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 325 records · Page 18Linked to original sources
PubMedDate not supplied

NF-kappaB in the survival and plasticity of neurons.

The transcription factor nuclear factor kappa-B (NF-kappaB) is involved in regulating responses of neurons to activation of several different signaling pathways in a variety of physiological and pathological settings. During development of the nervous system NF-kappaB is activated in growing neurons by neurotrophic factors and can induce the expression of genes involved in cell differentiation and survival. In the mature nervous system NF-kappaB is activated in synapses in response to excitatory synaptic transmission and may play a pivotal role in processes such as learning and memory. NF-kappaB is activated in neurons and glial cells in acute neurodegenerative conditions such as stroke and traumatic injury, as well as in chronic neurodegenerative conditions such as Alzheimer's disease. Activation of NF-kappaB in neurons can promote their survival by inducing the expression of genes encoding anti-apoptotic proteins such as Bcl-2 and the antioxidant enzyme Mn-superoxide dismutase. On the other hand, by inducing the production and release of inflammatory cytokines, reactive oxygen molecules and excitotoxins, activation of NF-kappaB in microglia and astrocytes may contribute to neuronal degeneration. Emerging findings suggest roles for NF-kappaB as a mediator of effects of behavioral and dietary factors on neuronal plasticity. NF-kappaB provides an attractive target for the development of novel therapeutic approaches for a range of neurological disorders.

Animals↗
PubMedDate not supplied

Recovery of neuroendocrine cells after injury in the aging brain of a mollusc.

Recovery after crush of neuroendocrine caudodorsal cells (CDCs) in the aging brain of the mollusc Lymnaea stagnalis, was determined as a measure of neuronal plasticity. Neuronal plasticity was determined in differently aged animals containing intact (young: 170 days) or morphologically and physiologically degraded (middle-aged: 305 days and old: 443 days) CDCs. Branching patterns and electrical and chemical connectivity and afterdischarge activity of CDCs were studied. Immediately after crush, electrical coupling and chemical transmission were absent. In all age groups partial recovery occurred within about 20 days. CDCs in old animals exhibited restricted recovery of electrical coupling and enhanced recovery of chemical transmission. In young and middle-aged animals normal afterdischarges occurred from day 8 on. In old animals abnormal afterdischarges occurred starting at day 0, becoming normal by day 12 after crush. Recovery of CDC branching was partial in all age groups. It is concluded that in the aging brain recovery of CDCs after injury does occur but is differentially restricted. Our results suggest that senescent degraded neurons still possess a considerable degree of plasticity.

Aging↗
PubMedDate not supplied

Effects of changes in dynamic equilibrium in microtubule and microfilament systems on the plastic responses of neurons.

Studies were carried out on the effects of disruption and stabilization of microtubules and microfilaments on the formation of neuronal plastic responses in isolated nerve cells of the mollusk Lymnaea stagnalis. Disruption of these cytoskeletal elements prevented the development of neuronal plastic responses. Microtubule stabilization produced a dynamic relationship between the development and retention of neuronal plastic responses and series of stimuli. Stabilization of microfilaments blocked the development but promoted the retention of these neuronal responses.

Actin Cytoskeleton↗
PubMed2004

Rapid fluctuations in rat barrel cortex plasticity.

Neuronal populations in the sensory cortex exhibit fluctuations in excitability, and the present experiments tested the hypothesis that these variations coincide with peaks and troughs in cortical modifiability. The activity of multiunit neuronal clusters under light urethane anesthesia was recorded through 100-microelectrode arrays implanted in the infragranular layers of rat barrel cortex. Spontaneous activity was characterized by "bursts" of spikes, synchronized across the barrel cortex. This allowed activity at one selected electrode to be taken as a reliable monitor of widespread cortical bursts. We used spikes at the selected electrode to trigger stimulation of two pairs of whiskers during a 50 min conditioning procedure: (1) for the "burst-conditioned" whisker pair, each stimulus was delivered 1 msec after the triggering spike, activating cortex coincident with the burst; and (2) for the "interburst-conditioned" whisker pair, each stimulus was delivered 300 msec after the triggering spike, activating cortex during the trough between bursts. The cross-correlation between cortical neurons in the pairs of columns matching the stimulated whisker pairs was estimated after the termination of the conditioning procedure. Conditioning produced a twofold increase in the degree of co-firing between infragranular neurons in columns receiving burst-conditioned costimulation but no significant change in connectivity between infragranular neurons in columns receiving interburst-conditioned costimulation, although the two pairs of columns received an equal number of sensory inputs. These findings suggest that the strength of co-activity between columns in the barrel cortex can be modified by sensory input patterns during discrete, intermittent intervals time-locked to bursts.

Action Potentials↗
PubMed2001

Operant conditioning of rat H-reflex affects motoneuron axonal conduction velocity.

This study assessed the effects of operant conditioning of the H-reflex on motoneuron axonal conduction velocity in the rat. After measurement of the control H-reflex size, rats were either exposed for at least 40 days to the HRup or HRdown conditioning mode, in which reward occurred only if the soleus H-reflex was greater than (HRup mode) or less than (HRdown mode) a criterion or continued under the control condition (HRcon mode) in which the H-reflex was simply measured. We then measured axonal conduction velocity of triceps surae motor units of HRup, HRdown, and HRcon rats by stimulating the axon in the ventral root and recording from the tibial nerve. Conduction velocity was 8% less in successful HRdown rats than in HRcon rats (P=0.02). Conduction velocity in HRup rats and unsuccessful HRdown rats was not significantly different from that in HRcon rats. Since recording bypassed the intra-spinal portion of the motoneuron, the change was clearly in the axon. This decrease was similar to the 6% decrease previously found in successful HRdown monkeys. Unsuccessful HRdown rats and monkeys did not show this decrease. This result suggests that the mechanism of HRdown conditioning is similar in rats and monkeys and provides further support for the hypothesis that HRdown conditioning decreases motoneuron excitability by producing a positive shift in firing threshold. While traditional theories of learning emphasize synaptic plasticity, neuronal plasticity may also contribute to operantly conditioned behavioral changes.

Action Potentials↗
PubMed2002

Nitric oxide down-regulates brain-derived neurotrophic factor secretion in cultured hippocampal neurons.

The regulation of neurotrophin (NT) secretion is critical for many aspects of NT-mediated neuronal plasticity. Neurons release NTs by activity-regulated secretion pathways, initiated either by neurotransmitters and/or by existing NTs by a positive-feedback mechanism. This process depends on calcium release from intracellular stores. Little is known, however, about potential pathways that down-regulate NT secretion. Here we demonstrate that nitric oxide (NO) induces a rapid down-regulation of brain-derived neurotrophic factor (BDNF) secretion in cultured hippocampal neurons. Similar effects occur by activating a downstream target of intracellular NO, the soluble guanylyl cyclase, or by increasing the levels of its product, cGMP. Furthermore, down-regulation of BDNF secretion is mediated by cGMP-activated protein kinase G, which prevents calcium release from inositol 1,4,5-trisphosphate-sensitive stores. Our data indicate that the NO/cGMP/protein kinase G pathway represents a signaling mechanism by which neurons can rapidly down-regulate BDNF secretion and suggest that, in hippocampal neurons, NT secretion is finely tuned by both stimulatory and inhibitory signals.

Animals↗
PubMed2004

Nitric oxide synthase and arginase expression changes in the rat perirhinal and entorhinal cortices following unilateral vestibular damage: a link to deficits in object recognition?

Previous studies have shown that peripheral vestibular damage causes long-term neurochemical changes in the hippocampus which may be related to spatial memory deficits. Since recent studies have also demonstrated deficits in non-spatial object recognition memory following vestibular lesions, the aim of the present study was to extend these investigations into the perirhinal cortex (PRC), which is known to be important for object recognition, and the related entorhinal cortex (EC). We examined the effects of unilateral vestibular deafferentation (UVD) on the expression of four enzymes associated with neuronal plasticity, neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), arginase I and arginase II (AI and II), in the rat EC and PRC using Western blotting. Tissue was collected at 10 hs, 50 hs and 2 weeks post-UVD. In the EC and PRC, nNOS protein expression decreased on the contralateral side at 2 weeks post-UVD but not before. At the same time, eNOS protein expression increased in both regions on the contralateral side. In the EC, AII protein expression increased on the ipsilateral side at 2 weeks post-UVD. In the PRC, AI increased and decreased on the contralateral and ipsilateral sides (respectively) at 2 weeks post-UVD. AII showed a bilateral increase in the PRC at 2 weeks post-UVD. These results demonstrate changes in NOS and arginase protein expression in the PRC and EC following UVD, which are unlikely to be due to the initial severity of the vestibular syndrome because they develop well after vestibular compensation has taken place. Neurochemical changes in these regions of the medial temporal lobe may be implicated in the development of object recognition deficits that contribute to cognitive dysfunction following peripheral vestibular damage.

Analysis of Variance↗
PubMed2005

SRF mediates activity-induced gene expression and synaptic plasticity but not neuronal viability.

Synaptic activity-dependent gene expression is critical for certain forms of neuronal plasticity and survival in the mammalian nervous system, yet the mechanisms by which coordinated regulation of activity-induced genes supports neuronal function is unclear. Here, we show that deletion of serum response factor (SRF) in specific neuronal populations in adult mice results in profound deficits in activity-dependent immediate early gene expression, but components of upstream signaling pathways and cyclic AMP-response element binding protein (CREB)-dependent transactivation remain intact. Moreover, SRF-deficient CA1 pyramidal neurons show attenuation of long-term synaptic potentiation, a model for neuronal information storage. Furthermore, in contrast to the massive neurodegeneration seen in adult mice lacking CREB family members, SRF-deficient adult neurons show normal morphologies and basal excitatory synaptic transmission. These findings indicate that the transcriptional events underlying neuronal survival and plasticity are dissociable and that SRF plays a prominent role in use-dependent modification of synaptic strength in the adult brain.

Animals↗
PubMed2003

Psychostimulant-induced plasticity of intrinsic neuronal excitability in ventral subiculum.

Psychostimulant drugs such as amphetamine are prescribed to increase vigilance, suppress appetite, and treat attention disorders, but they powerfully activate the dopamine system and have serious abuse potential. Repeated psychostimulant exposure induces neuronal plasticity within the mesolimbic dopamine system. Here we present evidence that repeated amphetamine exposure results in a suppression of intrinsic neuronal excitability in the ventral subiculum, a hippocampal region that activates dopamine neurotransmission. We used patch-clamp recordings from brain slices obtained at different times after withdrawal from repeated amphetamine exposure to determine the long-term effects of amphetamine on subicular excitability. Using several postsynaptic indices of sodium channel function, our results show that excitability is decreased for days, but not weeks, after repeated amphetamine exposure. The resulting increase in action potential threshold and decrease in postsynaptic amplification of excitatory synaptic input provide the first direct evidence that psychostimulants induce plasticity of hippocampal output and suggest one mechanism by which drug withdrawal may influence limbic dopamine-dependent learning and memory.

Action Potentials↗
PubMed2000

[Neuronal and synaptic properties: fundamentals of network plasticity].

Neurons, within the nervous system, are organized in different neural networks through synaptic connections. Two fundamental components are dynamically interacting in these functional units. The first one are the neurons themselves, and far from being simple action potential generators, they are capable of complex electrical integrative properties due to various types, number, distribution and modulation of voltage-gated ionic channels. The second elements are the synapses where a similar complexity and plasticity is found. Identifying both cellular and synaptic intrinsic properties is necessary to understand the links between neural networks behavior and physiological function, and is a useful step towards a better control of neurological diseases.

Animals↗
PubMed2002

Attenuated plasticity in neurons and astrocytes in the mouse model of Sanfilippo syndrome type B.

Sanfilippo syndrome type B (MPS III B) is a neurodegenerative disorder characterized by profound mental retardation and early death. It is caused by deficiency of a lysosomal enzyme involved in heparan sulfate (HS) degradation. Because HS accumulation can be a major feature of this disease, we have examined crucial molecular systems associated with HS function. Using a knockout mouse with disruption of the gene responsible for HS degradation, we evaluated the effects of possible HS accumulation on neuroplasticity that are within the spectrum of action of fibroblast growth factors (FGFs) and their receptor (FGFR). We found that levels of mRNA for the FGFR-1 were attenuated in the mutant mice by the age of 6 months, whereas the mRNAs for FGF-1 and FGF-2 were reduced or unchanged in the brain regions tested. Neurogenesis, in which FGF-2 is involved, was inhibited in the MPS III B mouse brain at both young and adult ages. We also examined the expression of the glial fibrillary acidic protein (GFAP) gene and GFAP-positive cell density in both normal and injured conditions to study the functional response of astrocytes to insult. We found that, although the mutation alone caused drastic induction of reactive astrocytes, acute injury to the mutant brains failed to induce additional reactive astrocytes. Our results showed important alterations in the expression of several genes involved in the maintenance of neuroplasticity in the MPS III B. This in turn may result in reduction of neuronal health and brain function.

Acetylglucosaminidase↗
PubMed1992

The role of protein phosphatases in synaptic transmission, plasticity and neuronal development.

In the past year significant advances have been made in our understanding of the role of protein dephosphorylation in the control of neuronal function. Molecular cloning has identified a large number of serine/threonine and tyrosine protein phosphatases in the nervous system. Many of these enzymes are selectively enriched in the nervous system, some are localized to specific neurons, and yet others are expressed only during specific periods of neuronal development. The availability of purified protein phosphatases and selective inhibitors has facilitated the analysis of these enzymes and their role in the regulation of neurotransmitter receptors and ion channels.

Animals↗
PubMed1999

Establishment and plasticity of neuronal polarity.

A fundamental feature of neurons is that they possess a polarized morphology, typified by a single long axon and several short dendrites. This cellular polarity forms the basis for directionalized rapid signaling, and for bi-directional trophic signaling, in neuronal circuits. While a catalog of structural, molecular, and functional differences between axons and dendrites is accumulating, the mechanisms involved in the establishment of neuronal polarity (also referred to as axogenesis) are not well understood. Cytoskeletal components, including microtubules and actin filaments, and cytoskeleton-regulating proteins such as microtubule-associated proteins (MAPs), actin-binding proteins, and "motor" proteins, likely play important roles in the establishment and maintenance of neuronal polarity. Polarized sorting of membranes and proteins occurs in neurons, and a better understanding of such sorting mechanisms will likely provide insight into the process of axogenesis. Calcium plays a pivotal role in the regulation of neurite elongation and growth cone motility. Studies in which intracellular calcium levels are measured and manipulated in embryonic neurons during the process of axogenesis suggest a necessary role for calcium gradients in the establishment of neuronal polarity. Experimental models in which developing neurons are induced to switch their polarity support central roles for calcium-regulated cytoskeletal reorganization and protein sorting in the process of axogenesis. Finally, recent findings suggest that mitochondria play an important role in organizing neuronal polarity, possibly by controlling local calcium and/or energy gradients. While considerable progress is being made in elucidating mechanisms that regulate neuronal polarity, the seminal event(s) underlying this process remain a mystery. J. Neurosci. Res. 57:577-589.

Animals↗
PubMed1999

Sending signals from the synapse to the nucleus: possible roles for CaMK, Ras/ERK, and SAPK pathways in the regulation of synaptic plasticity and neuronal growth.

The ability to learn and form memories depends on specific patterns of synaptic activity and is in part transcription dependent. However, the signal transduction pathways that connect signals generated at synapses with transcriptional responses in the nucleus are not well understood. In the present report, we discuss three signal transduction pathways: the Ca(2+)/calmodulin-dependent kinase (CaMK) pathway, the Ras/ERK pathway, and the SAPK pathways that might function to couple synaptic activity to long-term adaptive responses, in part through the regulation of new gene expression. Evidence suggests that these pathways become activated in response to stimuli that regulate synaptic function such as the influx of extracellular Ca(2+) and certain neurotrophin growth factors such as brain-derived neurotrophic factor. Once activated, the CaMK, Ras/ERK, and SAPK pathways lead to the phosphorylation and activation of transcription factors in the nucleus such as the cyclic AMP response element binding protein (CREB). Genes regulated by CREB or other transcription factor targets of the CaMK, Ras/ERK, and SAPK pathways could mediate important adaptive responses to changes in synaptic activity such as changes in synaptic strength and the regulation of neuronal survival and death.

Animals↗
PubMed1998

Gamma-frequency oscillations: a neuronal population phenomenon, regulated by synaptic and intrinsic cellular processes, and inducing synaptic plasticity.

Neurons are extraordinarily complicated devices, in which physical and chemical processes are intercoupled, in spatially non-uniform manner, over distances of millimeters or more, and over time scales of < 1 msec up to the lifetime of the animal. The fact that neuronal populations generating most brain activities of interest are very large-perhaps many millions of cells-makes the task of analysis seem hopeless. Yet, during at least some population activities, neuronal networks oscillate synchronously. The emergence of such oscillations generates precise temporal relationship between neuronal inputs and outputs, thus rendering tractable the analysis of network function at a cellular level. We illustrate this idea with a review of recent data and a network model of synchronized gamma frequency (> 20 Hz) oscillations in vitro, and discuss how these and other oscillations may relate to recent data on back-propagating, action potentials, dendritic Ca2+ transients, long-term potentiation and GABAA receptor-mediated synaptic potentials.

Animals↗