This document discusses neuronal plasticity, which refers to the brain's ability to change and adapt as a result of experience. It describes various types and mechanisms of neuroplasticity, including enhancement of existing connections through synapse development and strengthening, and formation of new connections through unmasking of silent synapses and axon sprouting. It also discusses cortical remapping in deaf individuals and long-term potentiation as the basis of neuronal plasticity. Synaptic plasticity can be measured in the hippocampus, where strong stimulation leads to calcium influx and activation of protein kinases that strengthen synapses.
2. What is neuronal plasticity? Plasticity is the quality of being ‘plastic’ or formative. Neuronal plasticity refers to the ability of the brain to change and adapt itself as a result of one’s experience.
3. Applications of Neuronal Plasticity ‘Learning new things’ ‘Making new memories’ ‘Rewiring circuits’
5. The NS is a series of connections Birth = 100 billion neurons 6 year old has twice as many synapses as an adult By late adolescence, synapses begin to disappear http://www.eng.yale.edu/synapses.htm
6. Types of Neuroplasticity TypeMechanismDuration 1. Enhancement of existing connections Synapse development Physiological ms-1 to hours Synapse strengthening Biochemical hours to days 2. Formation of new connections Unmasking Physiological minutes to days Sprouting Structural days to months 3. Formation of new cells Self-replication stem cell variable
7. Enhancement of existing connections Increased use of a synapse in existing pathways e.g. learning a new task Or alternative pathways following damage Cortical re-mapping (phantom limb)
11. Formation of new connections Unmasking of pre-existing pathways Sprouting of new pathways
12. Unmasking of silent synapses Possible reasons why some synapses could be ‘silent’ On distal dendrites Inhibited by dominant pathways Too little transmitter Too few receptors Don’t fire with other inputs
13. Unmasking – inhibition of subservient pathway by dominant pathway Parallel pathway; neurons with a comparable role Subservient pathway Dominant pathway + +
14. Unmasking Lesion to dominant pathway Subservient pathway is unmasked + + Activity is continued despite lesion
18. Sprouting Injury results in cell death Cell is re-innervated from alternative stimulus Sprouting may be a means of recovery; it may also produce unwanted effects
19. Neurogenesis Replacing dying or damaged neural cells with new ones New cells originate from stem cells Introduced stem cells are stimulated to produce neural cells by nerve growth factors (NGF) Stem cell /www.stanford.edu/group/hopes/rltdsci/nplast
26. From The Organization of Behavior by Donald Hebb, 1949: "When one cell repeatedly assists in firing another, the axon of the first cell develops synaptic knobs (or enlarges them if they already exist) in contact with the soma of the second cell." Hebb postulated that this behavior of synapses in neuronal networks would permit the networks to store memories.
28. Long Term Potentiation In neuroscience, long-term potentiation (LTP) is a long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously.
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30. Hippocampus Function: • Consolidation of New Memories • Emotions • Navigation • Spatial Orientation
31. Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits The post-synaptic region has both NMDA and AMPA receptors. Glutamate first activates AMPA receptors. NMDA receptors do not respond until enough AMPA receptors are stimulated and the neuron is partially depolarized.
32. Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits NMDA receptors at rest have a magnesium ion (Mg2+) block on their calcium (Ca2+) channels. After partial depolarization, the block is removed and the NMDA receptor allows Ca2+ to enter in response to glutamate.
33. Figure 17.22 Roles of NMDA and AMPA Receptors in the Induction of LTP in CA1 Region (Part 1)
34. Figure 17.22 Roles of NMDA and AMPA Receptors in the Induction of LTP in CA1 Region (Part 2)
35. Figure 17.22 Roles of NMDA and AMPA Receptors in the Induction of LTP in CA1 Region (Part 3)
36. Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits The large Ca2+ influx activates certain protein kinases – enzymes that add phosphate groups to protein molecules. One protein kinase is CaMKII – it affects AMPA receptors in several ways: Causes more AMPA receptors to be produced and inserted in the postsynaptic membrane.
37. Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits CaMKII : Moves existing nearby AMPA receptors into the active synapse. Increases conductance of Na+ and K+ ions in membrane-bound receptors. These effects all increase the synaptic sensitivity to glutamate. The activated protein kinases also trigger protein synthesis
38. Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits Strong stimulation of a postsynaptic cell releases a retrograde messenger that travels across the synapse and alters function in the presynaptic neuron. More glutamate is released and the synapse is strengthened.
39. Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits Somatic intervention experiments – pharmacological treatments that block LTP impair learning. Behavioral intervention experiments – show that training an animal in a memory task can induce LTP.
LTP can be induced either by strong tetanic stimulation of a single pathway to a synapse, or cooperatively via the weaker stimulation of many. When one pathway into a synapse is stimulated weakly, it produces insufficient postsynaptic depolarization to induce LTP. In contrast, when weak stimuli are applied to many pathways that converge on a single patch of postsynaptic membrane, the individual postsynaptic depolarizations generated may collectively depolarize the postsynaptic cell enough to induce LTP cooperatively.