Lecture 15: Experience-Dependent Plasticity Flashcards
Associative vs non-associative learning
1)Non-associative learning - learning based on repeated experience with a stimulus
– Habituation – decrease in effect
– Sensitization – increase in effect
2) Associative learning - learning relationships between stimuli, behaviours and/or events
– Respondent (Type 1) conditioning
– Operant (Type 2) conditioning
What are the two types of memory
1.Declarative/explicit
* Semantic - factual knowledge about the world
* Episodic – Events, Autobiographical
2. Non-declarative/implicit
* Procedural: IF….THEN… memories
* Skill learning, conditioning, non-associative
Who developed to idea of a memory engram
Karl Lashley - thought memories about learning to navigate a maze were encoded in an engram. He made lesions in different parts of the rats cortex and put it back in the maze, observing its behaviour and errors multiple times. Errors increased as lesions increased. Suggests the cortex was somehow responsible for this memory of learned behaviour. He couldn’t find the specific location though.
Discrete lesions of cortical areas did not interfere
with maze learning, but large areas of damage did.
What are Karl Lashley’s two principles
Principle of Equipotentiality: All cortical regions can mediate learning equally.
Principle of Mass action: Ability to learn is
proportional to the amount of cortex available.
What are the subcortical areas involved in learning and memory and how?
The hippocampus and the amygdala in the temporal lobe.
Hippocampus – declarative and spatial memories
(e.g., review case of H.M.)
* Cerebellum – procedural memories (simple
Pavlovian associations)
* Amygdala – emotional memories – Pavlovian
associations
* Frontal cortex – short-term/working memory
What brain connectivity did Pavlov speculate from formation of associations
That these associations create a new cortical connection where the auditory center of the brain connects to the food center of the brain and then the salivation center.
Give the growing research of what was known at the time about the brain
Neurogenesis: Creating Novel Circuits
* Predominant view prior to the mid-1990s:
– The mammalian brain does not make new neurons in adulthood
> There is now evidence that neurogenesis does occur in the mammalian brain
– Olfactory bulb, hippocampal formation, and possibly the neocortex
– Reason for neurogenesis is still unclear
Raising rats in enriched enclosures increases…
- Brain weight
– Dendritic length and complexity i.e. synaptic spines suggests more connections (‘Sholl analysis’)
– Vascular volume (more blood vessels)
– Number of synapses per neuron (synaptic spine counting)
– Mitochondrial volume (marker of greater metabolic activity) i.e. using more energy.
Overall environmental experiences alters brain morphology.
Are there different kinds of synapses in structure?
Yes some are thin, others more mushroom like and others more stubby. Researchers wondered if this is specific to learning in some way.
Thoughts on the synaptic basis of memory at the time
- New synapses could be generated to store
specific new memories. - Existing synapses could be modified to store the memories.
- A pool of new synapses could be continuously
generated in the brain, learning and memory
incorporates them into a functional storage
network.
Explain Donald Hebb’s idea related to synapses
New synapses are continuously generated
in the brain.
- New synapses are anatomically and
physiologically connected, but not part of a
memory network.
* Upon appropriate activation - synapses are
“strengthened” and incorporated into a memory network.
“When an axon of a cell A is near enough to excite a cell B and repeatedly or
persistently take part in firing it, some growth process or metabolic change
takes place in one or both cells that A’s efficacy, as one of the cells firing B, is
increased”
Key points:
* Simultaneous pre- and post synaptic activity
* Some sort of change in the connection between the neurons
* Increase in the influence that pre synaptic neuron has over postsynaptic
activity
“Cells that fire together, wire together”
What did the development of whole-cell electrophysiology allow for
Researchers were able to measure what happens at the post-synaptic neurons. They penetrate it with a glass pipette which allows for measuring the flow of ions coming into the cell. This was specifically done in the hippocampus as they are clearly aligned and connected.
What was the first evidence found for Hebbian learning and memory
Eric Kandel found that Stimulation of the siphon results in the withdrawal of the snail’s gill for protection. Stimulation activates sensory neurons in the siphon, which activates, directly or indirectly,
through interneurons, motor neurons that withdraw the gill. Habituation leads to a decrease in neurotransmitter release into the synapse with motor neurons and reduced EPSP at motor neurons. Communication is reduced as a result of habituation.
Define long-term potentiation
Long lasting changes in hippocampal synaptic efficacy following high frequency (tetanic) stimulation. I.e. strengthening of connection between two neurons. After a while after tetanic stimulation to allow the neurons to rest, they were stimulated again but there was an increase in the EPSP. This difference/increase is potentiation.
Define tetanic stimulation
Many stimulations within a small period of time ~ 100 stimulations per second.
Example of where tetanic stimulation happens
When learning a fear through association. It produces long term potentiation in the amygdala. Direct effect of learning on LTP.
Neurochemical basis of long term potentiation
Shows higher neurotransmitter release + many more receptors placed at the post-synaptic neuron to which the neurotransmitters bind to.
