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מצגת של PowerPoint
מצגת של PowerPoint

...  Consistent with these findings, responses to both eyes were up-regulated after BD. ...
The neuron Label the following terms: Soma Axon terminal Axon
The neuron Label the following terms: Soma Axon terminal Axon

... 10. Action  Potential     11. Myelin  Sheath  (Myelin)     12. Afferent  Neuron     13. Threshold     14.  Neurotransmitter     15. Efferent  Neurons   16. Axon  Terminal     17. Stimulus   18. Refractory  Period     19. Schwann     20. Nodes  o ...
Effects of the Metabotropic Glutamate Receptor Antagonist MCPG
Effects of the Metabotropic Glutamate Receptor Antagonist MCPG

... consequence of PI turnover is the generation of two second messengers, diacylglycerol and phosphatidylinositol trisphosphate, leading in turn to activation of protein kinase C and the release of intracellular calcium stores (Berridge, 1984). Thus, it has been suggested that differences in the patter ...
see p. A4b - Viktor`s Notes for the Neurosurgery Resident
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... NEUROTRANSMITTER – endogenous chemical agent that relays information from one neuron to another through synapse; released by presynaptic cell (upon excitation), crosses synapse to stimulate or inhibit* postsynaptic cell by binding to receptor. *final result (hyperpolarization or depolarization) is d ...
Development of glutamatergic and GABAergic synapses
Development of glutamatergic and GABAergic synapses

... L1 immunoglobulin family, along the PC soma-AIS axis, and such gradient requires ankyrinG, a membrane adaptor protein that recruits neurofascin (Ango et al. 2004). Interestingly, another member of the same family of adhesion molecules, CHL1, is localized along Bergmann glia fibers and stellate cells ...
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... React to stimuli in the external environment Usually found close to the body surface Example: receptors in the skin, vision apparatus of the eye, receptors in the ear Interoceptors (visceroceptors): respond to stimuli within the body Are found in the internal organs Include stretch receptors (found ...
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... Agrin is release by the presynaptic terminal and activates a receptor complex that includes MuSK At the intracellular side of the postsynaptic membrane, rapsyn is required for agrin-mediated clustering ...
I joined the Smith lab in the spring of 2000, as a
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... • First need to bring the presynaptic neuron to threshold at axon hillock. • Conduction down axon, length, R*C dependent. • Opening of voltage gated Ca channels. • Diffusion and action of Ca at release machinery. • Exocytosis and diffusion of transmitter in cleft. • Activation of postsynaptic recept ...
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... open, allowing calcium to enter the cell. This leads to the release of the neurotransmitters from the terminal into the synaptic cleft (space between the presynaptic and postsynaptic neuron). 5. Neurotransmitters, once released into the synaptic cleft, attach to receptors and alter activity of the p ...
Synaptic plasticity: taming the beast
Synaptic plasticity: taming the beast

... It has long been known that presynaptic activity that precedes postsynaptic firing or depolarization can induce LTP, whereas reversing this temporal order causes LTD11-13. Recent experimental results have expanded our knowledge of the effects of spike timing on LTP and LTD induction14-21. Although t ...
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... Information about the external world is conveyed through the nervous system via specialized sensory organs such as the vomeronasal organ (VNO). The VNO is crucial for pheromone detection and the regulation of social behavior in many mammals. Recent research has shown that purinergic signaling pathwa ...
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... but in STDP low-frequency stimulation can be used to induce both LTP and LTD. While in both types of protocols activation of N-methyl-D-aspartate (NMDA) subtype of glutamate receptors (NMDARs) (e.g., Refs. 13, 24, 65, 67, 119) and elevation of postsynaptic Ca2" level are required, the effectiveness ...
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... Gas exchange can now take place more quickly meaning exercise can be maintained at a higher intensity for longer. 20 of 28 ...
Spike Timing-Dependent Plasticity: From Synapse to Perception
Spike Timing-Dependent Plasticity: From Synapse to Perception

... but in STDP low-frequency stimulation can be used to induce both LTP and LTD. While in both types of protocols activation of N-methyl-D-aspartate (NMDA) subtype of glutamate receptors (NMDARs) (e.g., Refs. 13, 24, 65, 67, 119) and elevation of postsynaptic Ca2⫹ level are required, the effectiveness ...
Ramón y Cajal, 19 th century
Ramón y Cajal, 19 th century

... Neuronal activity changes the intracellular calcium. Via changes in intra-cellular calcium, neurons change their morphology with respect to their axonal and dendritic shape. This leads to changes in neuronal connectivity which, in turn, adapts neuronal activity. The goal is that by these changes neu ...
Neurons and how they communicate
Neurons and how they communicate

... Neurons influence each other through the release of neurotransmitters – chemical substances that carry signals across the synaptic cleft When the action potential reaches the end of the axon at its terminal button the neurotransmitters are released to travel across the synaptic cleft ...
< 1 ... 22 23 24 25 26 27 28 29 30 ... 41 >

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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