lecture 10/11- long term potentiation and depression Flashcards
what does long term potentiation mean
if 2 neurons are connected to a synapse and they fire at the same time, the synapse between them becomes stronger
where does LTP occur
hippocampus
describe the CA3/CA1 pathway
in hippocampus
CA3 is presynaptic
CA1 is postsynaptic
how does the CA3/CA1 pathway show input specificity
will only respond to certain input on pre or postsynaptic side
how does the CA3/CA1 pathway show co-operativity
if both membranes depolarised at the same time, then both pathways can be strengthened
what happens in LTP when one pathway is weaken than the other
the pathways help eachother
what are the 3 types of glutamate receptor involved in LTP
NMDA
AMPA
g protein coupled
is LTP a pre or post synaptic event
postsynaptic
which ion is very important for LTP
Ca2+
what is thew NMDA receptor blocked with and how is this overcome to activate the receptor
Mg2+ block
to activate you need glutamate and need to depolarise the membrane
what is the difference between early and late LTP
early- no protein synthesis
late- gene expression changes
what are the 3 possible cellular results of LTP
increased presynaptic release
increased synapses
increased post synaptic response
describe early phase LTP
1) Ca2+ activates calmodulin kinase 2
2) opens catalytic subunit
3)subunit becomes phosphorylated
4) this enhances the AMPA currents due to increase in no of receptors and increase in probability of receptors
describe late phase LTP
Need protein synthesis, cAMP signalling critical
1) cAMP goes into nucleus
2)CREB2 is swapped with CREB1
3)CREB1 is phosphorylated
4)gene expression occurs which strengthens synapses
describe the events that occur when NMDA is activated
1) Ca2+/ Calmodulin
2) adenylyl cyclase / CaMKII(-vely feeds back)
3) triggers pkA and then gene expression
describe the events that occur when AMPA is activated
Na+ released
depolarisation
what is evidence that LTP is linked to memory
mutations of CaMKII, NMDAs, and cAMP pathway all effect memory
drugs enhancing memory also enhance LTP
where does LTD occur
cerebellum
hippocampus
what are the 2 inputs of LTD in the cerebellum
mossy fibres -> granule cells
climbing fibres
both positive
which of the inputs for LTD causes massive depolarisation when stimulated
climbing fibres
what is the negative output for LTD in the cerebellum
purkinje fibres
how is a response caused in the purkinje cells
when purkinje fibres and climbing fibres are stimulated at the same time
which receptors are involved in LTD in the cerebellum
voltaged gated Ca2+ receptors from climbing fibres to purkinje
AMPA
G alpha Q pathway
from parallel fibre to purkinje
describe the G alpha Q pathway
DAG
PKC
This phosphorylates AMPA
why is co-activation needed for LTD
Ca2+ obtained from parallel fibre activation
Ca2+ obtained from climbing fibres
together these cause deactivation of AMPA receptors
describe hippocampal LTD
stimulate CA3-CA1 synapse with low frequency
what is the overall effect of a small increase in Ca2+ in the hippocampus
protein phosphatase activated
decrease AMPA efficacy
LTD
what is the overall effect of a large increase in Ca2+ in the hippocampus
protein kinase activated
increased AMPA efficacy
LTP
