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Flashcards in LTP Deck (18):

Entorhinal cortex links to the denture gyrus which links to CA3 which links to CA1. Which of these structures lie within the hippocampus? What are the names of the pathways running from each structure to the next? Where are they located on a hippocampus diagram?

Dentate gyrus, CA3 & CA1. The perforant path, the mossy fibre path & the Schaffer collaterals in that order (PMS). The DG is at the bottom, CA3 is on the left & CA1 is at the top


What is the evidence by Bliss & Lomo (1973) for LTP existing in the rabbit? N.B. this is not evidence for LTP underlying learning

They anaesthesised a rabbit, stimulated the perforant path at low F & recorded from the DG, then stimulated the perforant path at a high F & finally re-stimulated the perforant path at a low F to find that the new DG field potential was larger than before


Where in the brain was the control recording by Bliss & Lomo (1973) taken?

In cells not connected to the cells which have been stimulated


The problem with using anaesthesised rabbits is that the anaesthetic may...Therefore the results were replicated with...

Suppress activity which is then renewed by the stimulation & was actually present all along. Conscious, awake, freely-moving rabbits


Name and describe 3 important properties of LTP

1) Co-operativity: LTP can be induced by strong stimulation of 1 or weak stimulation of co-operating pathways which converge onto the same cell, 2) Input specificity: LTP at one synapse does not spread to other synapses of the same cell, 3) Associativity: if weak stimulation of pathway A is insufficient to induce LTP, simultaneous strong stimulation of pathway B will induce LTP in the cell's synapse with both A & B


In terms of Schaffer collateral axons between CA3 & CA1, what is the evidence for LTP and LTD?

Repetitive, high F stimulation of CA3 potentiates CA1 field potentials in response to future CA3 signals. Repetitive, low F stimulation of CA3 depresses CA1 field potentials in response to future CA3 signals


Why does strong (high F) but not weak (low F) stimulation induce LTP?

Because prior depolarisation of the postsynaptic membrane by the opening of AMPA channels is required in order to unblock voltage- & ligand-gated glumatergic NMDA channels


What is the evidence that LTP depends on the NMDA Rs? Name 3 e.g.s of such drugs

Drugs which block NMDA Rs block LTP induction without affecting baseline responses. 1) AP5 = competitive, 2) MK-801 = non-competitive, 3) 7-chlorokynurenic acid = glycine antagonist (must bind as well as Glu)


What is the difference between a competitive and non-competitive antagonist?

Increasing the amount of agonist required to fully open the channel vs. reducing the max post synaptic current which can be achieved with any amount of agonist


What is the evidence that LTP relies on a rise in postsynaptic terminal intracellular Ca2+ levels as a result of opening NMDA Rs?

1) Drugs which deplete Ca2+ stores block LTP induction. This prevents the initial Ca2+ influx from triggering the release of more Ca2+ within the postsynaptic terminal
2) Ca2+ tracers signal its presence during HFS of the axon connecting to the cell


Is there evidence that LTP relies on presynaptic Ca2+ influxes?

Yes, mossy fibre LTP relies on an NMDA-independent presynaptic increase in Ca2+, which makes sense given the need for presynaptic Calcium to initiate vesicle fusion


How can the role of Ca2+ in LTP & synaptic transmission in general be described as a chain reaction?

Because there is a signalling cascade: Ca2+ influx at the POSTsynaptic terminal raises Ca2+ levels at that same cell's PREsynaptic terminal etc


Name 1 presynaptic and 3 postsynaptic mechanisms for the expression (not induction) of LTP

1) increased P (Glu release/ AP), 2) improved functional characteristics of AMPA Rs, 3) insertion of existing AMPA Rs into the membrane for synaptic use, 4) increase in the number of AMPA Rs by protein synthesis


PTP can be seen even when no further stage of LTP can be induced because of ___

Saturation: the connection strength is at maximum


Early LTP but not PTP nor STP can be be blocked by.... Early LTP enhances the ___ of existing AMPA Rs by phosphorylation of the ___ subunit

Protein kinase inhibitors. Conductivity. GluA1


What does Ca2+ entry into the postsynaptic terminal do re: AMPA Rs during LTP?

It assembles AMPA sub-units ready for anchoring to the membrane


What 2 substances block L-LTP? Name one of these

Protein synthesis inhibitors e.g. ZIP & transcriptional blockers given that genetic transcription is required to make new proteins


Name a substance which maintains LTP and when inhibited 20 hours after LTP induction reverses LTP, leaving responses as they were before LTP was induced. What is its role?

Kinase PKM-zeta. To act as a synaptic tag I.e. identify which synapse is to be kept potentiated and ensure input specificity