Control of GABA Release at Mossy Fiber-CA3 Connections in the Developing Hippocampus.
Victoria F. Safiulina,Maddalena D. Caiati,Sudhir Sivakumaran,Giacomo Bisson,Michele Migliore,Enrico Cherubini +5 more
TLDR
Combining calcium transients associated with network-driven giant depolarizing potentials or GDPs generated by the synergistic action of glutamate and GABA with MF activation increased the probability of GABA release and caused the conversion of silent synapses into conductive ones suggesting that GDPs act as coincident detector signals for enhancing synaptic efficacy.Abstract:
In this review some of the recent work carried out in our laboratory concerning the functional role of GABAergic signalling at immature mossy fibres (MF)-CA3 principal cell synapses has been highlighted. While in adulthood MF, the axons of dentate gyrus granule cells release onto CA3 principal cells and interneurons glutamate, early in postnatal life they release GABA, which exerts into targeted cells a depolarizing and excitatory action. We found that GABAA-mediated postsynaptic currents (MF-GPSCs) exhibited a very low probability of release, were sensitive to L-AP4, a group III metabotropic glutamate receptor agonist, and revealed short-term frequency-dependent facilitation. Moreover, MF-GPSCs were down regulated by presynaptic GABAB and kainate receptors, activated by spillover of GABA from MF terminals and by glutamate present in the extracellular medium, respectively. Activation of these receptors contributed to the low release probability and in some cases to synapses silencing. By pairing calcium transients, associated with network-driven giant depolarizing potentials or GDPs (a hallmark of developmental networks thought to represent a primordial form of synchrony between neurons), generated by the synergistic action of glutamate and GABA with MF activation increased the probability of GABA release and caused the conversion of silent synapses into conductive ones suggesting that GDPs act as coincident detector signals for enhancing synaptic efficacy. Finally, to compare the relative strength of CA3 pyramidal cell output in relation to their MF glutamatergic or GABAergic inputs in adulthood or in postnatal development, respectively, a realistic model was constructed taking into account different biophysical properties of these synapses.read more
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Harnessing neuroplasticity for clinical applications
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TL;DR: Integration of information across disciplines should enhance opportunities for the translation of neuroplasticity and circuit retraining research into effective clinical therapies.
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13 reasons why the brain is susceptible to oxidative stress.
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TMS and drugs revisited 2014
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TL;DR: This up-dated review will highlight important knowledge and recent advances in the contribution of pharmaco-TMS-EMG and pharmacological characterization of the TMS-evoked EEG potentials to understanding of normal and dysfunctional excitability, connectivity and plasticity of the human brain.
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An integrative model of tinnitus based on a central gain controlling neural sensitivity.
TL;DR: A model highlighting the putative connections between hearing loss and the phantom perception of tinnitus is proposed, suggesting that central hyperactivity in the central auditory system could result from a central gain increase.
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Cerebral plasticity: Windows of opportunity in the developing brain.
TL;DR: It is proposed that critical and sensitive periods of brain development in health and disease can create "windows of opportunity" for neuromodulatory interventions that are not commonly seen in adult brain and probably augment plasticity responses and improve clinical outcomes.
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