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https://www.readbyqxmd.com/read/29704282/amyloid-fibrils-induce-dysfunction-of-hippocampal-glutamatergic-silent-synapses
#1
Bihua Bie, Jiang Wu, Joseph F Foss, Mohamed Naguib
Silent glutamatergic synapses lacking functional AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate) receptors exist in several brain regions including the hippocampus. Their involvement in the dysfunction of hippocampal glutamatergic transmission in the setting of Alzheimer's disease (AD) is unknown. The present study demonstrated a decrease in the percentage of silent synapses in rats microinjected with amyloid fibrils (Aβ1-40 ) into the hippocampal CA1. Also, pairing low-frequency electric stimuli failed to induce activation of the hippocampal silent synapses in the modeled rats...
April 27, 2018: Hippocampus
https://www.readbyqxmd.com/read/29617653/removing-4e-bp-enables-synapses-to-refine-without-postsynaptic-activity
#2
Yumaine Chong, Natasha Saviuk, Brigitte Pie, Nathan Basisty, Ryan K Quinn, Birgit Schilling, Nahum Sonenberg, Ellis Cooper, A Pejmun Haghighi
Throughout the developing nervous system, considerable synaptic re-organization takes place as postsynaptic neurons extend dendrites and incoming axons refine their synapses, strengthening some and eliminating others. It is well accepted that these processes rely on synaptic activity; however, the mechanisms that lead to this developmental reorganization are not fully understood. Here, we explore the regulation of cap-dependent translation, a mechanism known to play a role in synaptic growth and plasticity...
April 3, 2018: Cell Reports
https://www.readbyqxmd.com/read/29603470/a-silent-eligibility-trace-enables-dopamine-dependent-synaptic-plasticity-for-reinforcement-learning-in-the-mouse-striatum
#3
Tomomi Shindou, Mayumi Shindou, Sakurako Watanabe, Jeffery Wickens
Dopamine-dependent synaptic plasticity is a candidate mechanism for reinforcement learning. A silent eligibility trace - initiated by synaptic activity and transformed into synaptic strengthening by later action of dopamine - has been hypothesized to explain the retroactive effect of dopamine in reinforcing past behaviour. We tested this hypothesis by measuring time-dependent modulation of synaptic plasticity by dopamine in adult mouse striatum, using whole-cell recordings. Presynaptic activity followed by postsynaptic action potentials (pre-post) caused spike-timing-dependent long-term depression in D1-expressing neurons, but not in D2 neurons, and not if postsynaptic activity followed presynaptic activity...
March 30, 2018: European Journal of Neuroscience
https://www.readbyqxmd.com/read/29244810/synaptic-augmentation-in-a-cortical-circuit-model-reproduces-serial-dependence-in-visual-working-memory
#4
Daniel P Bliss, Mark D'Esposito
Recent work has established that visual working memory is subject to serial dependence: current information in memory blends with that from the recent past as a function of their similarity. This tuned temporal smoothing likely promotes the stability of memory in the face of noise and occlusion. Serial dependence accumulates over several seconds in memory and deteriorates with increased separation between trials. While this phenomenon has been extensively characterized in behavior, its neural mechanism is unknown...
2017: PloS One
https://www.readbyqxmd.com/read/29224722/nrap-1-is-a-presynaptically-released-nmda-receptor-auxiliary-protein-that-modifies-synaptic-strength
#5
Ning Lei, Jerry E Mellem, Penelope J Brockie, David M Madsen, Andres V Maricq
NMDA receptors (NMDARs) are a subtype of postsynaptic ionotropic glutamate receptors that function as molecular coincidence detectors, have critical roles in models of learning, and are associated with a variety of neurological and psychiatric disorders. To date, no auxiliary proteins that modify NMDARs have been identified. Here, we report the identification of NRAP-1, an auxiliary protein in C. elegans that modulates NMDAR function. NMDAR-mediated currents were eliminated in nrap-1 mutants, as was NMDA-dependent behavior...
December 20, 2017: Neuron
https://www.readbyqxmd.com/read/29169997/psd95-a-synaptic-protein-implicated-in-schizophrenia-or-autism
#6
REVIEW
Austin A Coley, Wen-Jun Gao
The molecular components of the postsynaptic density (PSD) in excitatory synapses of the brain are currently being investigated as one of the major etiologies of neurodevelopmental disorders such as schizophrenia (SCZ) and autism. Postsynaptic density protein-95 (PSD-95) is a major regulator of synaptic maturation by interacting, stabilizing and trafficking N-methyl-d-aspartic acid receptors (NMDARs) and α-amino-3-hydroxy-5-methyl-4-isox-azoleproprionic acid receptors (AMPARs) to the postsynaptic membrane...
March 2, 2018: Progress in Neuro-psychopharmacology & Biological Psychiatry
https://www.readbyqxmd.com/read/29107522/-silent-nmda-synapses-enhance-motion-sensitivity-in-a-mature-retinal-circuit
#7
Santhosh Sethuramanujam, Xiaoyang Yao, Geoff deRosenroll, Kevin L Briggman, Greg D Field, Gautam B Awatramani
Retinal direction-selective ganglion cells (DSGCs) have the remarkable ability to encode motion over a wide range of contrasts, relying on well-coordinated excitation and inhibition (E/I). E/I is orchestrated by a diverse set of glutamatergic bipolar cells that drive DSGCs directly, as well as indirectly through feedforward GABAergic/cholinergic signals mediated by starburst amacrine cells. Determining how direction-selective responses are generated across varied stimulus conditions requires understanding how glutamate, acetylcholine, and GABA signals are precisely coordinated...
December 6, 2017: Neuron
https://www.readbyqxmd.com/read/29091767/metaplasticity-at-ca1-synapses-by-homeostatic-control-of-presynaptic-release-dynamics
#8
Cary Soares, Kevin F H Lee, Jean-Claude Béïque
Hebbian and homeostatic forms of plasticity operate on different timescales to regulate synaptic strength. The degree of mechanistic overlap between these processes and their mutual influence are still incompletely understood. Here, we report that homeostatic synaptic strengthening induced by prolonged network inactivity compromised the ability of CA1 synapses to exhibit LTP. This effect could not be accounted for by an obvious deficit in the postsynaptic capacity for LTP expression, since neither the fraction of silent synapses nor the ability to induce LTP by two-photon glutamate uncaging were reduced by the homeostatic process...
October 31, 2017: Cell Reports
https://www.readbyqxmd.com/read/29076975/acute-spinal-cord-injury-diminishes-silent-synapses-in-the-rat-hippocampus
#9
Yingli Jing, Fan Bai, Hui Chen, Hao Dong
Spinal cord injury (SCI) can promote profound functional modification in various brain centers. However, the question of whether SCI can affect the generation of silent synapses that regulate neuronal plasticity in the hippocampus remains unclear. In the present studies, we demonstrated that acute SCI diminished silent synapses in hippocampus of lesioned rats. Furthermore, the SCI induced decline in silent synapses appeared to require the activation of NR2B-containing N-methyl-D-aspartate receptors. Our data show that SCI impaired synaptic plasticity in the hippocampus, suggesting that this region may serve as a potential therapeutic target for meliorating impaired brain functions after SCI...
December 6, 2017: Neuroreport
https://www.readbyqxmd.com/read/29030051/determinants-of-axon-growth-plasticity-and-regeneration-in-the-context-of-spinal-cord-injury
#10
REVIEW
Angela R Filous, Jan M Schwab
The mechanisms that underlie recovery after injury of the central nervous system have rarely been definitively established. Axon regrowth remains the major prerequisite for plasticity, regeneration, circuit formation, and eventually functional recovery. The attributed functional relevance of axon regrowth, however, will depend on several subsequent conditional neurobiological modifications, including myelination and synapse formation, but also pruning of aberrant connectivity. Despite the ability to revamp axon outgrowth by altering an increasing number of extracellular and intracellular targets, disentangling which axons are responsible for the recovery of function from those that are functionally silent, or even contributing to aberrant functions, represents a pertinent void in our understanding, challenging the intuitive translational link between anatomical and functional regeneration...
January 2018: American Journal of Pathology
https://www.readbyqxmd.com/read/29026183/developmental-emergence-of-sparse-coding-a-dynamic-systems-approach
#11
Vahid Rahmati, Knut Kirmse, Knut Holthoff, Lars Schwabe, Stefan J Kiebel
During neocortical development, network activity undergoes a dramatic transition from largely synchronized, so-called cluster activity, to a relatively sparse pattern around the time of eye-opening in rodents. Biophysical mechanisms underlying this sparsification phenomenon remain poorly understood. Here, we present a dynamic systems modeling study of a developing neural network that provides the first mechanistic insights into sparsification. We find that the rest state of immature networks is strongly affected by the dynamics of a transient, unstable state hidden in their firing activities, allowing these networks to either be silent or generate large cluster activity...
October 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28979189/uncorrelated-neural-firing-in-mouse-visual-cortex-during-spontaneous-retinal-waves
#12
Matthew T Colonnese, Jing Shen, Yasunobu Murata
Synchronous firing among the elements of forming circuits is critical for stabilization of synapses. Understanding the nature of these local network interactions during development can inform models of circuit formation. Within cortex, spontaneous activity changes throughout development. Unlike the adult, early spontaneous activity occurs in discontinuous population bursts separated by long silent periods, suggesting a high degree of local synchrony. However, whether the micro-patterning of activity within early bursts is unique to this early age and specifically tuned for early development is poorly understood, particularly within the column...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28890050/modulation-of-hippocampal-synapse-maturation-by-activity-regulated-e3-ligase-via-non-canonical-pathway
#13
Pushpa Kumari, Balakumar Srinivasan, Sourav Banerjee
Development of functional synapses is crucial for the transmission and storage of information in the brain. Post establishment of the initial synaptic contact, synapses are stabilized through neuronal activity-induced signals. Emerging studies have implicated ubiquitination; a reversible posttranslational modification, as a key regulatory switch that modulates synapse development through proteasomal degradation. Ubiquitination of proteins is precisely regulated by E3 ligases, a set of enzymes that bind to specific substrates to facilitate the conjugation of monomeric or polymeric ubiquitin...
November 19, 2017: Neuroscience
https://www.readbyqxmd.com/read/28826488/silent-synapses-generate-sparse-and-orthogonal-action-potential-firing-in-adult-born-hippocampal-granule-cells
#14
Liyi Li, Sébastien Sultan, Stefanie Heigele, Charlotte Schmidt-Salzmann, Nicolas Toni, Josef Bischofberger
In adult neurogenesis young neurons connect to the existing network via formation of thousands of new synapses. At early developmental stages, glutamatergic synapses are sparse, immature and functionally 'silent', expressing mainly NMDA receptors. Here we show in 2- to 3-week-old young neurons of adult mice, that brief-burst activity in glutamatergic fibers is sufficient to induce postsynaptic AP firing in the absence of AMPA receptors. The enhanced excitability of the young neurons lead to efficient temporal summation of small NMDA currents, dynamic unblocking of silent synapses and NMDA-receptor-dependent AP firing...
August 8, 2017: ELife
https://www.readbyqxmd.com/read/28746826/electrophysiological-properties-of-neurons-and-synapses-in-the-lateral-habenular-complex-lhb
#15
REVIEW
Franziska Wagner, Torsten Weiss, Rüdiger W Veh
Animal including human behavior is highly sophisticated. Besides reflective actions it is largely based on the desire for magnificent internal feelings, which are provided by the reward system. Its counterpart an "anti-reward" system is mainly composed of the lateral habenular complex (LHb) and its extensive interconnections with the monoaminergic cell groups in the mid- and hindbrain. The present review focuses on the neuronal composition and the internal signaling in the LHb. Morphologically six distinct types of neurons (spherical, fusiform-1, fusiform-2, polymorphic, vertical, neurogliaform) can be identified...
November 2017: Pharmacology, Biochemistry, and Behavior
https://www.readbyqxmd.com/read/28658619/peripheral-sensory-deprivation-restores-critical-period-like-plasticity-to-adult-somatosensory-thalamocortical-inputs
#16
Seungsoo Chung, Ji-Hyun Jeong, Sukjin Ko, Xin Yu, Young-Hwan Kim, John T R Isaac, Alan P Koretsky
Recent work has shown that thalamocortical (TC) inputs can be plastic after the developmental critical period has closed, but the mechanism that enables re-establishment of plasticity is unclear. Here, we find that long-term potentiation (LTP) at TC inputs is transiently restored in spared barrel cortex following either a unilateral infra-orbital nerve (ION) lesion, unilateral whisker trimming, or unilateral ablation of the rodent barrel cortex. Restoration of LTP is associated with increased potency at TC input and reactivates anatomical map plasticity induced by whisker follicle ablation...
June 27, 2017: Cell Reports
https://www.readbyqxmd.com/read/28604739/autism-like-behaviours-and-enhanced-memory-formation-and-synaptic-plasticity-in-lrfn2-salm1-deficient-mice
#17
Naoko Morimura, Hiroki Yasuda, Kazuhiko Yamaguchi, Kei-Ichi Katayama, Minoru Hatayama, Naoko H Tomioka, Maya Odagawa, Akiko Kamiya, Yoshimi Iwayama, Motoko Maekawa, Kazuhiko Nakamura, Hideo Matsuzaki, Masatsugu Tsujii, Kazuyuki Yamada, Takeo Yoshikawa, Jun Aruga
Lrfn2/SALM1 is a PSD-95-interacting synapse adhesion molecule, and human LRFN2 is associated with learning disabilities. However its role in higher brain function and underlying mechanisms remain unknown. Here, we show that Lrfn2 knockout mice exhibit autism-like behavioural abnormalities, including social withdrawal, decreased vocal communications, increased stereotyped activities and prepulse inhibition deficits, together with enhanced learning and memory. In the hippocampus, the levels of synaptic PSD-95 and GluA1 are decreased...
June 12, 2017: Nature Communications
https://www.readbyqxmd.com/read/28462940/chronic-nicotine-alters-corticostriatal-plasticity-in-the-striatopallidal-pathway-mediated-by-nr2b-containing-silent-synapses
#18
Jianxun Xia, Allison M Meyers, Jeff A Beeler
Smoking is the leading cause of preventable death in the United States and success rates for quitting remain low. High relapse rates are attributed to pervasive nicotine-reinforced associative learning of incentive cues that is highly resistant to extinction. Why such learning is so persistent is poorly understood but may arise as a consequence of neuroadaptations in synaptic plasticity induced by chronic nicotine. We used whole-cell patch clamp recording to investigate the effect of chronic nicotine (cNIC) on synaptic plasticity in dopamine D2 receptor-expressing medium-spiny neurons in the indirect, striatopallidal pathway in dorsolateral striatum...
November 2017: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/28445587/cb1-receptors-down-regulate-a-camp-epac2-plc-pathway-to-silence-the-nerve-terminals-of-cerebellar-granule-cells
#19
Beatris Alonso, David Bartolomé-Martín, José Javier Ferrero, Jorge Ramírez-Franco, Magdalena Torres, José Sánchez-Prieto
Cannabinoid receptors mediate short-term retrograde inhibition of neurotransmitter release, as well as long-term depression of synaptic transmission at excitatory synapses. The responses of individual nerve terminals in VGLUT1-pHluorin transfected cerebellar granule cells to cannabinoids have shown that prolonged activation of cannabinoid type 1 receptors (CB1Rs) silences a subpopulation of previously active synaptic boutons. Adopting a combined pharmacological and genetic approach to study the molecular mechanisms of CB1R-induced silencing, we found that adenylyl cyclase inhibition decreases cAMP levels while it increases the number of silent synaptic boutons and occludes the induction of further silencing by the cannabinoid agonist HU-210...
August 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28424166/applying-fluid-biomarkers-to-alzheimer-s-disease
#20
REVIEW
Henrik Zetterberg
Alzheimer's disease (AD) is a common neurodegenerative disease that starts with a clinically silent phase of a decade or more during which brain pathologies accumulate predominantly in the medial temporal lobe but also elsewhere in the brain. Network dysfunction and clinical symptoms typically appear when senile plaque (amyloid-β) and neurofibrillary tangle (tau) pathologies meet in the brain parenchyma, producing synapse and neuronal loss. For plaque and tangle pathologies, reliable fluid biomarkers have been developed...
July 1, 2017: American Journal of Physiology. Cell Physiology
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