Flashcards in Principles of Neuroscience Lecture 20 Memory II Deck (18)
What is LTP?
Long term potentiation: strengthening between synapses, memory forming
What is LTD?
Lond term depression; the eventual weakening of the connection between neurons
Loss of a memory
Describe the experiment investigating LTP and LTD
A neuron was stimulated with
b. low frequency tetanus
In a., there was long term potentiation
In b., there was long term depression
Low frequency tetanus stimulation of a neuron results in ...
What is the mechanism for LTP?
Outline the steps
1. Glutamate release by the pre synaptic neuron when the synaptic vesicles fuse with the membrane
2. Glutamate binds to NMDA receptors, calcium rushes into the cell
3. Influx of calcium activates protein kinases (CaMKII)
4. Protein kinases phosphorylate and being about the insertion of AMPA in the membrane, and increasing the effectiveness of AMDA already in the membrane
Differentiate between AMPA and NMDA receptors
AMPA: excited by glutamate
NMDA: unblocked by glutamate, calcium rushes through
What is CaMKII?
Calcium-calmodulin dependent Kinase II
What are the different regions of CaMKII?
What is the activity of CaMKII when it is phosphorylated?
It is constitutively active (that is, until a phosphatase removes the phosphate)
Describe the multimer structure of CaMKII?
The CaMKII are found in rings.
Once Ca/calmodulin disown its some of them, they all become activated and phosphorylated.
What is CaMKII's role in LTP?
When there is calcium influx into a cell, the calcium activates and brings about phosphorylation of the CaMKII
What is required for true long term memory?
Protein synthesis alteration
Receptor deposition, receptor sensitivity and phosphorylation aren't enough for long term change
Describe how protein synthesis can be altered in memory storage
1. CREB-2 replaced with CREB-1 when there is activity in a certain neuron
2. CREB-1 is phosphorylated, and that gene will undergo transcription
What are the different ways that calcium can enter a neuron?
1. NMDA receptor
2. Intracellular stores: inside the cell, glutamate binds to a receptor on the ER membrane, prompting Ca release from the ER
3. Back propagating dendritic action potentials open voltage gated Ca channels
What is spike timing dependent plasticity?
This is when the dependence of memory formation (LTP, LTD) on the timing of the action potential
Describe how LTP is dependent on spike timing dependent plasticity
If the action potential occurs after EPSP --> LTP
Describe how LTD is dependent on spike timing dependent plasticity
If the action potential occurs before EPSP --> LTD