Learning and Memory Flashcards
Learning
Changes in the structure and function of neurons and their synapses in response to experiences or stimuli.
Memory
How these changes are maintained over time and how they are expressed (recall)
When do we start remembering things?
Memory consolidation takes time, event initiates a molecular cascade
Where takes memory consolidation place?
Hippocampus and associated cortical structures. Memories are then distributed probably over the cerebral cortex (but still unsure)
How does it happen?
Synaptic reorganisation is crucial. Modulation of structural, adhesion neurotransmission proteins
Example HM
H.M., was a patient who underwent a surgical procedure called a bilateral medial temporal lobe resection in 1953 to treat his epilepsy. The surgery involved the removal of the hippocampus and surrounding tissue in both brain hemispheres.
The surgery was initially successful in reducing H.M.’s seizures, but it had a dramatic and unforeseen effect on his memory.
H.M. developed severe anterograde amnesia, meaning he was unable to create new memories or learn new information after the surgery. He retained some memories from before the surgery, but he was unable to remember anything that happened after the surgery, including the surgery itself.
Main learning outcomes from patient HM
-> Some brain regions seem to be more important for some kinds of memory
-> Forming (consolidating) new episodic memories is dependent on the medial temporal lobe
declarative memory (explicit)
things you know that you can tell others
procedural memory(non-explicit)
things you know you can do by showing
Hippocampus x memory consoliation
HM suggests that hippocampus and related cortical areas are important for consolidating episodic memories for long-term storage in other cortical areas
Over time, memories are stored in distributed networks of cortical areas and become less and less connected to the hippocampus (hippocampal-neocortical reactivation theory)
-> Engram = change in the brain that represents a memory
-> In order to understand it, you need to systematically test which brain areas are important for memory storage.(Examples what we know so far below)
Hippocampus x memory consoliation
HM suggests that hippocampus and related cortical areas are important for consolidating episodic memories for long-term storage in other cortical areas
Over time, memories are stored in distributed networks of cortical areas and become less and less connected to the hippocampus (hippocampal-neocortical reactivation theory)
-> Engram = change in the brain that represents a memory
-> In order to understand it, you need to systematically test which brain areas are important for memory storage.(Examples what we know so far below)
Cellular Basis of Learning and Memory
- Long-term potentiation (LTP): LTP is a long-lasting increase in the strength of a synapse, or the junction between two neurons, in response to repeated or strong stimulation. LTP is thought to be a key mechanism underlying learning and memory, and it involves changes in the number and function of receptors and ion channels at the synapse.
- Long-term depression (LTD): LTD is a long-lasting decrease in the strength of a synapse in response to weak or repetitive stimulation. LTD is thought to play a role in the modification of existing memories and in the process of forgetting.
- Synaptic plasticity: Synaptic plasticity refers to the ability of synapses to change in strength in response to activity or experience. Both LTP and LTD are forms of synaptic plasticity, and they involve changes in the number and function of receptors and ion channels at the synapse.
- Gene expression: Learning and memory can also involve changes in gene expression, which is the process by which the information in a gene is used to synthesize a protein. Learning and memory can be associated with the activation or suppression of specific genes, leading to changes in the abundance or function of proteins in the brain.
Forgetting
If a memory is no longer needed or rarely recalled = corresponding synapse is weakened and eventually disappear
Long Term Potentation (LTP)
refers to long-lasting enhancement of the strength of connection between two neurons that results from repeated activation of those neurons.
- High frequency (strong experience)
- Repeating (studying, revising)
It can occur at most excitatory synapses in the brain but it is best studied at the glutamate synapse at the hippocampus.
When a glutamatergic neuron is stimulated -> action potentials travel down its Axon and trigger the release of glutamate into the synaptic cleft -> glutamate then binds to its receptors on the postsynaptic neuron
(the two main glutamate receptors that often coexist in a synapse or AMPA and NMDA receptors) -> these are ion channels that activate upon binding to glutamate when the presynaptic neuron is stimulated by -> a weak signal only a small amount of glutamate is released although both receptors are bound by the glutamate only AMPA is activated by weak stimulation sodium influx (NA+) -> results in a slight depolarization of the postsynaptic membrane the
NMDA channel remains closed because it’s poor is blocked by magnesium ions -> when the presynaptic neuron is stimulated by a strong or repeating signal a large amount of glutamate is released the AMPA receptor stays open for a longer time admitting more sodium into the cell
-> thus, resulting in a greater depolarization
-> increased influx of positive ions expels magnesium from the NMDA channel which now activates
allowing not only sodium but also calcium into the cell: calcium is the mediator of LTP induction
LTP can be divided into two phases
In the early phase (induction phase), calcium initiates signaling pathways that activate several proteins kinases that enhance synaptic communication in two ways. There is a rapid increase in the strength of the synapse in response to a series of high frequency stimuli.
- They phosphorylate the existing AMPA receptors thereby increasing AMPA conductance to sodium (a) and help to bring more AMPA receptors from intracellular stores to the postsynaptic membrane (b)
(a) (b)
This phase is thought to be the basis of short-term memory which lasts for several hours.
In the late phase (maintenance phase) new proteins are made and gene expression is activated to further enhance the connection between the two neurons.
This process is slower but leads to a more sustained increase in the strength of a synapse.
These include newly synthesized AMPA receptors and expression of other proteins that are involved in the growth of new dendritic spines and synaptic connections.
The late phase may correlate with formation of long-term memory.
