Flashcards in Nondeclarative memory Deck (25):
What is the simplest case of nondeclarative memory? Name 3 measures of it which can be used
Habituation which allows us to ignore a large number of irrelevant, unimportant and familiar stimuli in the world. Reduced visual fixation time, reduced heart rate, reduced respiratory rate
Simple animals can habituate to biologically IRrelevant stimuli. Give an example of such animals. Which 2 parts of them habituate? How is this measured?
Aplysia. The withdrawal response of the aplysia's gill and syphon as a result of being tickled. Microelectrode recordings also reveal reduced neural firing as the tickle becomes familiar
Describe the layout of the siphon neuron, interneuron, gill and siphon neural circuit in aplysia. What changes in the excitatory APs recorded in the IN and MN are observed after habituation?
The SN is connected to an IN and 2 MNs. One of the MNs is connected to the gill and the other is connected to the siphon. The IN connects to both MNs. There is also a SN-siphon connection. Weaker IN and MN post synaptic potentials. This synaptic depression lasts for as long as the behavioural habituation
What causes habituation in aplysia at the presynaptic terminal?
Reduced fusing of vesicles to the presynaptic membrane and resultant reduced neurotransmitter release
If the SN is stimulated once, how long does habituation and reduced neurotransmitter release last? If the SN is stimulated several times, how long does habituation last? To achieve LT habituation of > 1 week, how many stimulations are required?
Several minutes, 10-15 minutes, 10 stimulations/ day
How is LT habituation caused at the neural level?
Synaptic pruning, including the inactivation of connections and structural changes
Name 4 differences between habituation and sensitisation
H: decrease in synaptic strength, S: increase in synaptic strength
H: learning about benign stimuli, S: learning about noxious stimuli
H: a response is made to the same stimulus which was presented, S: a response is made to stimulus A as a result of presenting noxious stimulus B. H: homosynaptic, S: heterosynaptic
How does short term sensitisation work in aplysia?
Serotonin binds to metabotropic Rs, activating the G protein & the enzyme adenylyl-cyclase. This activates cAMP. This activates protein kinase A. This enhances vesicle mobilisation & release and closes K+ channels to prolong APs at the PREsynaptic terminal
What are the main differences between ionotropic and metabotropic Rs?
Duration of the effect, the presence of ion channels or not which undergo a conformational change or not, activation of G proteins and 2nd messengers or not. N.B. metabotropic Rs still cause K+ and Ca2+ channels to open eventually
Describe in brief the sequence of AP transmission across a synapse
AP arrives, Ca2+ channels open, vesicle fusion, transmitter release, postsynaptic channels open, Na+ floods in
How is LT sensitisation mediated in aplysia?
Through synaptic growth. A protein called CREB activates genes which initiate growth
Aplysia show withdrawal responses to classically conditioned stimuli. What is the presynaptic mechanism responsible for such?
Arrival of an AP (from the neutral stimulus) opens Ca2+ channels at the presynaptic terminal. Ca2+ binds to calmodulin. This makes adenylyl cylase more effective which catalyses cAMP production. This activates PKA. This leads to more transmitter release IF a serotonin signal (from the US) arrives from an IN soon after
What is the postsynaptic mechanism responsible for classical conditioning in aplysia?
Na+ entry - after transmitter binding to AMPA Rs - depolarises the postsynaptic membrane, which unblocks the NMDA R by removing Mg2+. This enables Ca2+ entry
Order "behaviour", "circuit" and "physiology" in terms of which was specified first to last in the case of nondeclarative memory in aplysia and LTP-mediated declarative memory
Nondeclarative: behaviour, circuit, physiology
Declarative: physiology, circuit, behaviour
According to studies on rabbits which neural structure is important for learning & retention of EBCC (eye-blink classical conditioning)?
The cerebellum and not the hippocampus
What is perceptual learning?
The ability to learn about the sensory qualities of stimuli and as a result make finer distinctions between similar stimuli with repeated exposure
How can perceptual learning be demonstrated at a behavioural level?
Stimuli which have benefited from perceptual learning support especially rapid learning in subsequent associative learning tasks
How is the behavioural finding re: the perceptual learning of stimuli explained by psychological and physiological theories?
Psychological theories: the associations learnt latch onto stimuli elements which make the stimuli most discriminable I.e. strong associations are formed between unique features, whilst inhibitory associations are formed between shared features. Physiological theories: expansion of cortical representations
How does Gaffan (1996) refute the psychology theory's explanation of perceptual learning?
By finding that macaques can learn to discriminate not only between similar scenes but also between similar colours and e.g. different shades of blue cannot have unique "elements". N.B. this study also found that perceptual learning about red generalises to blue!
Give 2 pieces of evidence for perceptual learning at the physiological level in terms of expanded cortical representations
1) expanded representations of digits in the somatosensory cortex of owl-monkeys after learning
2) expanded representations of the reading finger in the somatosensory cortex of Braille readers
Hippocampal lesion patients show intact perceptual learning for ___ but disrupted perceptual learning for ___ (Graham, 2006). This suggests the MTL does perform some nondeclarative memory tasks in a ___-___ manner
Faces. Scenes. Domain-specific
Name 2 types of patient who DO show impairments on perceptual motor skill learning in the serial RT task. Who shows little vs. no reduction in RTs across trials? Which block contained the random pattern of asterisk presentation?
Parkinson's disease and cerebellum degeneration patients. PD patients show a little learning. CD patients show no learning (Pascual-Leone, 1993). Block 6
Why is the problem of circular reasoning when applied to defining declarative memory?
Declarative memory has been defined by Squire as referring to any type of memory which is impaired as a result of a MTL lesion. But some types of nondeclarative memory are impaired by MTL lesions e.g. HM is impaired at 10-pair, habit, concurrent discrimination learning
Can HM's habit learning deficit be explained by Squire?
Not unless he refers to non-MTL damage as the cause