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Neuroscience_topics
Neuroscience: CNS disease, pain, brain research, ion channels, synaptic transmission, channelopathies, neuronal network
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Very long-term memories may be stored in the pattern of holes in the perineuronal net

Very long-term memories may be stored in the pattern of holes in the perineuronal net | Neuroscience_topics | Scoop.it

A hypothesis and the experiments to test it propose that very long-term memories, such as fear conditioning, are stored as the pattern of holes in the perineuronal net (PNN), a specialized ECM that envelops mature neurons and restricts synapse formation. The 3D intertwining of PNN and synapses would be imaged by serial-section EM. Lifetimes of PNN vs. intrasynaptic components would be compared with pulse-chase 15N labeling in mice and 14C content in human cadaver brains. Genetically encoded indicators and antineoepitope antibodies should improve spatial and temporal resolution of the in vivo activity of proteases that locally erode PNN. Further techniques suggested include genetic KOs, better pharmacological inhibitors, and a genetically encoded snapshot reporter, which will capture the pattern of activity throughout a large ensemble of neurons at a time precisely defined by the triggering illumination, drive expression of effector genes to mark those cells, and allow selective excitation, inhibition, or ablation to test their functional importance. The snapshot reporter should enable more precise inhibition or potentiation of PNN erosion to compare with behavioral consequences. Finally, biosynthesis of PNN components and proteases would be imaged. (...) - By Roger Y. TsienPNAS July 23, 2013 vol. 110 no. 3012456-12461

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[Review] Epigenetic Mechanisms of Depression and Antidepressant Action

[Review] Epigenetic Mechanisms of Depression and Antidepressant Action | Neuroscience_topics | Scoop.it

[Abstract] Epigenetic mechanisms, which control chromatin structure and function, mediate changes in gene expression that occur in response to diverse stimuli. Recent research has established that environmental events and behavioral experience induce epigenetic changes at particular gene loci and that these changes help shape neuronal plasticity and function and hence behavior. Some of these changes can be stable and can even persist for a lifetime. Increasing evidence supports the hypothesis that aberrations in chromatin remodeling and subsequent effects on gene expression within limbic brain regions contribute to the pathogenesis of depression and other stress-related disorders such as post-traumatic stress disorder and other anxiety syndromes. Likewise, the gradually developing but persistent therapeutic effects of antidepressant medications may be achieved in part via epigenetic mechanisms. This review discusses recent advances in our understanding of the epigenetic regulation of stress-related disorders and focuses on three distinct aspects of stress-induced epigenetic pathology: the effects of stress and antidepressant treatment during adulthood, the lifelong effects of early-life stress on subsequent stress vulnerability, and the possible transgenerational transmission of stress-induced abnormalities. - by Vialou V et al., Annual Review of Pharmacology and Toxicology, 53(1):59

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Functional maps within a single neuron

Functional maps within a single neuron | Neuroscience_topics | Scoop.it

The presence and plasticity of dendritic ion channels are well established. However, the literature is divided on what specific roles these dendritic ion channels play in neuronal information processing, and there is no consensus on why neuronal dendrites should express diverse ion channels with different expression profiles. In this review, we present a case for viewing dendritic information processing through the lens of the sensory map literature, where functional gradients within neurons are considered as maps on the neuronal topograph. Under such a framework, drawing analogies from the sensory map literature, we postulate that the formation of intraneuronal functional maps is driven by the twin objectives of efficiently encoding inputs that impinge along different dendritic locations and of retaining homeostasis in the face of changes that are required in the coding process. In arriving at this postulate, we relate intraneuronal map physiology to the vast literature on sensory maps and argue that such a metaphorical association provides a fresh conceptual framework for analyzing and understanding single-neuron information encoding. We also describe instances where the metaphor presents specific directions for research on intraneuronal maps, derived from analogous pursuits in the sensory map literature. We suggest that this perspective offers a thesis for why neurons should express and alter ion channels in their dendrites and provides a framework under which active dendrites could be related to neural coding, learning theory, and homeostasis. by Narayanan R & Johnston DJournal of Neurophysioly, November 1, 2012 vol. 108 no. 9 2343-2351

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MicroRNAs Shape the Neuronal Landscape

MicroRNAs Shape the Neuronal Landscape | Neuroscience_topics | Scoop.it

[Review] The nervous system equips us with capability to adapt to many conditions and circumstances. We rely on an armamentarium of intricately formed neural circuits for many of our adaptive strategies. However, this capability also depends on a well-conserved toolkit of different molecular mechanisms that offer not only compensatory responses to a changing world, but also provide plasticity to achieve changes in cellular state that underlie a broad range of processes from early developmental transitions to life-long memory. Among the molecular tools that mediate changes in cellular state, our understanding of posttranscriptional regulation of gene expression is expanding rapidly. Part of the “epigenetic landscape” that shapes the deployment and robust regulation of gene networks during the construction and the remodeling of the brain is the microRNA system controlling both levels and translation of messenger RNA. Here we consider recent advances in the study of microRNA-mediated regulation of synaptic form and function. - By McNeil E & Vactor D van in Neuron 75(3), 9 August 2012

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Neuronal plasticity and antidepressant actions

Neuronal plasticity and antidepressant actions | Neuroscience_topics | Scoop.it

Antidepressant treatments enhance plasticity and increase neurogenesis in the adult brain, but it has been unclear how these effects influence mood. We propose that, like environmental enrichment and exercise, antidepressant treatments enhance adaptability by increasing structural variability within the nervous system at many levels, from proliferating precursors to immature synaptic contacts. Conversely, sensory deprivation and chronic stress reduce this structural variability. Activity-dependent competition within the mood-related circuits, guided by rehabilitation, then selects for the survival and stabilization of those structures that best represent the internal or external milieu. Increased variability together with competition-mediated selection facilitates normal function, such as pattern separation within the dentate gyrus and other mood-related circuits, thereby enhancing adaptability toward novel experiences. - by Castren E. & Hen R.Trends in Neurosciences04 February 2013

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Ion channels in genetic and acquired forms of epilepsy

Ion channels in genetic and acquired forms of epilepsy | Neuroscience_topics | Scoop.it
[Abstract] Genetic mutations causing dysfunction of both voltage- and ligand-gated ion channels make a major contribution to the cause of many different types of familial epilepsy. Key mechanisms comprise defective Na+ channels of inhibitory neurons or GABAA receptors affecting pre- or postsynaptic GABAergic inhibition, or a dysfunction of different types of channels at axon initial segments. Many of the mentioned ion channel mutations have been modelled in mice which has largely contributed to the understanding of where and how the ion channel defects lead to neuronal hyperexcitability. Defects of ion channel function are also associated with forms of acquired epilepsies. Animal models of febrile seizures or mesial temporal epilepsy have shown that dendritic K+ channels, hyperpolarization-activated cation channels and T-type Ca2+ channels play important roles in the generation of seizures. For the latter, it has been shown that suppression of their function by pharmacological mechanisms or in knock-out mice can antagonize epileptogenesis. Autoantibodies directed against ion channels or associated proteins, such as K+ channels, LGI1 or NMDA receptors, have been identified in epileptic disorders which are summarized under the term limbic encephalitis comprising limbic seizures, status epilepticus and psychiatric symptoms. We conclude that ion channels and associated proteins are important players for different types of genetic and acquired epilepsies. Nevertheless, the molecular bases for most common forms of epilepsy are not yet clear, and evidence to be discussed indicates just how much more we need to understand about the complex mechanisms that underlie epileptogenesis. - Lerche H et al., The Journal of Physiology, doi:
10.1113/jphysiol.2012.240606
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Sleep Oscillations in the Thalamocortical System Induce Long-Term Neuronal Plasticity

Sleep Oscillations in the Thalamocortical System Induce Long-Term Neuronal Plasticity | Neuroscience_topics | Scoop.it

Highlights

  • Slow-wave sleep induces long-term potentiation of evoked responses
  • In vitro, stimulation mimicking SWS replicated these results
  • Potentiation of responses was postsynaptic, Ca2+, AMPA, and NMDA dependent
  • The mechanism of potentiation was compatible with the classical LTP mechanism

Summary

Long-term plasticity contributes to memory formation and sleep plays a critical role in memory consolidation. However, it is unclear whether sleep slow oscillation by itself induces long-term plasticity that contributes to memory retention. Using in vivo prethalamic electrical stimulation at 1 Hz, which itself does not induce immediate potentiation of evoked responses, we investigated how the cortical evoked response was modulated by different states of vigilance. We found that somatosensory evoked potentials during wake were enhanced after a slow-wave sleep episode (with or without stimulation during sleep) as compared to a previous wake episode. In vitro, we determined that this enhancement has a postsynaptic mechanism that is calcium dependent, requires hyperpolarization periods (slow waves), and requires a coactivation of both AMPA and NMDA receptors. Our results suggest that long-term potentiation occurs during slow-wave sleep, supporting its contribution to memory.

Sylvain Chauvette, Josée Seigneur, Igor TimofeevNeuron, Volume 75, Issue 6, 1105-1113, 20 September 2012

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