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Learning and Memory Flashcards

1
Q

Give the definition of learning

A

An adaptive change in behaviour from experience

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2
Q

Define memory

A

The retention of learning

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3
Q

Describe the mechanism of learning

A

Fill in later

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4
Q

Name the two types of memory and their availability, formation, short term storage, and long term storage attributes

A

Fill in later

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5
Q

Disorders of declarative memory stem from…….

Give a case study which supports this

A

…. damage to the medial temporal lobe

Case Study: HM - had epilepsy from 10 y/o. Had a bilateral resection of MTL which controlled epilepsy. HM could recall early memories and IQ of 112 was unchanged but he had severe anterograde amnesia

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6
Q

Give three features of declarative memory and evidence for each

A

1: DM is distributed in various cortical sites

Evidence: Karl Lashley (1920’s) - Rats with brain lesions given maze tasks. Showed location of lesion wasn’t significant, only extent of lesion and task difficulty - ‘MASS ACTION PRINCIPLE’

2: Hippocampus is the organisational centre for DM

Evidence: Hippocampal inputs (afferents) match outputs (efferents) - place where recall happens as well as learning

3: Different regions of MTL are responsible for different aspects of DM

Evidence: Daselaar et al (2006) - subjects given 120 english and 80 non-words (2 s/item), after 30 mins they were tested on recall and familiarity and brain activity measured. Recollection - Highest activity in posterior hippocampus; Familiarity - Highest activity in posterior parahippocampal cortex; Novelty - Highest activity in anterior hippocampus and rhinal cortex

Epstein and Kanwisher (1998) - Post Para Hippocampal place (PPA). Subjects were shown pictures and their brain activity measured. PPA is strongly activated by spatial information, but not objects or faces. People with damaged PPA have trouble navigating novel environments

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7
Q

Describe the basic mechanism of non-declarative memory

A

Input enters cerebellum - striatum (doing part of brain) - motor cortex - action

When two signals reach the cerebellum at the same time, the become associated
e.g. Tone + Airpuff = Eye blink -> Tone = Eye blink

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8
Q

Describe how MRI and fMRI works

A

MRI - Uses strong magnetic field to align protons. Burst of radio waves flip protons out of alignment. When protons flip back, the energy change is recorded

fMRI - measures areas with higher levels of oxygenated blood (activity) - Not infallible: people have taken readings from dead salmon

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9
Q

Give a brief summary of declarative memory encoding

A
  • Object information is represented by the perirhinal cortex (relational information comes from neo cortex)
  • Contextual information processed by the para hippocampal cortex
  • The two types of info are integrated by the hippocampus
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10
Q

Describe Hebb’s postulate and Hebb’s learning rules

A

The synaptic connection between cells A and B is affected (strengthened) because A keeps firing B

Learning Rules:
Correlated pre- and post-synaptic activity causes synaptic strengthening/stabilisation (A + B firing)
Uncorrelated pre- and post- synaptic activity causes synapse weakening/elimination (A firing, B not)

“CELLS THAT FIRE TOGETHER, WIRE TOGETHER”

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11
Q

Define Synaptic Potential

A

Depolarising/hyper-polarising potential die to activation of neurotransmitter receptors

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12
Q

Define EPSP

A

Excitatory post synaptic potential - measure of synaptic strength at excitatory synapse

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13
Q

Describe a study which shows the associativity of LTP

A

Nicoll et al (1998)

Tetanic stimulation of a weak input does not produce a high enough EPSP to fire the post-synaptic cell (No LTP occurs)

Tetanic stimulation of a strong input causes the post-synaptic cell to fire (resulting in LTP)

Tetanic stimulation of strong and weak inputs at the same time causes firing of the post synaptic cells and causes LTP in both strong and weak pathways

Example: Pavlovs dogs -
Strong signal = Food
Weak signal = Bell

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14
Q

State how LTD occurs

A

Generated by repetitive low frequency stimulation of input - results in persistently reduced synapse strength

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15
Q

Describe Bliss and Lomo’s 1973 study and it’s findings

A

To do later

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16
Q

Give the mechanisms of pre-synaptic plasticity

A

Probability of release
Filling of vesicle
Transmitter concentration in synaptic cleft

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17
Q

Describe the mechanism of retrograde messages in terms of synaptic plasticity

A

Signals that can diffuse out of the post synaptic terminal and influence activity of the pre-synaptic terminal
e.g. NO, CO, neutrophins

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18
Q

Give the mechanisms of post-synaptic plasticity

A

Insertion of new receptors

Gating of existing receptors

19
Q

Describe how Ca2+ is involved in short term plasticity

A

Paired paired pulse facilitation

Seen when two pulses are delivered in very quick succession (less than half a second apart). Pulse B results in higher excitation

Caused by residual Ca2+ in cell from pulse A. excitation is Ca2+ dependant

20
Q

Briefly describe the synaptic vesicle cycle

A

Filling, Docking -ATP-> Priming -Ca2+-> Exocytosis and fusion -Ca2+-> Endocytosis

21
Q

Describe and give examples of four types of protein required for the synaptic vesicle cycle

A

Glutamate Transporters - required for vesicle content (KO = decrease in neurotransmission)

Synapsins - mobilisation of synaptic vesicles

Rab3/RIM1 alpha - Docking and priming of vesicles

SNAREs, munc18 - Synaptic vesicle fusion

22
Q

Name the protein required for synaptic vesicle mobilisation and state how they are required.

A

Synapsins

Vesicles mobilised by synapsins which bind them to the actin cytoskeleton

23
Q

Describe the process of vesicle docking and name the proteins involved

A

Rab3 (“Passport of vesicle trafficking”) which is a GTPase

GDP bound form is inactive. GTP bound form binds to vesicle and binds an effector (RIM1) on the membrane. This allows docking.

Once exocytosis occurs, Rab3 is hydrolysed and released from the vesicle

24
Q

Explain the process of synaptic vesicle fusion

A

Uses SNARE proteins (Synaptobrevin - vesicle associated, Syntaxin - embedded in membrane, SNAP-25 - present on membrane, Synaptotagmin - vesicle associated)

Synaptobrevin, Syntaxin and SNAP-25 form coiled coil and energy from ‘zippering’ brings membranes together

Synaptotagmin mediated Ca2+ dependant process

Vesicle tethered by Rab3 which brings the vesicle into membrance, munc18 is removed from membrane SNARE complex (priming). Full SNARE complex forms on membrane - zippering allowed once Ca2+ has bound to synaptotagmin. Fusion occurs, NT released, NSF and SNAP disassemble (ATP dependant)

25
Describe studies to show the critical nature of synaptotagmin
Critical for Ca2+ dependence of vesicle fusion. Difficult to prove. KO mouse dies before birth (mutants in Ca2+ chelating Amino acids are lethal) Mutant in R233 amino acid in Ca2+ binding site (R233Q) reduces affinity of Ca2+ to synaptotagmin and also Ca2+ affinity of NT release
26
Describe the two types of neurotransmitter receptor
Ionotropic (Ligand gated ion channels) - NT binds, conformational change in channel helices, ions flow in. 'Fast' receptor Metabotropic (G-protein coupled) - NT binds, G protein a subunit binds to effector protein which send intracellular messages to ion channel. 'Slow' but potentially longer lasting
27
Give properties of NMDA and AMPA receptors
NMDA and AMPA: Tetrameric, homodimers, glutamate binds in M3, M4 loop, NMDA/AMPA looks similar glutamate (only binds its respective receptor) NMDA: Gates Ca2+ and Na+, D-AP5 is a blocker, in the absence of glycine the receptor does not function, Mg2+ block in the ion pore (voltage dependant, depolarisation removes Mg2+) AMPA: Gates primarily Na+ and sometimes Ca2+, NBQX is a blocker
28
Describe the Yeast 2 Hybrid Assay
Used to study protein-protein interactions Bait is protein of choice, go 'fishing' in solution of protein (i.e. mushed up brain) and pull out what binds to bait In post-synaptic setting - Get a transcription factor, split it in half, attach bait to one half and express the other half at the end of genes expressed in yeast, If they come together, transcription of the gene will occur
29
Give an advantage and disadvantage of using aplysia as a model organism
Adv: Neurons arranged in ganglia, cell bodies are large Dis: Relies on v. simple learning paradigms (i.e. tail shock, touching siphon)
30
Give the definition of habituation
Reduction of psychological or behavioural response occuring when a specific stimulus occurs repeatedly
31
Give the definition of sensitisation
The process of becoming susceptible to a given stimulus that previously had no effect or significance
32
Describe habituation in Aplysia
Touch siphon -> Gill withdrawal Gill withdrawal weaker after repeated stimulation of siphon
33
Describe sensitisation in Aplysia and give methods for long and short term sensistisation
Pairs electrical stimulation of tail with light touch of siphon Light touch of siphon -> Strong gill withdrawal Short term: Single tail shock and siphon touch lasts a few hours (post translational modification) Long term: Multiple trains of shocks ( 4 trains of 10 for four days) cause sensitisation to last days (requires structural changes at synapse - protein synthesis)
34
Describe how Habituation and sensitisation affects the neural circuitry of Aplysia
Habituation: Glutamate release by sensory neuron decreases - responsible for decrease in behavioural response Sensitisation: Serotonin is released from inter-neuron on to sensory neuron (skin) and enhances the action of glutamate (via PKA) (and skin sensory neuron)
35
Describe structural changes seen at Aplysia synapses after sensitisation
Synaptic bouton number increases/decreases during sensitisation/habituation (Long term only) Habituation decreases Sensitisation increases This requires gene expression and protein synthesis
36
Describe the effect of PKA on sensitisation
When serotonin is released from inter-neurons to to sensory neurons, PKA is activated. PKA activity increases NT release in sensory neuron PKA is required for short and long term sensitisation
37
Describe fear conditioning in rodents
Classical: Sound paired with aversive foot shock. Association of sound with shock - fear of sound. Extinction of fear requires exposure to sound with no shock Operant: Skinner box - reinforcement positive (food) /negative (electric shock). Rewarded behaviour is repeated
38
Describe spatial learning in rodents
Morris Water Maze - Hidden platform under water, rat must find platform - After 10 trials, rat goes straight to platform (WT) - Rats with hippocampal lesions do not improve (PPA damage) Latency, platform crossings and time spent in quadrants is measured Rodents use surrounding areas to orientate themselves (i.e. chairs, clocks). Move objects and they struggle to find platform Mutants in CREB struggle at improving with one trial per day, 4 trials per day see improvement similar to wild type
39
Briefly summarise short term plasticity
Dependant on Post-synaptic activation of AMPA receptors and NMDA receptors Ca2+ influs through AMPAR starts depolarisation. This removes the Mg2+ block in NMDAR. Ca2+ modulated signalling pathways (Calmodulin Kinase II and Proetin Kinase C) are initiated and substrate phosphorylation occurs, leading to the insertion of additional AMPA receptors
40
For long term plasticity to persist beyond 2 hrs...
...synaptic signalling pathways initiated at the synapse (kinases) are required effect changes in the nucleus
41
Give evidence that long term LTP requires gene transcription
in CA3:CA1 pathway, give multiple trains of 100Hz. Control shows normal long term LTP, Add actinomycin D (transcription inhibitor) or anisomycin (protein synthesis inhibitor) before tetanic stimulus and early LTP is demonstrated but late LTP is blocked Apply inhibitors after stimulus and it has no effect suggesting that gene expression changes are induced early
42
Give evidence that long term facilitation requires gene transcription
Simulation of pairing tail shock with gill withdrawal in Aplysia. Apply serotonin to cell (in bath) for 5 mins. Look at EPSP immediately after and 24 hrs later (response similar each time) . 5 doses of 5 mins spaced 15 mins apart of serotonin shows long term faciliation of the neuron. 24hrs later, there is a huge enhancement of the response (Application of actinomysin D or anisomycin at time of serotonin application blocks LTF)
43
Name some Immediate early genes (IEGs) and give the role
Regulatory genes (encode for TFs): c-fos, zif268, c-jun Effector IEGs: - Arc - protein involved in exocytosis of AMPA receptor - BDNF - Growth factor that alows synapse growth and can potentiate NT release - Homer1a - Scaffolding protein that links proteins in post synaptic density ALL ARE TARGETS OF CREB
44
Describe the action or Arc as an effector IEG
Associate with Endophilin and Dynemin - mediates AMPA receptor endocytosis Interacts with Wave3 (involved in actin remodelling) - possibly involved in structural plasticity of LTP

Biology (12 decks)

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