Synaptic plasticity

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21 Terms

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Early theories of cellular mechanisms of memory

  • Santiago Ramon y Cajal - neuron doctrine 1894 → memories might be formed by strengthening if connections between neurons

  • Donald Herb: the organisation of behaviour 1949 (book)

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Hebb’s law

→ when an axo of cell A is near enough to excite cell B, and repeatedly fires it, some growth processes/metabolic change takes place in one/both cells so cell A’s efficiency to fire B is increased

  • ‘neurons that fire together wire together’

<p>→ when an axo of cell A is near enough to excite cell B, and repeatedly fires it, some growth processes/metabolic change takes place in one/both cells so cell A’s efficiency to fire B is increased</p><ul><li><p>‘neurons that fire together wire together’ </p></li></ul><p></p>
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Synaptic plasticity

→ change in strength of synaptic communication

  • the strength of synaptic communication between two neurons is not fixed

  • Short and long term potentiation exists = brain processes that temporarily or permanently alter synaptic strength

<p>→ change in strength of synaptic communication </p><ul><li><p>the strength of synaptic communication between two neurons is not fixed </p></li><li><p>Short and long term potentiation exists = brain processes that temporarily or permanently alter synaptic strength</p></li></ul><p></p>
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Who were Bliss and Lomo?

  • First description of long term potentiation (LTP) of synaptic strength in 1973

  • Recorded fEPSPs (field excitatory postsynaptic potentials) in the performance pathway of anaesthetised rabbits

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What is LTP

Persistent strengthening of synapses based on patterns of recent activity

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What did Bliss and Lomo do in their study?

  1. Low frequency baseline stimulation→ stimulate the performant pathway and record fEPSP amplitude

  2. High frequency conditioning stimulus→ continue to measure fEPSP, shows an increase in amplitude of synaptic response, remains increased overtime

  3. Low frequency stimulation again→ after conditioning, the response is larger, follows Hebb’s law

<ol><li><p>Low frequency baseline stimulation→ stimulate the performant pathway and record fEPSP amplitude</p></li><li><p>High frequency conditioning stimulus→ continue to measure fEPSP, shows an increase in amplitude of synaptic response, remains increased overtime </p></li><li><p>Low frequency stimulation again→ after conditioning, the response is larger, follows Hebb’s law</p></li></ol><p></p>
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Properties of LTP: input specificity

  • change in synaptic strength occurs specifically at synapses that are activated e.g. between A and B that are simultaneously fired together

  • Spiking in A&B increases strength between A&B but not between A and others.

<ul><li><p>change in synaptic strength occurs specifically at synapses that are activated e.g. between A and B that are simultaneously fired together</p></li><li><p>Spiking in A&amp;B increases strength between A&amp;B but not between A and others. </p></li></ul><p></p>
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Properties of LTP: associativity

  • a weak stimulus in one pathway is not sufficient to elicits LTP

  • When paired with activity in another stronger pathway, LTP occurs in both

<ul><li><p>a weak stimulus in one pathway is not sufficient to elicits LTP</p></li><li><p>When paired with activity in another stronger pathway, LTP occurs in both</p></li></ul><p></p>
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Properties of LTP: cooperativity

  • same as associativity but doesn’t require the second pathway to have a strong stimulus, just requires a second pathway active at the same time

  • Even if A and C are equal in stimulation = LTP in both

<ul><li><p>same as associativity but doesn’t require the second pathway to have a strong stimulus, just requires a second pathway active at the same time</p></li><li><p>Even if A and C are equal in stimulation = LTP in both</p></li></ul><p></p>
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Properties of LTP: persistence

  • changes in synaptic strength will last across time

  • “Long” term

<ul><li><p>changes in synaptic strength will last across time</p></li><li><p>“Long” term</p></li></ul><p></p>
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Mechanism of LTP induction

  • NMDA receptors are required for LTP

  • They act as coincidence detectors to detect pre and post synaptic activity at the same time

  • NMDA receptors activate at depolarised potentials and Mg2+ bock is removed

<ul><li><p>NMDA receptors are required for LTP</p></li><li><p>They act as coincidence detectors to detect pre and post synaptic activity at the same time</p></li><li><p>NMDA receptors activate at depolarised potentials and Mg2+ bock is removed</p></li></ul><p></p>
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When does LTP occur/not occur?

  • no postsynaptic spiking = Mg block→ no LTP

  • Postsynaptic spiking but no glutamate = Mg block removed but no glutamate to open NMDA receptor

  • Glutamate from A and Mg unblocked in B = LTP!!!

<ul><li><p>no postsynaptic spiking = Mg block→ no LTP</p></li><li><p>Postsynaptic spiking but no glutamate = Mg block removed but no glutamate to open NMDA receptor</p></li><li><p>Glutamate from A and Mg unblocked in B = LTP!!!</p></li></ul><p></p>
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Why does NMDA activation lead to LTP

  • NMDA receptors also allow Ca2+ into the cell, which activates intracellular signalling cascades

  • These cascades drive LTP in downstream effectors, strengthening the synaptic connection

<ul><li><p>NMDA receptors also allow Ca2+ into the cell, which activates intracellular signalling cascades</p></li><li><p>These cascades drive LTP in downstream effectors, strengthening the synaptic connection</p></li></ul><p></p>
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Proof of Ca2+ role in LTP

CA1 hippocampal recording of control (LTP occurring)

  • one group injected with nitr-5 (Ca2= chelator - binds to free calcium)

  • Nitr-5 group had significant decrease in LTP, shows calcium’s role in LTP

<p>CA1 hippocampal recording of control (LTP occurring)</p><ul><li><p>one group injected with nitr-5 (Ca2= chelator - binds to free calcium)</p></li><li><p>Nitr-5 group had significant decrease in LTP, shows calcium’s role in LTP</p></li></ul><p></p>
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Potential mechanisms where LTP is expressed

  1. Change in release properties→ presynaptic

  • increased probability of release

  • Increase no. Of release sites

  • Increase cleft glutaate conc

  1. Chnage in AMPAR properties→ postsynaptic

  • increase channel open-time

  • Increase in probability of opening of channel

  • Increase in gamma

  1. Chnage in AMPAR no.→ postsynaptic

  • unsilencing AMPAR insertion

  • Insertion of additional AMPARs

<ol><li><p>Change in release properties→ presynaptic</p></li></ol><ul><li><p>increased probability of release</p></li><li><p>Increase no. Of release sites</p></li><li><p>Increase cleft glutaate conc</p></li></ul><ol start="2"><li><p>Chnage in AMPAR properties→ postsynaptic</p></li></ol><ul><li><p>increase channel open-time</p></li><li><p>Increase in probability of opening of channel</p></li><li><p>Increase in gamma</p></li></ul><ol start="3"><li><p>Chnage in AMPAR no.→ postsynaptic</p></li></ol><ul><li><p>unsilencing AMPAR insertion</p></li><li><p>Insertion of additional AMPARs</p></li></ul><p></p>
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Long term depression

→ a persistent decrease in synaptic strength

  • found in many synapses in the brain, including the hippocampus

  • Usually achieved by prolonged ow frequency stimulation

<p>→ a persistent decrease in synaptic strength</p><ul><li><p>found in many synapses in the brain, including the hippocampus</p></li><li><p>Usually achieved by prolonged ow frequency stimulation</p></li></ul><p></p>
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LTD dependence on NMDA Proof

  • some forms of LTD are dependant on NMDA receptors

  • Proof = D-APV which is a NMDA receptors antagonist, shown to block LTD

  • Collingridge et.al.

  • After D-APV was applied, LTD did not occur

<ul><li><p>some forms of LTD are dependant on NMDA receptors</p></li><li><p>Proof = D-APV which is a NMDA receptors antagonist, shown to block LTD</p></li><li><p>Collingridge et.al.</p></li><li><p>After D-APV was applied, LTD did not occur</p></li></ul><p></p>
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Proof LTD depends on Ca2+ entry

  • some forms of LTD depend on postsynaptic Ca2+ entry

  • Used intracellular Ca2+ chelation using BAPTA to block LTD

  • With BAPTA applied, no LTD occurred

<ul><li><p>some forms of LTD depend on postsynaptic Ca2+ entry</p></li><li><p>Used intracellular Ca2+ chelation using BAPTA to block LTD</p></li><li><p>With BAPTA applied, no LTD occurred </p></li></ul><p></p>
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LTD alternative inducing mechanisms

  1. Metabotropic glutamate receptors

  2. Muscarinic acetylchoine receptors

<ol><li><p>Metabotropic glutamate receptors</p></li><li><p>Muscarinic acetylchoine receptors </p></li></ol><p></p>
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How do neuronal networks remember things?

Encoding first, then consolidation second, then each time after that is recal

<p>Encoding first, then consolidation second, then each time after that is recal</p><p></p>
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Summary of mechanisms of LTP vs LTD

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