Lecture 7 Flashcards
What did Hebb state about memory?
Memory results form synaptic modifications (hebbian plasticity)
What did Kandel discover?
Molecular mechanisms lead to synaptic plasticity
- simple invertebrates
What are the 2 stages of learning/memory?
Acquisition of short-term memory
Consolidation of long-term memory
How does short-term memory work?
Physical modification of brain caused by incoming sensory information
- modifies synaptic transmission between neurons
How does long-term memory work?
Requires new gene expression and protein synthesis
- protein synthesis inhibitors - deficits in learning and memory
What is special about the neural network model?
Unique pattern/ratio of activity of neuronal activity
- distributed memory
- no single neuron represents specific memory
What is the advantage of the neural network model?
Memories survive damage to individual neurons
What leads to memory loss?
Degradation of memory = neuron loss
- physical change of memory = change in synaptic weight
Explain Henry Molaison’s case.
Seizures @ age 10 that became more frequent and severe with age (convulsions, tongue biting, and loss of consciousness)
- @ Age 27, surgery removed 8 cm of medial temporal lobe, including cortex, underlying amygdala, and 2/3 hippocampus
- Lead to no more seizures but unable to learn new information
What are 3 things that can happen to the memory model?
1) Increases/decrease in synaptic weights: shift neuronal selectivity and store information
2) Synaptic plasticity (long term potentiation and long term depression)
3) Trisynaptic circuit of the hippocampus
- entorhinal cortex -> dentate gyrus synapse -> CA3 synapse -> CA1 synapses
Explain the mechanism of LTP in CA1
1) Glutamate receptors mediate excitatory synaptic transmission
- NMDA and AMPA receptors
2) Calcium influx through NMDA receptors triggers alteration in AMPA receptors
3) Activation of kinases that phosphorylate AMPA receptors (already in synapse) increase permeability
4) Calcium mediated insertion of additional AMPA receptors at the synapse
How is LTD produced?
Low-frequency electrical stimulation of excitatory pathway
What are the 2 forms of homosynaptic LTD at CA1 synapse?
mGluRs: G-protein coupled metabotropic glutamate receptors
NMDA receptors: rise in [Ca++] triggers LTD
What 2 rules lead bidirectional plasticity of LTP vs. LTD?
1) Synapses during strong depolarization of postsynaptic neuron causes LTP
2) Synapses during weak depolarization of postsynaptic neuron causes LTD
How can long-term memory be stabilized if phosphorylation of a protein isn’t permanent?
Protein synthesis and structural changes
