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Lecture 10
Synaptic Plasticity. Simple Forms of Behavior and Underlying Mechanisms
Question | Answer |
---|---|
What is conceptual learning? | Learning in which animal (or human) is trained to classify objects. Emphasizes the kinds of things one is able to do with the information one has acquired. |
What is operant conditioning? | Conditioning that involves association of a response with a meaningful stimulus (reward or punishment). Also called trial and error training because the animal is free to try various responses before finding the one that is rewarded. |
What is classical conditioning? | Involves associating stimulus that evokes a response (unconditional stimulus) with a second (conditional) stimulus) that normally doesn’t evoke this response. The subject learns that one stimulus predicts another stimulus |
What molecular changes are implicated in imprinting? | c-fos gene expression up-regulation in GABAergic neuron, increase in the pool of releasable GABA, phosphorylation of AMPA receptors, postsynaptic density modifications, phosphorylation of NMDA receptors |
What is imprinting? | A very rapid learning that occurs during a short window after birth and establishes long-lasting behavioral responses to a specific object or individual |
What contributes to learning, memory and complex behaviors in mammals? | LTP in hippocampal synapses |
. What provides cellular substrate for long-term synaptic changes? | Dynamic changes in dendritic spines number/morphology |
What molecular attributes of long-term synaptic changes are associated with learned behavior? | Ca2+ signaling mechanisms, activation of CaMKII kinase and up-regulation of CREB |
What are the two phases of LTP? | Early phase that involves post-translation mechanisms, such as activation of protein kinases. A later phase that entails changes in gene expression and synthesis of new proteins |
What is the mechanism underlying LTP? | The NMDA channels open only if the postsynaptic cell is sufficiently depolarized. The Ca2+ ions that enter the cell through the channel activate postsynaptic protein kinases. These kinases may act postsynaptically to increase the sensitivity to glutamate. |
Why are NMDA & AMPA receptors important in LTP? | Intrinsic properties of NMDA receptors (voltage-dependent Mg2+ block, Ca2+ permeability) and activity-dependent insertion/internalization of AMPA receptors provide |
What does associativity contribute to LTP and learning? | Simultaneous stimulation of two pathways to one cell is causing LTP in both synaptic pathways (even if one of the pathways produces no LTP when solely stimulated. This property may be linked to associative learning (e.g. classical conditioning). |
What does specificity contribute to LTP and memory formation? | LTP induced by activation of one synapse doesn't occur in another (inactive) synapse. This property may be linked to a selective storage of information at synapses. |
What must be paired to cause LTP? | Presynaptic and postsynaptic stimulation |
What are the three properties of LTP? | Strong activity of presynaptic and postsynaptic neurons is required. Specificity and associativity. |
What is long-term depression (LTD)? | A form of plasticity that is associated with long-lasting decrease in synaptic strength. |
What is long-term potentiation (LTP)? | A form of synaptic plasticity that is associated with long-lasting increase in synaptic strength. |
What is long-term plasticity? | Caused by longer lasting sensitization due to presynaptic enhancement. This enhancement involves: prolonged PKA activation, CREB activation - persistent PKA activation, and regulation of other downstream genes - addition of synaptic terminals |
What is the mechanism of presynaptic enhancement underlying sensitization? | Serotonin GCPRS activation; cAMP-activation of PKA; proteins (K+ channels) phosphorylation; presynaptic Ca2+ increase; more vesicles are fused |
What is sensitization? | An increase in the response to a non-noxious stimulus when it follows noxious stimulus. Allows generalization of an aversive response elicited by a noxious stimulus to a variety of non-noxious stimuli. Presynaptic enhancement in glutamate release underli |
What is habituation? | Process that cause the animal to become less responsive to repeated occurrences of a stimulus. Happens when no reward or punishment follows the repeated stimulation. Underlined by synaptic depression in Aplysia due to reduced transmitter. |
What is synaptic potentiation (PTP)? | Increase in synaptic strength, form of synaptic plasticity that occurs on the time scale of tens of seconds , elicited by repeated synaptic activity, increases neurotransmitter released, observed after tetanic stimulation |
What is synaptic augmentation? | Increase in synaptic strength, form of synaptic plasticity that occurs on the time scale of few seconds (when extracellular Ca2+ is low), due to tetanic activity at the presynapse |
What is synaptic depression? | Decrease in synaptic strength caused by prolong elevation of presynaptic calcium concentration that, in turn, leads to depletion of ready-to-be released pool of synaptic vesicles |
What is synaptic facilitation? | Increase in synaptic strength cause by elevation of presynaptic calcium concentration that, in turn, facilitates vesicular transmitter release. Occurs when more than 1 AP arrives to the presynaptic terminal within < 50 milliseconds |
What kinds of short term plasticity are there? | Facilitation, depression, synaptic augmentation and synaptic potentiation (PTP) |
What does long term plasticity require? | Changes in gene expression, new protein synthesis and growth (or elimination) of new synapses |
What does short term plasticity involve? | Posttranslational modifications of existing proteins |
What two types of synaptic plasticity are there? | Short-term plasticity and long-term plasticity |
What is synaptic plasticity? | . Reorganization at synapse resulting in synaptic strength that can lead to changes in circuit function, and ultimately, to behavior plasticity. |