AMPA receptor: Difference between revisions

From The School of Biomedical Sciences Wiki
Jump to navigation Jump to search
← Older editNewer edit →
No edit summary
No edit summary
Line 1: Line 1:
<xmlns:texthelpns rwthpgen="1">AMPA receptors are </xmlns:texthelpns>[[Ligand-gated ion channel|Ligand gated ion channels]]<xmlns:texthelpns rwthpgen="1">.The ligand (signalling molecule) they are complementary to is a </xmlns:texthelpns>[[Glutamate|Glutamate]]&nbsp;<xmlns:texthelpns rwthpgen="1">which is the main excitatory&nbsp;</xmlns:texthelpns>[[Neurotransmitter|neurotransmitter]]&nbsp;<xmlns:texthelpns rwthpgen="1">in the </xmlns:texthelpns>[[Central nervous system|CNS]]<xmlns:texthelpns rwthpgen="1">, this means there is a high proportion of these AMPA receptors on postsynaptic neurons in the brain.&nbsp;</xmlns:texthelpns>
AMPA receptors are [[Ligand-gated_ion_channel|Ligand gated ion channels]] .The ligand (signalling molecule) they are complementary to is a[[Glutamate|Glutamate]] which is the main excitatory[[Neurotransmitter|neurotransmitter]] in the[[Central_nervous_system|CNS]], this means there is a high proportion of these AMPA receptors on postsynaptic neurons in the brain.<br>When Glutamate binds to AMPA receptors it causes a conformational change and the ion channel opens allowing Na+ ions to flood into the postsynaptic cell. The increase in Na+ concentration causes depolarisation of the postsynaptic membrane generating an[[EPSP|EPSP]] ( which if strong enough can go on to initiate an [[Action_potential|action potential]] at the axon hillock). Repetitive stimulation of these synapses in the brain can cause LTP [[Long_term_potentiation|(Long-term potentiation]]) , due to more Glutamate being released across the synaptic cleft binding to more AMPA receptors which leads to a higher influx of Na+ ions into the cell generating a stronger EPSP. This strong depolarisation of the post-synaptic member aids to the activation of [[NMDA_receptor|NMDA receptors]] ( along with glutamate binding) which allow Ca2+ ions to enter the post synaptic cell. This increase in Ca 2+ concentration can cause new AMPA receptors to be inserted in to the post-synaptic membrane increasing the sensitivity of the post-synaptic cell to Glutamate. <ref>Bruce Alberts, e. a., 2008. Molecular Biology of the cell. 5th ed (pg 690). New York: Garland Science.</ref><br>


<xmlns:texthelpns rwthpgen="1"></xmlns:texthelpns><xmlns:texthelpns rwthpgen="1">When Glutamate binds to AMPA receptors it causes a conformational change and the ion channel opens allowing Na+ ions to flood into the postsynaptic cell.&nbsp;</xmlns:texthelpns><xmlns:texthelpns rwthpgen="1">The increase in Na+ concentration causes depolarisation of the postsynaptic membrane generating an&nbsp;</xmlns:texthelpns>[[EPSP|EPSP]]&nbsp;<xmlns:texthelpns rwthpgen="1">( which if strong enough can go on to initiate an </xmlns:texthelpns>[[Action potential|action potential]]&nbsp;<xmlns:texthelpns rwthpgen="1">at the axon hillock).</xmlns:texthelpns><xmlns:texthelpns rwthpgen="1">Repetitive stimulation of these synapses in the brain can cause LTP (</xmlns:texthelpns>[[Long term potentiation|Long-term potentiation]]<xmlns:texthelpns rwthpgen="1">) , due to more Glutamate being released across the synaptic cleft binding to more AMPA receptors which leads to a higher influx of Na+ ions into the cell generating a stronger EPSP.&nbsp;</xmlns:texthelpns><xmlns:texthelpns rwthpgen="1">This strong depolarisation of the post-synaptic member aids to the activation of </xmlns:texthelpns>[[NMDA receptor|NMDA receptors]]&nbsp;<xmlns:texthelpns rwthpgen="1">( along with glutamate binding) which allow Ca2+ ions to enter the post synaptic cell.</xmlns:texthelpns><xmlns:texthelpns rwthpgen="1">This increase in Ca 2+ concentration can cause new AMPA receptors to be inserted in to the post-synaptic membrane increasing the sensitivity of the post-synaptic cell to Glutamate.</xmlns:texthelpns><xmlns:texthelpns rwthpgen="1">&nbsp;</xmlns:texthelpns><ref>Bruce Alberts, e. a., 2008. Molecular Biology of the cell. 5th ed (pg 690). New York: Garland Science.</ref><br>  
<u>'''References'''</u>


<u>'''References'''</u>  
<u</u><references />
 
<references />

Revision as of 15:01, 9 November 2013

AMPA receptors are Ligand gated ion channels .The ligand (signalling molecule) they are complementary to is aGlutamate which is the main excitatoryneurotransmitter in theCNS, this means there is a high proportion of these AMPA receptors on postsynaptic neurons in the brain.
When Glutamate binds to AMPA receptors it causes a conformational change and the ion channel opens allowing Na+ ions to flood into the postsynaptic cell. The increase in Na+ concentration causes depolarisation of the postsynaptic membrane generating anEPSP ( which if strong enough can go on to initiate an action potential at the axon hillock). Repetitive stimulation of these synapses in the brain can cause LTP (Long-term potentiation) , due to more Glutamate being released across the synaptic cleft binding to more AMPA receptors which leads to a higher influx of Na+ ions into the cell generating a stronger EPSP. This strong depolarisation of the post-synaptic member aids to the activation of NMDA receptors ( along with glutamate binding) which allow Ca2+ ions to enter the post synaptic cell. This increase in Ca 2+ concentration can cause new AMPA receptors to be inserted in to the post-synaptic membrane increasing the sensitivity of the post-synaptic cell to Glutamate. [1]

References

<u

  1. ↑ Bruce Alberts, e. a., 2008. Molecular Biology of the cell. 5th ed (pg 690). New York: Garland Science.
Retrieved from "https://teaching.ncl.ac.uk/bms/wiki//index.php?title=AMPA_receptor&oldid=9402"