Learning and Memory Flashcards
What is a neuronal explanation of learning?
Process causing lasting changes in synapses and/ore neuronal activity
What is a neuronal explanation of memory?
Changes in synaptic/neuronal activity that persist
How can memory be classified in terms of time course?
Short term memory (working memory)
Long term memory
What categories can long term memory be further divided into?
Declarative - episodic + semantic
Non-declarative - implicit
What is episodic memory and what brain areas is it associated with?
memory for events
temporal lobe and hippocampus
What is semantic memory and what brain areas is it associated with?
Memory of different facts
Involves many brain areas with some being category specific
What brain areas are associated with implicit memory?
Amygdala, striatum, neocortex, cerebellum and spinal cord
What is priming and what are the two types?
Where exposure to one stimulus influences a later stimulus response can be:
conceptual or perceptual
What is procedural memory and what are the two stages?
Proceeds with repetition
Cognitive: pay attention to performance (parietal and inferior temporal cortex)
Autonomous: skills executed without much conscious effort (inferior temporal)
What are the two types of conditioning?
Classical (two stimuli) and operant (action and consequence)
What is nonassociative learning?
About a single stimulus can be:
Habituation - response weakens following bening stimuli
Sensitization - response strengthens following noxious stimuli
How does habituation occur is aplysia?
Short term: fewer vesicles available for release from sensory neuron to motor neuron (depression of glutaminergic release)
Long term: decreased number of synaptic contacts
How does sensitization occur in aplysia?
Tail shock activates tail sensory neuron which activates a modulatory interneuron which releases serotonin on to the presynaptic area of where the siphon sensory neuron connects to the motor and interneuron. This enhances vesicle release and increases excitation.
What is the biochemical explanation for increased glutaminergic release in aplysia during short term sensitisation?
- Seretonin released my facilatory interneuron binds to either G coupled receptor or PLC coupled receptor
- Activated G protein dissociates from receptor and activates adenylyl cyclase going on to activate cAMP
- cAMP binds to PKA, releasing catalytic subunits capable of phosphorylating K channels
- When depolarisation occurs, fewer open K channels means that Ca2+ enters cell for longer allowing more vesicles to be released
- PLC activates second messenger DAG which facilitates movement of vesicles
What is the biochemical explanation for increased glutaminergic release in aplysia during long term sensitisation?
- Increased training leads to cAMP (activated by G coupled protein) to release catalytic unit and bind to CREB (cAMP response element binding-protein) which bond to CRE (cAMP response elements)
- This increases transcription of downstream genes causing increases in proteins such as ubiquitin hydroxylase which causes a degredation of the regulatory subunit of PKA, causing some catalytic units to be persistently active no longer requiring seretonin
- Also increases transciption of C/EPB which is another transcription factor which aids in the transciption of other unknown genes believed to increase number of synaptic contacts
How does classical conditioning occur within aplysia?
Same as sensitisation with addition of:
- Ca2+ influx binds with calmodulin
- Binds to adenyl cyclase (coupled with G protein receptor - remeber sensitisation) enhancing reception of serotonin
- Leads to more cAMP and more facilitation
What are the cortex related mechanisms of fear conditioning?
- Increased activity in the lateral nucleus of the amygdala
- In mouse whose feet are shocked when tone is heard, stimuli from ears and feet either take a direct or indirect pathway from the thalamus and glutaminergic inputs converge on the lateral amygdala causing facilitation
What are the short term mechanisms of fear conditioning at a neuronal level?
- NMDAR and voltage gated calcium channel activation
- Ca2+ influx
- Inseration of AMPARs (enhanced transmitter release)
What are the long term mechanisms of fear conditioning?
- cAMP-dependent PKA and MAPK
- Activation of CREB and gene expression increasing synaptic connections
What are the mechanisms of procedural learning?
- LTP forms at synapse from cortex to striatum
- LTP mediated by NMDARs
- Maintenance of LTP involves CREB function
What brain areas are associated with explicit learning?
STM - prefrontal cortex (short term)
LTM - hippocampus (hours-lifetime)
Cortex - permanent storage? (permanent storage)
How is working memory belived to be maintained?
Through peristent firing maintained by intrinsic properties
- Depolarisation of pyramidal entorhinal neuron causes opening of v-gated Ca2+ channels
- These activate Ca2+-active non selective cation channels (CAN)
- Causes further depolarisation (after depolarisation - ADP) with positive feedback loop that can persist for several minutes
Name 3 other mechanisms that can cause persistent firing?
Long range - between different brain regions such as the inferior temporal, prefrontal and parietal
Local feedback between neuron groups in a certain area
Mutual inhibition networks (half centre hypothesis)
What are the two mechanisms whereby long-term explicit learning is carried out
Direct and Trisynaptic take input from entorhinal cortex
3 regions with 4 glutaminergic synapses all capable of forming LTP
What is the direct prefrontal pathway?
- Non-associative LTP, requires strong activation on presynapse
- Dependent on NMDA and v-dependent receptors
What is the schaffer collateral pathway?
Associative LTP formation where NMDARs are essential
1. Have V-dependent Mg2+ block which is removed by post synaptic APs
2. Binding of glutamate predicts presynaptic activity
Increased Ca2+ activity triggers cellular cascade leading to LTP induction
Hebbs Law - Neurons that fire together wire together
How is the CA1 pertinent to spatial memory?
- NMDAR NRI mutation in this region results in failure to induce LTP in mice and poor performance in a water maze
- NMDAR NR2B overexpression causes smart mice
How does long term depression rely on NMDARs?
Low levels Ca2+ activate phosphatase calcineurin leading to the endocytosis of AMPARs and therefore LTD
What is the hypothesized role of LTD in spatial memory?
Needed for preventing LTP saturation
Mutant mouse with phosphatase 2A inhibited causes failure to form LTD in CA1 region also take longer to adjust to a change in location in the water maze
What are place cells?
- Found in CA3 and CA1 region
- Only fire when animal is in certain location in certain environment
- Formed within minutes and are stable for weeks/months
What are grid cells?
Found in the medial entohrinal cortex and fire only when animals are in regular triangular knots in the environment
different grid cells have different knot positions/distances
Independent of visual cues, speed and direction (measure distance)
Describe LTP formation at the Mossy Fibre pathway (granule and pyramidal cells)
- non-associative (no post-synaptic activity)
- tetanic stimulation leads to a greater Ca2+ influx and an activation of Ca2+-Calmodulin dependent adenlyl cyclase
- cAMP increase leads to PKA activation which phosophorylates RIM1a on vesicles
- Results in enhanced vesicle release
- Subcellular changes depend on PKA activity
What is the early phase and the late phase of the Schaffer pathway?
Early - insertion of AMPARs on post synaptic membrane and enhancement of transmitter release
Late - New synapses
