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Molecular anatomical investigation of the 2
Molecular anatomical investigation of the 2

... translates the extent of anterograde transmission into a retrograde feedback signal. Excess presynaptic activity activates perisynaptic metabotropic glutamate receptors, which then leads to 2-AG production. The retrograde signal attenuates futher presynaptic transmitter release as a synaptic circuit ...
Human Vision: Electrophysiology and Psychophysics
Human Vision: Electrophysiology and Psychophysics

... used to solve problems in fields as diverse as • pattern recognition • optimisation • locomotion and spatial recognition • sequence prediction ...
Pathophysiology of Epilepsy
Pathophysiology of Epilepsy

... – Ionotropic: fast synaptic transmission. NMDA, AMPA, kinate. Gated Ca and Na channels – Metabotropic: slow synaptic transmission. Modulation of second messengers, e.g. Inositol, cAMP ...
MMNeuropharm2011
MMNeuropharm2011

... exposure. At baseline, all AMPARs contain GluA2 while after the cocaine treatment some synapses express GluA2-lacking AMPARs. Further investigations indicate that this AMPAR redistribution depends on PICK1, a trafficking protein specifically interacting with GluA2 (Bellone and Lüscher, 2006). Moreover ...
Powerpoint version
Powerpoint version

... Signal at the synapse excites or inhibits the postsynaptic neuron Excitatory synapse:  Causes an influx of Na+ into postsynaptic neuron.  This produces an EPSP and depolarizes the neuron. ...
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Nervous system and neurons

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Stochastic Modeling the Tripartite Synapse and Applications
Stochastic Modeling the Tripartite Synapse and Applications

... stochastic spiking model [1] accounts for the firing randomness, while a sequence of signal amplifiers model the nodes of Ranvier found in a myelinated axon. The inter-neuronal communication unit represents the pre-synaptic calcium gateway (CaG), the neurotransmitter diffusion in the synaptic cleft ...
Full-Text PDF
Full-Text PDF

... D-serine in regulating NMDAR function in vivo [22,23]. Recent evidence suggests that whether particular NMDARs utilize glycine or D-serine may be dependent on the type of synapse examined [24] or the localization of the receptors [25]. Both D-serine and glycine are already found in the CNS at birth ...
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초록리스트

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Molecular heterogeneity of central synapses: afferent and target
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Synaptic plasticity: taming the beast
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Ch 25 - Molecular Mechanisms of Learning and Memory
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seminario - Instituto Cajal
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Neurotransmitters - Shifa College of Medicine
Neurotransmitters - Shifa College of Medicine

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... features including symptoms of disrupted colonic motility and visceral pain. To better understand and treat these conditions, it is necessary to elucidate the neural mechanisms responsible for altered gut functions and to develop targeted therapeutic strategies. The objectives of my dissertation stu ...
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Long-term depression

Long-term depression (LTD), in neurophysiology, is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress. LTD in the hippocampus and cerebellum have been the best characterized, but there are other brain areas in which mechanisms of LTD are understood. LTD has also been found to occur in different types of neurons that release various neurotransmitters, however, the most common neurotransmitter involved in LTD is L-glutamate. L-glutamate acts on the N-methyl-D- asparate receptors (NMDARs), α-amino-3-hydroxy-5-methylisoxazole-4-propionicacid receptors (AMPARs), kainate receptors (KARs) and metabotropic glutamate receptors (mGluRs) during LTD. It can result from strong synaptic stimulation (as occurs in the cerebellar Purkinje cells) or from persistent weak synaptic stimulation (as in the hippocampus). Long-term potentiation (LTP) is the opposing process to LTD; it is the long-lasting increase of synaptic strength. In conjunction, LTD and LTP are factors affecting neuronal synaptic plasticity. LTD is thought to result mainly from a decrease in postsynaptic receptor density, although a decrease in presynaptic neurotransmitter release may also play a role. Cerebellar LTD has been hypothesized to be important for motor learning. However, it is likely that other plasticity mechanisms play a role as well. Hippocampal LTD may be important for the clearing of old memory traces. Hippocampal/cortical LTD can be dependent on NMDA receptors, metabotropic glutamate receptors (mGluR), or endocannabinoids. The result of the underlying-LTD molecular mechanism is the phosphorylation of AMPA glutamate receptors and their elimination from the surface of the parallel fiber-Purkinje cell (PF-PC) synapse.LTD is one of several processes that serves to selectively weaken specific synapses in order to make constructive use of synaptic strengthening caused by LTP. This is necessary because, if allowed to continue increasing in strength, synapses would ultimately reach a ceiling level of efficiency, which would inhibit the encoding of new information.
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