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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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Learning and reconsolidation implicate different synaptic mechanisms

Learning and reconsolidation implicate different synaptic mechanisms | Neuroscience_topics | Scoop.it

Synaptic mechanisms underlying memory reconsolidation after retrieval are largely unknown. Here we report that synapses in projections to the lateral nucleus of the amygdala implicated in auditory fear conditioning, which are potentiated by learning, enter a labile state after memory reactivation, and must be restabilized through a postsynaptic mechanism implicating the mammalian target of rapamycin kinase-dependent signaling. Fear-conditioning–induced synaptic enhancements were primarily presynaptic in origin. Reconsolidation blockade with rapamycin, inhibiting mammalian target of rapamycin kinase activity, suppressed synaptic potentiation in slices from fear-conditioned rats. Surprisingly, this reduction of synaptic efficacy was mediated by post- but not presynaptic mechanisms. These findings suggest that different plasticity rules may apply to the processes underlying the acquisition of original fear memory and postreactivational stabilization of fear-conditioning–induced synaptic enhancements mediating fear memory reconsolidation. - by Li Y. et al., PNASvol. 110 no. 12, 47984803


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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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Brain mapping reveals neurological basis of decision-making in rats

Brain mapping reveals neurological basis of decision-making in rats | Neuroscience_topics | Scoop.it

Scientists at UC San Francisco have discovered how memory recall is linked to decision-making in rats, showing that measurable activity in one part of the brain occurs when rats in a maze are playing out memories that help them decide which way to turn. The more they play out these memories, the more likely they are to find their way correctly to the end of the maze. (...) - by UCSF, ScienceBlog

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Metabotropic NMDA receptor function is required for NMDA receptor-dependent long-term depression

NMDA receptor (NMDAR) activation controls long-term potentiation (LTP) as well as long-term depression (LTD) of synaptic transmission, cellular models of learning and memory. A long-standing view proposes that a high level of Ca2+ entry through NMDARs triggers LTP; lower Ca2+ entry triggers LTD. Here we show that ligand binding to NMDARs is sufficient to induce LTD; neither ion flow through NMDARs nor Ca2+ rise is required. However, basal levels of Ca2+ are permissively required. Lowering, but not maintaining, basal Ca2+levels with Ca2+ chelators blocks LTD and drives strong synaptic potentiation, indicating that basal Ca2+levels control NMDAR-dependent LTD and basal synaptic transmission. Our findings indicate that metabotropic actions of NMDARs can weaken active synapses without raising postsynaptic calcium, thereby revising and expanding the mechanisms controlling synaptic plasticity. (...) - by Nabavi S. et al.PNAS 2013 110 (10) 4027-4032

Julien Hering, PhD's insight:

A great article from R. Malinov's team about fine mechanisms controlling synaptic plasticity through levels of calcium 

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