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Results for “Neuronal Plasticity”

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At least 181 records · Page 10Linked to original sources
PubMed1999

Postsynaptic actin and neuronal plasticity.

In the adult brain, actin is concentrated in dendritic spines where it can produce rapid changes in their shape. Through various synaptic junction proteins, this postsynaptic actin is linked to neurotransmitter receptors, influencing their function and, in turn, being influenced by them. Thus, the actin cytoskeleton is emerging as a key mediator between signal transmission and anatomical plasticity at excitatory synapses.

Actins↗
PubMed2005

Airway-related vagal preganglionic neurons express brain-derived neurotrophic factor and TrkB receptors: implications for neuronal plasticity.

Recent evidence indicates that brain-derived neurotrophic factor (BDNF) is present in neurons and may affect neurotransmitter release, cell excitability, and synaptic plasticity via activation of tyrosine kinase B (TrkB) receptors. However, whether airway-related vagal preganglionic neurons (AVPNs) produce BDNF and contain TrkB receptors is not known. Hence, in ferrets, we examined BDNF and TrkB receptor expression in identified AVPNs using in situ hybridization and immunohistochemistry. BDNF protein levels were measured within the rostral nucleus ambiguus (rNA) region by ELISA. We observed that the subpopulation of AVPNs, identified by neuroanatomical tract tracing, within the rNA region express BDNF mRNA, BDNF protein, as well as TrkB receptor. In addition, brain tissue from the rNA region contained measurable amounts of BDNF that were comparable to the hippocampal region of the brain. These data indicate, for the first time, that the BDNF-TrkB system is expressed by AVPNs and may play a significant role in regulating cholinergic outflow to the airways.

Animals↗
PubMed2003

Calcineurin regulation of neuronal plasticity.

From the most basic of nervous systems to the intricate circuits found within the human brain, a fundamental requirement of neuronal function is that it be malleable, altering its output based upon experience. A host of cellular proteins are recruited for this purpose, which themselves are regulated by protein phosphorylation. Over the past several decades, research has demonstrated that the Ca(2+) and calmodulin-dependent protein phosphatase calcineurin (protein phosphatase 2B) is a critical regulator of a diverse array of proteins, leading to both short- and long-term effects on neuronal excitability and function. This review describes many of the influences of calcineurin on a variety of proteins, including ion channels, neurotransmitter receptors, enzymes, and transcription factors. Intriguingly, due to the bi-directional influences of Ca(2+) and calmodulin on calcineurin activity, the strength and duration of particular stimulations may cause apparently antagonistic functions of calcineurin to work in concert.

Calcineurin↗
PubMed1990

Neuronal plasticity in the developing chick brain: interaction of ethanol and neuropeptides.

We have examined the influence of ethanol on cholinergic and catecholaminergic neuronal expression in the chick embryonic brain using choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) activities as respective neuronal markers. Ethanol (5-20 mg/50 microliters/day), administered to embryos in ovo from day 1 to 3 of development produced a dose-dependent decrease in ChAT activity while TH activity exhibited a dose-dependent increase when embryos were sacrificed on embryonic day 8. The optimal neurotoxic dose of ethanol following this paradigm was 15 mg/day and the LD50 was 17.5 mg/day for the 3 days. Subsequently, embryos were administered ethanol (15 mg) either alone or concomitantly with growth hormone-releasing hormone (GH-RH; 100 ng/50 microliters/day). Previous studies from this laboratory have demonstrated both potent cholinotropic and catecholaminotropic effects for this neuropeptide, results confirmed in this study. Co-administration of ethanol and GH-RH resulted in a significant increase in ChAT activity as compared to both saline- and ethanol-treated controls when examined on day 8 of embryonic growth. No additive effect was observed in TH activity following co-administration of ethanol and GH-RH. The findings from this study are interpreted to mean that GH-RH represents a potent secondary signal to undifferentiated neuroblasts which may lead to a restoration of the cholinergic neuronal population following neurotoxic insult by ethanol.

Animals↗
PubMed1993

[The effect of a decrease in the mobilization of Ca+ and its chemo-controlled intake into the cytoplasm on the modulation of cholinoreceptor neuronal plasticity in Helix lucorum snails by 15-hydroxyeicosatetraenoic acid].

The effects of extracellular solution without Ca2+ and inhibitors of Ca2+ mobilization dependent of Ca2+ (tetracaine) and inositol-1,4,5-trisphosphate (TMB-8) on the modulation of cholinoreceptor (ChR) plasticity of identified Helix lucorum RPa3 and LPa3 neurons by 15(S)-hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid (15-HETE) were investigated. Using the double-electrode voltage-clamp technique, the inward current, induced by local ionophoretic acetylcholine application (ACh-current), was recorded. ChR plasticity was evaluated by extinction of ACh-current developed in a process of rhythmic ACh applications on the soma with an interval 60-240 s. Tetracaine and TMB-8 disturbed long-latent modulatory effect of 15-HETE and did not influence short-latent one. Extraction of Ca2+ from extracellular solution did not affect the modulatory effect of 15-HETE. It was concluded that one of the molecular mechanisms of ChR plasticity deepening due 15-HETE (in long-latent phase) induces potentiation of Ca(2+)- and inositol-1,4,5-trisphosphate-dependent Ca2+ mobilization evoked by 5-lipoxygenase eicosanoids.

Acetylcholine↗
PubMed1992

Activity-dependent neuronal plasticity following tissue injury and inflammation.

Increases in neuronal activity in response to tissue injury lead to changes in gene expression and prolonged changes in the nervous system. These functional changes appear to contribute to the hyperalgesia and spontaneous pain associated with tissue injury. This activity-dependent plasticity involves neuropeptides, such as dynorphin, substance P and calcitonin gene-related peptide, and excitatory amino acids, such as NMDA, which are chemical mediators involved in nociceptive processing. Unilateral inflammation in the hindpaw of the rat results in an increase in the expression of preprodynorphin and preproenkephalin mRNA in the spinal cord, which parallels the behavioral hyperalgesia associated with the inflammation. Cellular intermediate-early genes, such as c-fos, are also expressed in spinal cord neurons following inflammation and activation of nociceptors. Peripheral inflammation results in an enlargement of the receptive fields of many of these neurons. Dynorphin applied to the spinal cord also induces an enlargement of receptive fields. NMDA antagonists block the hyperexcitability produced by inflammation. A model has been proposed in which dynorphin, substance P and calcitonin gene-related peptide enhance excitability at NMDA receptor sites, leading first to dorsal horn hyperexcitability and then to excessive depolarization and excitotoxicity.

Animals↗
PubMed2000

Activity-dependent regulation of neuronal plasticity and self repair.

Plasticity is an essential characteristic of the brain: it is part of how the brain functions and is continuous while the brain interacts with the outer world. The state of activation and the level of activity of the entire organism affect the brain's plastic response. Brain plasticity has many substrates, ranging from synapses to neurites and entire cells. The production of new neurons is part of plasticity even in the adult and old brain, but under normal conditions neurogenesis only occurs in two privileged regions of the adult brain: hippocampus and olfactory system. At least in the hippocampus, physical activity stimulates neurogenesis by acting on the proliferation of neuronal stem cells. More specific functions such as learning may be able to recruit new neurons from the pool of cells with neurogenic potential. In a broader context neuronal stem cells can likely be found throughout the brain. Therefore, novel approaches to neuroregeneration will, when most effective, make use of the activity-related effects on neuronal stem cells in the adult brain to activate these stem cells in a targeted manner to enhance brain function.

Animals↗
PubMed1997

Adenosine and neuronal plasticity.

Adenosine is considered an important neuromodulator of the nervous system acting at pre-, post- and non-synaptic levels. In the present review we describe how adenosine modifies paired-pulse facilitation (PPF), posttetanic depression (PTD), long-term potentiation (LTP), long-term depression (LTD) and depotentiation at the hippocampus, and therefore how this nucleoside modulates synaptic plasticity.

Adenosine↗