus, are programmed to produce a defined amount of axon and terminal field, with any developmental loss resulting in a 'pruning effect' such that the total terminal field appears conserved. Given the specificity of the hyperinnervation, inductive influences from the target nuclei probably play a major role in determining the pattern of the noradrenergic innervation.

Animals↗

PubMed2005

Premotor neuronal plasticity in monkeys adapting to a new dynamic environment.

Recent evidence indicates that premotor cortex (PM) in addition to their well-established motor functions, also play a role in nonmotor processes such as spatial attention and working memory. In the present study, neuronal activities in dorsal PM (PMd) and ventral PM (PMv) were recorded in a force field adaptation task. This study found that PM neurons show learning-related plasticity and that a neuron demonstrates either one type or multiple types of properties (i.e. kinematic, dynamic, and memory). The current study reveals that memory properties could be displayed by one or a combination of the cell activity parameters [i.e. average firing rate (AFR), dynamic range (DR), and preferred direction (PD)]. A predominant percentage of cells displayed memory properties with AFR or AFR plus other parameters. This study investigated the memory properties vs. the time sequence of the task trial [i.e. delay time (DT), movement time (MT), and target holding time (THT)] and found that: (i) most neurons display memory properties only in one time window; (ii) few neurons display memory properties in three time windows, and (iii) there are significantly more cells showing memory properties during MT than during any other time windows. There are cells that show memory I (changing their tuning curves in the force field and retaining those changes after the force field was removed), memory II (changing their tuning curves after the force field was removed), or both properties. Significantly more cells display one type of memory property (memory I or memory II) rather than both types of memory properties (memory I and memory II).

Adaptation, Physiological↗

PubMed1995

Mamillothalamic tract transection blocks anterior thalamic training-induced neuronal plasticity and impairs discriminative offidance behavior in rabbits.

Rabbits with bilateral transecting lesions of the mamillothalamic tract, control (tract-sparing and sham) lesions, or no lesions, and chronic, fixed-position anterior ventral (AV) and medial dorsal (MD) thalamic and posterodorsal subicular complex unit recording electrodes were trained to step in an activity wheel in response to a 0.5 sec tone (CS+) in order to avoid a brief foot shock. The rabbits also learned to ignore a different tone (CS-) not predictive of shock. Behavioral acquisition was significantly retarded in rabbits with mamillothalamic tract transection compared to controls. When trained, transected rabbits failed to avoid the shock more often than controls. Mamillothalamic tract transection abolished and control lesions attenuated AV thalamic discriminative training-induced activity (i.e., development with training of greater discharges in response to the CS+ than to the CS-). Transection and control lesions attenuated AV thalamic excitatory training-induced activity (greater elicited activity during training than during unpaired tone-shock presentations before training) as well as AV thalamic "spontaneous" baseline unit activity. CS-elicited discharge magnitude was reduced by control lesions and it was further reduced by tract transecting lesions. Significant lesion-related changes were not found in the subicular or MD thalamic neuronal receptor. Mamillothalamic tract afferent information flow is thus essential for AV thalamic discriminative training-induced activity, excitatory training-induced activity, tone-elicited discharges and maintenance of conditioned avoidance responses. The effects of the control lesions suggested that afferents which course in parallel with and near the mamillothalamic tract may contribute to AV thalamic spontaneous activity and excitatory training-induced activity.

Animals↗

PubMed1999

Nuclear calcium-activated gene expression: possible roles in neuronal plasticity and epileptogenesis.

Nuclear calcium signals associated with electrical activation of neurons are critical regulators of gene expression and may cause changes in neuronal structure and function. Recent studies have identified a key component of the transcriptional machinery, the coactivator CREB binding protein (CBP), as a target for a nuclear calcium signalling pathway. Because the regulation of many genes involves transcription factors that function through their interaction with CBP, this mechanism, termed 'the coactivator control model', may modulate the expression of a large number of genes. During normal working of the brain, nuclear calcium increases may be transient and initiate transcriptional responses that are important for learning and memory. However, more intense or sustained stimulations of neurons (for example those used in the kindling model) may overactivate nuclear calcium-regulated processes. This may initiate inappropriate gene expression responses and could lead to the formation of epileptic neuronal circuits and disorders of neuronal excitability.

Animals↗

PubMed2003

Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for difficult-to-treat depression.

There is growing evidence from neuroimaging and ostmortem studies that severe mood disorders, which have traditionally been conceptualized as neurochemical disorders, are associated with impairments of structural plasticity and cellular resilience. It is thus noteworthy that recent preclinical studies have shown that critical molecules in neurotrophic signaling cascades (most notably cyclic adenosine monophosphate [cAMP] response element binding protein, brain-derived neurotrophic factor, bcl-2, and mitogen activated protein [MAP] kinases) are long-term targets for antidepressant agents and antidepressant potentiating modalities. This suggests that effective treatments provide both trophic and neurochemical support, which serves to enhance and maintainnormal synaptic connectivity, thereby allowing the chemical signal to reinstate the optimal functioning of critical circuits necessary for normal affective functioning. For many refractory patients, drugs mimicking "traditional" strategies, which directly or indirectly alter monoaminergic levels, may be of limited benefit. Newer "plasticity enhancing" strategies that may have utility in the treatment of refractory depression include N-methyl-D-aspartate antagonists, alpha-amino-3-hydroxy-5-methylisoxazole propionate (AMPA) potentiators, cAMP phosphodiesterase inhibitors, and glucocorticoid receptor antagonists. Small-molecule agents that regulate the activity f growth factors, MAP kinases cascades, and the bcl-2 family of proteins are also promising future avenues. The development of novel, nonaminergic-based therapeutics holds much promise for improved treatment of severe, refractory mood disorders.

Animals↗

PubMed1986

Neuronal plasticity in the nigrostriatal system of the rat after unilateral removal of vibrissae.

The vibrissae of rats were shaved from one side of the face daily for 10 days. To see whether or not this treatment had an effect on crossed and uncrossed striatal afferent connections from the midbrain, the tract tracer horseradish peroxidase was applied to the caudate-putamen on day 11. When the tracer was deposited on the side opposite the vibrissae removal, more labeled cells were found in the contralateral substantia nigra than when it was applied on the same side as the vibrissae removal, or placed in animals with intact vibrissae. Unilateral removal of vibrissae did not affect uptake of the tracer by the cells which give rise to the homolateral nigrostriatal projections. These changes in HRP labeling in the crossed projection from the substantia nigra were seen after 10 days of unilateral removal of the vibrissae; i.e., at a time when the animals have had opportunity to learn to compensate for vibrissotomy-induced behavioral asymmetries.

Animals↗

PubMed2000

Functional triads consisting of ryanodine receptors, Ca(2+) channels, and Ca(2+)-activated K(+) channels in bullfrog sympathetic neurons. Plastic modulation of action potential.

Fluorescent ryanodine revealed the distribution of ryanodine receptors in the submembrane cytoplasm (less than a few micrometers) of cultured bullfrog sympathetic ganglion cells. Rises in cytosolic Ca(2+) ([Ca(2+)](i)) elicited by single or repetitive action potentials (APs) propagated at a high speed (150 microm/s) in constant amplitude and rate of rise in the cytoplasm bearing ryanodine receptors, and then in the slower, waning manner in the deeper region. Ryanodine (10 microM), a ryanodine receptor blocker (and/or a half opener), or thapsigargin (1-2 microM), a Ca(2+)-pump blocker, or omega-conotoxin GVIA (omega-CgTx, 1 microM), a N-type Ca(2+) channel blocker, blocked the fast propagation, but did not affect the slower spread. Ca(2+) entry thus triggered the regenerative activation of Ca(2+)-induced Ca(2+) release (CICR) in the submembrane region, followed by buffered Ca(2+) diffusion in the deeper cytoplasm. Computer simulation assuming Ca(2+) release in the submembrane region reproduced the Ca(2+) dynamics. Ryanodine or thapsigargin decreased the rate of spike repolarization of an AP to 80%, but not in the presence of iberiotoxin (IbTx, 100 nM), a BK-type Ca(2+)-activated K(+) channel blocker, or omega-CgTx, both of which decreased the rate to 50%. The spike repolarization rate and the amplitude of a single AP-induced rise in [Ca(2+)](i) gradually decreased to a plateau during repetition of APs at 50 Hz, but reduced less in the presence of ryanodine or thapsigargin. The amplitude of each of the [Ca(2+)](i) rise correlated well with the reduction in the IbTx-sensitive component of spike repolarization. The apamin-sensitive SK-type Ca(2+)-activated K(+) current, underlying the afterhyperpolarization of APs, increased during repetitive APs, decayed faster than the accompanying rise in [Ca(2+)](i), and was suppressed by CICR blockers. Thus, ryanodine receptors form a functional triad with N-type Ca(2+) channels and BK channels, and a loose coupling with SK channels in bullfrog sympathetic neurons, plastically modulating AP.

Action Potentials↗

PubMed1987

Neuronal plasticity in the mammalian brain: relevance to behavioral learning and memory.

Much recent activity in the neurosciences relates to the search for the brain mechanisms underlying learning and memory. In recent years a brain circuit in cerebellum and brainstem has been discovered that is responsible for the learning of a simple motor response (nictitating membrane movement). This has provided a model for neuroscientists to use in understanding the brain circuits involved in this simple form of learning and, by extension, to more complex forms ultimately, and a means of exploring the changes in neural function underlying the learning. An enduring change in neural function is represented by long-term potentiation (LTP), an alteration in synaptic efficacy seen in hippocampus and other areas. LTP can be induced experimentally and occurs as a concomitant of learning. We review data suggesting that different brain circuits may underlie different forms of learning and memory. Several current theories of learning and memory with respect to hippocampal and other brain circuit involvement are considered. We conclude with the behavioral and physiological effects of exposure to teratogens or toxins and the CNS alterations associated with dementia.

Animals↗

PubMed2006

Nidogen and nidogen-associated basement membrane proteins and neuronal plasticity.

Extracellular matrix (ECM) proteins are thought to subserve structural functions as, for example, tissue barriers as well as guidance structures during cell growth, differentiation and tissue repair. Deletion of basement membrane (BM) components results in malformations of different organs, including the brain. Recent data, however, suggest that interference with cellular membrane-associated proteins interacting with ECM can alter neuronal excitability and synaptic plasticity without obvious underlying structural damage. This does not only apply to classical ECM proteins such as laminin, reelin and tenascin, but also to molecules of a rather specialized ECM, the BM. Here, nidogen (also termed entactin) appears to subserve a function in neuronal plasticity. Nidogen ablation leads to epileptic activity in vivo and the appearance of spontaneous epileptiform activity in vitro. This raises the intriguing question whether the BM protein nidogen may directly influence neuronal function in the CNS, opening the possibility of modulatory mechanisms of synaptic plasticity and excitability reaching beyond classical processes confined to cellular interactions.

Animals↗

PubMed2001

Neuronal plasticity in hippocampal mossy fiber-CA3 synapses of mice lacking the inositol-1,4,5-trisphosphate type 1 receptor.

In the present study, we used inositol-1,4,5-trisphosphate (IP3) type 1 receptor (IP3R1) knockout mice to examine the role of this receptor in the induction of LTP, LTD, and DP at mossy fiber-CA3 synapses. No difference in synaptically induced field-EPSPs was seen between the wild-type (IP3R1(+/+)) and IP3R1 knockout mice (IP3R1(-/-)), showing that basic synaptic transmission does not involve IP3R1 activation. Tetanus induced LTP in both wild-type and IP(3)R1(-/-) mice, but the magnitude of LTP was significantly greater in IP3R1(-/-) mice (149.8+/-3.5%, mean+/-S.E.M., n=15) than in wild-type mice (132.4+/-1.5%, n=17), suggesting that the IP3R1 has a suppressive effect on LTP induction. To determine whether this effect involved N-methyl-D-aspartate receptor (NMDAR)-dependent LTP, the effect of tetanus was tested in the present of the NMDAR antagonist, D,L-AP5 (50 microM); under these conditions, the LTP in both IP3R1(-/-) and IP3R1(+/+) mice was not significantly reduced. In addition, group I mGluR activation was shown to be necessary for LTP induction, as the LTP was almost blocked by the group I mGluR antagonist, RS-4CPG (500 microM) in both IP3R1(-/-) (117.6+/-1.7%, n=8) and IP3R1(+/+) (116.9+/-1.8%, n=5) mice. The IP3R1 also plays an essential role in LTD induction, as low-frequency stimulation (LFS) failed to induce LTD in the mutant mice (104.5+/-2.1%, n=10). DP was induced in both IP3R1(-/-) and wild-type mice.

Animals↗

PubMed2005

A role for caveolin-1 in post-injury reactive neuronal plasticity.

Remodeling and plasticity in the adult brain require cholesterol redistribution and synthesis for the formation of new membrane components. Caveolin-1 is a cholesterol-binding membrane protein involved in cellular cholesterol transport and homeostasis. Evidence presented here demonstrates an up-regulation of caveolin-1 in the hippocampus, which was temporally correlated with an increase in synaptophysin during the reinnervation phase in a mouse model of hippocampal deafferentation. Using an in vitro model of neuronal reactive plasticity, we examined the effect of virally mediated overexpression of caveolin-1 on injured differentiated PC12 cells undergoing terminal remodeling. Three days post lesion, caveolin-1-overexpressing cells revealed increases in synaptophysin and GAP-43, two markers of neurite sprouting and synaptogenesis. Morphologically, caveolin-1-overexpressing cells showed a decrease in primary neurite outgrowth and branching as well as an increase in neurite density. Caveolin-1-overexpressing cells also revealed the presence of terminal swelling and beading along processes, consistent with a possible alteration of microtubules stability. Moreover, a focal enrichment of caveolin-1 immunofluorescence was observed at the bases of axonal and dendritic terminals of mouse primary hippocampal neurons. Altogether, these results indicate that caveolin-1 plays an active role in the regulation of injury-induced synaptic and terminal remodeling in the adult CNS.

Animals↗