Lecture 18 - Learning and Memory 2 Flashcards
Model systems for studying the neural basis of learning and memory: links to behaviour:
- LTP is a neural correlate for a change in synaptic strength during learning
- What is the cellular basis of associative conditioning – learn relationships in predicted environments (dogs – ringing bell – started salivating)? This makes us increase our chances of survival
- If a pathway was particularly active, then it would become stronger as it was constantly activated and branching would occur
Learning in Invertebrates:
- Caenorhabditis elegans (nematode worm (CNS - 302 neurons))
- Drosophila melanogaster (fruit flies)
- Learning mutants
1. Involvement of cAMP signalling cascade
2.
e.g. dunce shows deficits in olfactory associative conditioning: cAMP phosphodiesterase mutation.
Aplysia californica – the sea hare:
Gill withdrawal reflex
- Shows habituation, sensitisation, classical conditioning
- Highly influential in the nervous system
- Heavily folded gills that has oxygen pass through it
Aplysia abdominal ganglion:
- Control movements of the gill and pick up sensory information
- Accessible brains easily detected
- Nerve cells are the brown structure
- Sensory neurons pick up information from the siphon and the motor neurons pick them out at the MN
- Response in the gill which is the effector
Stimulus – response relationship:
mild stimulus so contraction of the gill to protect itself
- can measure how big the response is by measuring the total area of the gill before and after the response is given
- the smaller the gill, the greater the response
Habituation of gill withdrawal response:
- Non-associative learning
- Habituation is when you get the same stimulus over and over that you stop responding and it becomes the norm
- 100% response to begin with
- gradually response gets smaller
Synaptic depression at sensory neuron-motorneuron synapse:
- pre-synaptic neuron is constantly stimulated to produce and action potential (EPSP) in motor neuron
- became smaller and smaller in the post-synaptic leading to habituation responses
Habituation of gill withdrawal involves synaptic depression – a form of synaptic plasticity:
- Synaptic efficacy is reduced with repeated use - due to a reduction in Ca2+ influx per action potential and hence reduced neurotransmitter release
- Learning = change in synaptic function (monosynaptic)
Sensitisation of gill withdrawal response: (adaptive form of learning)
Non-associative learning
- Can re-stimulate by adding a different stimulus, in this case, an electric shock
- Shows that sensitisation can be short term or long term
- Long term changes require long term stimulation (lots of it) to allow synthesis process to occur
Sensitisation of gill withdrawal involves presynaptic facilitation – a form of synaptic plasticity:
- Single shock to the tail creates another pathway by 3 synaptic arrangements onto the sensory neuron
- Connections back to the tail – heterosynpatic – as there’s 2 synapses
- This can modify the activity (green affects brown)
Short-term:
5HT which binds to receptors that activates the G-proteins which allows the intracellular cAMP to protein kinases to stimulate a response to the motor neurons by opening and closing sodium channels
- this causes repolarisation
- 5HT applied, longer action potentials in the sensory neuron
- leads to increased neurotransmitter release which leads to greater action by the motor neurons
Long Term:
- shock the tail a few times and the synapses becomes sensitised and strengthened
- involves gene expression and protein synthesis
- enzyme – ubiquitin hydrolase is produced which causes protein kinase A that causes the persistent release of the neurotransmitter and the voltage-gated K+ channels remain open – broadening of the action potentials
- cAMP enzymes also led to structural changes
- Using EM, the area of the synaptic transmission was increased
- Number of sites between a sensory and motor neuron was also increased and actually became stronger structurally and functionally
- Doesn’t mirror LTP – the one above is all in the pre-synaptic neuron
Sensitisation of the gill withdrawal response involves:
- Increased neurotransmitter release at sensory neuron motoneuron synapse (functional plasticity)
- Activation of cAMP signalling cascade, leading over the long term to changes in gene expression
- Increased number and area of active synaptic zones (structural plasticity)
Classical (associative) conditioning of the withdrawal response:
- Involves similar cellular/molecular processes to sensitisation
- Tail shock (US) → gill/siphon withdrawal (R)
- CS is weak tactile stimulation of siphon
- Graph shows response to CS alone
- Underlie what makes animal behaviour so adaptive
- Learn to associate events to occur – time
- Graph shows that in the experimental group (2 stimuli were paired in time), the response to the weak conditioning stimulus was greatly enhanced after training
- Weak stimulus associated with the electric shock which was painful
- Memory would gradually stay for days
- When unconditioned stimulus was given alone then sensitisation occurred
Classical conditioning of gill withdrawal response:
¥ When CS and US are paired, there is greater activation of adenylyl cyclase in the presynaptic terminal than with either stimulus by itself
¥ 5HT and normal stimulus arrives at the same time, you get more of a response as cAMP is enhanced in its activity
¥ This is because the CS action potential admits Ca2+ into the presynaptic terminal
¥ The Ca2+ (by interacting with a protein called calmodulin) increases the response of adenylyl cyclase to G-proteins
