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Previous lecture
Previous lecture

... Magee & Johnston, J Physiol (1995) ...
Synaptic Transmission
Synaptic Transmission

... message and can be inhibitory. When they bind to the post-synaptic neuron, they let potassium out instead of sodium in, which makes the neuron even more negative! ...
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Neuroscience in PT: Introduction and Review
Neuroscience in PT: Introduction and Review

... of presynaptic facilitation and inhibition? • Describe the structure of a chemical synapse and the events of signal transmission at the synapse. • Compare and contrast neurotransmitters versus neuromodulators. • Discuss the functions of neurotransmitters and the associated clinical implications. ...
doc Nerve and synapses
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1 Introduction to Neurobiology Rudolf Cardinal NST 1B
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overview of neural f..
overview of neural f..

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Ca 2+
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Brainsignals, Synaptic Transmission and Short
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Molecular basis of learning in the hippocampus and the amygdala

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... On the postsynaptic side, neurotransmitter binds to a receptor (9). Ionotropic receptors open an ion channel (10) for some ion, allowing a current to flow. The effect of the synapse depends on which ion the channel conducts. Metabotropic receptors are coupled to G-proteins and/or kinases which prod ...
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... AMPA: a-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate NMDA: N-methyl-D-aspartate Kainate: Kainic acid ...
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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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