Disease relevance of Neuronal Plasticity

• The excessive activation of NR2B-PP1-GSK3beta-PP1 circuitry may contribute to the deficits of CREB-dependent neuronal plasticity in neurodegenerative diseases [1].
• In this study we tested a neuroplasticity/learning origins hypothesis for repetitive strain injuries (RSIs), including occupationally induced focal dystonia [2].
• It also suggests that fMRI can evidence the active processes of neuroplasticity contributing to mask the clinical cognitive expression of brain pathology at the earliest stage of MS [3].
• The data suggest that while capsaicin-sensitive primary afferents may be involved in neuronal plasticity induced by peripheral tissue inflammation, changes in the capsaicin-insensitive WDR and NS populations are sufficient to produce thermal and mechanical hyperalgesia after the loss of capsaicin-sensitive primary afferents [4].
• Effects of chronic blockade of N-methyl-D-aspartate receptors by MK-801 on neuroplasticity of the micturition reflex pathway after partial urethral obstruction in the rat [5].

Psychiatry related information on Neuronal Plasticity

• As 5-HT and oestrogen are involved in mood disorders, our data suggest that the positive regulation of cell proliferation and neuroplasticity by these two factors may contribute to restore hippocampal connectivity in depressive patients [6].
• These effects are often discussed in terms of nicotine-induced glutamate release with subsequent glutamate-dependent stimulation of dopamine metabolism and neuronal plasticity in brain areas critically involved in drug-addiction mechanisms [7].
• Apolipoprotein E and neuronal plasticity following experimental de-afferentation and in Alzheimer's disease [8].
• Slow-wave sleep: serotonin, neuronal plasticity, and seizures [9].

High impact information on Neuronal Plasticity

• The activity of tPA in neural tissue is correlated with neurite outgrowth, regeneration and migration, suggesting that it might be involved in neuronal plasticity [10].
• Persistent neuronal plasticity, including that observed at some hippocampal synapses, requires N-methyl-D-aspartate (NMDA)-mediated transmission [11].
• The effect of antidepressant treatments on the function of cAMP-responsive element binding protein (CREB), a transcription factor that regulates expression of several genes involved in neuroplasticity, cell survival, and cognition, has been extensively studied [12].
• A mutation was identified in the alpha-synuclein gene, which codes for a presynaptic protein thought to be involved in neuronal plasticity, in the Italian kindred and in three unrelated families of Greek origin with autosomal dominant inheritance for the PD phenotype [13].
• Thus, acetylcholine and norepinephrine have a permissive role in use-dependent neuronal plasticity [14].

Chemical compound and disease context of Neuronal Plasticity

• Preoperative epidural fentanyl, neuroplasticity, and postoperative pain [15].
• The pathological cascade after severe hypoxia or ischemia includes decreased ATP, influx of Ca2+ and Na+ with decrease in intracellular K+ leading to depolarization, release of glutamate, noradrenaline and acetylcholine, changes in neuronal plasticity, cell death, and cognitive impairment [16].

Biological context of Neuronal Plasticity

• Thus, CaMKII phosphorylation of slo Thr107 works as a 'molecular dimmer switch' that could mediate tolerance to alcohol, a form of neuronal plasticity [17].
• The extracellular signal-regulated kinase (ERK1,2 or ERK) pathway is an essential component of NMDAR signal transduction controlling the neuroplasticity underlying memory processes, neuronal development, and refinement of synaptic connections [18].
• Several recent studies suggest that CREB and related transcription factors regulate gene expression necessary for neuronal plasticity and LTM [19].
• Serotonin neurons, neuroplasticity, and homeostasis of neural tissue [20].
• Thus, the sedative action of diazepam is correlated with a selective down-regulation of transcripts involved in the regulation of neuronal plasticity and neurotrophic responses [21].

Anatomical context of Neuronal Plasticity

• In the adult rat brain, transcription of t-PA is an immediate-early response in the hippocampus following treatments that induce neuronal plasticity [22].
• Microtubule-associated protein 1B (MAP1B) is a major constituent of the neuronal cytoskeleton that is expressed at high levels during early brain development and plays a role in axonal growth and neuronal plasticity [23].
• The N-methyl-D-aspartate (NMDA) receptor plays an important role in glutamate-mediated neuronal plasticity and neurotoxicity in the central nervous system [24].
• To reveal the underlying mechanisms of direct current (DC)-induced neuroplasticity, we combined tDCS of the motor cortex with the application of Na(+)-channel-blocking carbamazepine (CBZ) and the N-methyl-D-aspartate (NMDA)-receptor antagonist dextromethorphan (DMO) [25].
• Furthermore, CCSP-NGF-tg mice developed an increased reactivity of sensory neurons in response to inhaled capsaicin demonstrating NGF-mediated neuronal plasticity [26].

Associations of Neuronal Plasticity with chemical compounds

• Glutamate neurotransmission is an essential component of many forms of neuronal plasticity, however, the intracellular mechanisms that mediate plasticity are only beginning to be elucidated [27].
• The available data indicate that there is a high degree of steroid-induced neuronal plasticity in the POM, including changes in neuronal function, in protein synthesis, and in specific inputs [28].
• Accessories to addiction: G protein regulators play a key role in cocaine seeking and neuroplasticity [29].
• Tissue-type plasminogen activator (tPA) is a highly specific serine proteinase expressed in the CNS during events that require neuronal plasticity [30].
• The Drosophila learning mutant, rutabaga, is deficient in the calmodulin-sensitive adenylate cyclase, and studies of associative learning in Aplysia have implicated this enzyme in neuroplasticity [31].

Gene context of Neuronal Plasticity

• Although Reln is secreted by GABAergic neurons, its target are not the GABA receptors, but rather may be extrasynaptically located in perineuronal nets and concerned with the modulation of neuronal plasticity [32].
• Neuronal plasticity associated with learning, memory and development is controlled, in part, by NMDA receptors, which are complexes consisting of the subunit NMDAR1 (NR1) and one or more NMDAR2 subunits (NR2A-NR2D) [33].
• The observed transcriptional modulation of the components of dystrophin-dystroglycan complexes indicates their involvement in injury-induced neuronal plasticity and suggests a role in other forms of plasticity such as those required in learning and memory, functions often impaired in Duchenne muscular dystrophy patients [34].
• Inducible cAMP early repressor (ICER) in the nervous system--a transcriptional regulator of neuronal plasticity and programmed cell death [35].
• Voluntary exercise induces a BDNF-mediated mechanism that promotes neuroplasticity [36].

Analytical, diagnostic and therapeutic context of Neuronal Plasticity

• Confocal microscopy was used to assess activity-dependent neuroplasticity in neurotransmitter innervation of vasopressin immunoreactive magnocellular neurons in the supraoptic nucleus (SON) [37].
• Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity [38].
• Urine samples were assayed for different soluble mediators using immunoassays for tryptase (a marker for mast cell activation), neurotrophic factors (markers of neuronal plasticity) and chemokines (markers of inflammatory cell activity) [39].
• Nitric oxide (NO)-mediated mechanisms have been assigned a role in cortical perfusion, learning and memory as well as in neuronal plasticity [40].
• We performed microarray analysis on rat hippocampal tissue following kainic acid treatment in order to study the signaling mechanisms underlying these diverse processes in an attempt to increase our current understanding of mechanisms contributing to such fundamental processes as neuronal protection and neuronal plasticity [41].

References