Presentation is loading. Please wait.

Presentation is loading. Please wait.

Chapter 13: Biology of Learning and Memory. Learning, Memory, Amnesia, and Brain Functioning An early influential idea regarding localized representations.

Similar presentations


Presentation on theme: "Chapter 13: Biology of Learning and Memory. Learning, Memory, Amnesia, and Brain Functioning An early influential idea regarding localized representations."— Presentation transcript:

1 Chapter 13: Biology of Learning and Memory

2 Learning, Memory, Amnesia, and Brain Functioning An early influential idea regarding localized representations of memory in the brain suggested physical changes occur when we learn something new. One popular idea was that connections grow between areas of the brain.

3 Learning, Memory, Amnesia, and Brain Functioning Ivan Pavlov researched classical conditioning in which pairing of two stimuli changes the response to one of them. –Presentation of a conditioned stimulus (CS) is paired with an unconditioned stimulus (UCS). –Automatically results in an unconditioned response (UCR). After several pairings, response can be elicited by the CS without the UCS, which is known as a conditioned response (CR).

4 Learning, Memory, Amnesia, and Brain Functioning In operant conditioning, responses are followed by reinforcement or punishment that either strengthen or weaken a behavior. –Reinforcers are events that increase the probability that the response will occur again. –Punishment are events that decrease the probability that the response will occur again.

5 Fig. 13-1, p. 385

6 Learning, Memory, Amnesia, and Brain Functioning Pavlov believed that conditioning strengthened connections between the CS center and UCS center in the brain. Karl Lashley set out to prove this by searching for such engrams, or physical representations of what had been learned. –Believed that a knife cut should abolish the newly learned response.

7 Fig. 13-2, p. 386

8 Learning, Memory, Amnesia, and Brain Functioning Lashley’s studies attempted to see if disrupting certain connections between cortical brain areas would disrupt abilities to learn associations. Found that learning and memory did not depend on connections across the cortex Also found that learning did not depend on a single area of the cortex.

9 Learning, Memory, Amnesia, and Brain Functioning Lashley proposed two key principles about the nervous system: Equipotentiality – all parts of the cortex contribute equally to complex functioning behaviors (e.g. learning) Mass action – the cortex works as a whole, not as solitary isolated units.

10 Learning, Memory, Amnesia, and Brain Functioning Modern day research by Richard F. Thompson and colleagues has suggested that the engram for classical conditioning is located in the cerebellum, not the cortex. During conditioning, changes occur in cells of one nucleus of the cerebellum called the lateral interpositus nucleus (LIP). However, a change in a brain area does not necessarily mean that learning necessarily took place in that area.

11 Fig. 13-4, p. 388

12 Learning, Memory, Amnesia, and Brain Functioning Suppression of activity in the LIP led to a condition in which the subject displayed no previous learning. As suppression wore off, the animal began to learn at the same speed as animals that had no previous training. But suppression of the red nucleus also led to a similar condition. Later assumed that the learning did occur in the LIP, as it was the last structure that needed to be awake for learning to occur.

13 Learning, Memory, Amnesia, and Brain Functioning Hebb (1949) differentiated between two types of memory: Short-term memory – memory of events that have just occurred. Long-term memory – memory of events from previous times.

14 Learning, Memory, Amnesia, and Brain Functioning Differences between STM and LTM –Short-term memory has a limited capacity; long-term memory does not. –Short-term memory fades quickly without rehearsal; long-term memories persist. –Memories from long-term memory can be stimulated with a cue/ hint; retrieval of memories lost from STM do not benefit from the presence of a cue.

15 Learning, Memory, Amnesia, and Brain Functioning Later research has weakened the distinction between STM and LTM. –Some memories do not qualify as distinctly short-term or long-term. Working Memory –Proposed by Baddeley & Hitch as an alternative to short-term memory. –Emphasis on temporary storage of information to actively attend to it and work on it for a period of time.

16 Learning, Memory, Amnesia, and Brain Functioning Three major components of working memory include: Phonological loop – Stores auditory input Visuospatial sketchpad – Stores visual input. Central Executive – Directs attention and determines which items to store.

17 Learning, Memory, Amnesia, and Brain Functioning The delayed response task is a test of working memory which requires responding to a stimulus that one heard or saw a short while earlier. Increased activity in the prefrontal cortex during the delay indicates storing of the memory. The stronger the activation, the better the performance.

18 Fig. 13-7, p. 394

19 Learning, Memory, Amnesia, and Brain Functioning Older people often have impairments in working memory. Changes in the prefrontal cortex assumed to be the cause. Declining activity of the prefrontal cortex in the elderly is associated with decreasing memory. Increased activity is indicative of compensation for other regions in the brain.

20 Learning, Memory, Amnesia, and Brain Functioning Amnesia is the loss of memory. Studies on amnesia help to clarify the distinctions between and among different kinds of memories and their mechanisms. Different areas of the hippocampus are active during memory formation and retrieval. –Damage results in amnesia.

21 Learning, Memory, Amnesia, and Brain Functioning Patient HM is a famous case study in psychology who had his hippocampus removed to prevent epileptic seizures. Afterwards Patient HM had great difficulty forming new long-term memories. STM or working memory remained intact. Suggested that the hippocampus is vital for the formation of new long-term memories.

22 Fig. 13-5ab, p. 391

23 Learning, Memory, Amnesia, and Brain Functioning Patient HM showed massive anterograde amnesia after the surgery. Two major types of amnesia include: Anterograde amnesia – the loss of the ability to form new memory after the brain damage occurred. Retrograde amnesia – the loss of memory events prior to the occurrence of the brain damage.

24 Learning, Memory, Amnesia, and Brain Functioning Patient HM had difficulty with declarative and episodic memory. –Episodic memory: ability to recall single events. –Declarative memory: ability to put a memory into words. Patient HM’s procedural memory remained intact. –Procedural memory: ability to develop motor skills (remembering or learning how to do things).

25 Learning, Memory, Amnesia, and Brain Functioning Patient HM also displayed greater “implicit” than “explicit” memory. Explicit memory – deliberate recall of information that one recognizes as a memory. Implicit memory – the influence of recent experience on behavior without realizing one is using memory.

26 Learning, Memory, Amnesia, and Brain Functioning Research in differences in hippocampus size has revealed conflicting results. Some evidence suggests that a smaller hippocampus is associated with better memory performance. –Hypothesis is that apoptosis improves hippocampus functioning. Generally, hippocampus activity is more associated with memory performance than is the size.

27 Learning, Memory, Amnesia, and Brain Functioning Research of the function of the hippocampus suggests the following: 1.The hippocampus is critical for declarative (especially episodic) memory functioning. 2.The hippocampus is especially important for spatial memory. 3.The hippocampus is especially important for configural learning and binding.

28 Learning, Memory, Amnesia, and Brain Functioning Research in the role of the hippocampus in episodic memory shows damage impairs abilities on two types of tasks: Delayed matching-to-sample tasks – a subject sees an object and must later choose the object that matches. Delayed non-matching-to-sample tasks– subject sees an object and must later choose the object that is different than the sample.

29 Fig. 13-7, p. 394

30 Learning, Memory, Amnesia, and Brain Functioning Damage to the hippocampus also impairs abilities on spatial tasks such as: Radial mazes – a subject must navigate a maze that has eight or more arms with a reinforcer at the end. Morris search task – a rat must swim through murky water to find a rest platform just underneath the surface.

31 Learning, Memory, Amnesia, and Brain Functioning Hippocampus damage also impairs configural learning and binding. –Configural learning – learning in which the meaning of a stimulus depends on what other stimuli are paired with it. –Animals with damage can learn configural tasks but learning is slow. Indicates hippocampus is not necessary for configural learning, but is involved.

32 Learning, Memory, Amnesia, and Brain Functioning Evidence suggests that the hippocampus is important in the process of “consolidation”. Consolidation is the process of strengthening short-term memories into long-term memories. Damage to the hippocampus impairs recent learning more than older learning. –The more consolidated a memory becomes, the less it depends on the hippocampus.

33 Learning, Memory, Amnesia, and Brain Functioning Reverberating circuits of neuronal activity were thought to be the mechanisms of consolidation. Consolidation is also influenced by the passage of time and emotions. –Small to moderate amounts of cortisol activate the amygdala and hippocampus where they enhance storage and consolidation of recent experiences. –Prolonged stress impairs memory.

34 Fig. 13-11, p. 398

35 Learning, Memory, Amnesia, and Brain Functioning Different kinds of brain damage result in different types of amnesia. Two common types of brain damage include: 1.Korsakoff’s syndrome 2.Alzheimer’s disease

36 Learning, Memory, Amnesia, and Brain Functioning Korsakoff’s syndrome – prolonged thiamine (vitamin B1) deficiency impedes the ability of the brain to metabolize glucose. Leads to a loss of or shrinkage of neurons in the brain. Often due to chronic alcoholism. Symptoms include apathy, confusion, and forgetting and confabulation (taking guesses to fill in gaps in memory).

37 Learning, Memory, Amnesia, and Brain Functioning Alzheimer’s disease is associated with a gradually progressive loss of memory often occurring in old age. Affects 50% of people over 85. Early onset seems to be influenced by genes, but 99% of cases are late onset. About half of all patients with late onset have no known relative with the disease.

38 Fig. 13-13, p. 401

39 Learning, Memory, Amnesia, and Brain Functioning Alzheimer’s disease is associated with an accumulation and clumping of the following brain proteins: Amyloid beta protein 42 which produces widespread atrophy of the cerebral cortex, hippocampus and other areas. An abnormal form of the tau protein, part of the intracellular support system of neurons.

40 Learning, Memory, Amnesia, and Brain Functioning Accumulation of the tau protein results in: –Plaques – structures formed from degenerating neurons. –Tangles – structures formed from degenerating structures within a neuronal body.

41 Learning, Memory, Amnesia, and Brain Functioning A major area of damage is the basal forebrain and treatment includes enhancing acetylcholine activity. One experimental treatment includes the stimulation of cannabinoid receptors that limits overstimulation by glutamate. Research with mice suggests the possibility of immunizing against Alzheimer’s by stimulating the production of antibodies against amyloid beta protein.

42 Learning, Memory, Amnesia, and Brain Functioning Lessons from studying amnesiac patients include: –There can be deficiencies of very different aspects of memory. –There are independent kinds of memory. –Various kinds of memory depend on different brain areas.

43 Storing Information in the Nervous System (con’t) Activity in the brain results in physical changes. Patterns of activity leave a path of physical changes. Not every change is a specific memory as was once originally believed.

44 Storing Information in the Nervous System A Hebbian synapse occurs when the successful stimulation of a cell by an axon leads to the enhanced ability to stimulate that cell in the future. –Increases in effectiveness occur because of simultaneous activity in the presynaptic and postsynaptic neurons. –Such synapses may be critical for many kinds of associative learning.

45 Storing Information in the Nervous System Studies of how physiology relates to learning often focus on invertebrates and try to generalize to vertebrates. The aplysia is a slug-like invertebrate that is often studied due to its large neurons. This allows researchers to study basic processes such as: –Habituation. –Sensitization.

46 Storing Information in the Nervous System Habituation is a decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli. –Results in a change in the synapse between the sensory neurons and the motor neurons. –Sensory neurons fail to excite motor neurons as they did previously.

47 Storing Information in the Nervous System Sensitization is an increase in response to a mild stimulus as a result to previous exposure to a more intense stimulus. Changes at identified synapses include: –Serotonin released from a facilitating neuron blocks potassium channels in a presynaptic neuron. –Prolonged release of transmitter from that neuron results in prolonged sensitization.

48 Storing Information in the Nervous System Long-term Potentiation (LTP) occurs when one or more axons bombard a dendrite with stimulation. –Leaves the synapse “potentiated” for a period of time and the neuron is more responsive.

49 Storing Information in the Nervous System Properties of LTP that suggest it as a cellular basis of learning and memory include: –Specificity –Cooperativity –Associativity

50 Storing Information in the Nervous System –Specificity – only synapses onto a cell that have been highly active become strengthened. –Cooperativity – simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by a single axon. –Associativity – pairing a weak input with a strong input enhances later responses to a weak input.

51 Storing Information in the Nervous System Long-term depression (LTD) is a prolonged decrease in response at a synapse that occurs when axons have been active at a low frequency. –The opposite of LTP

52 Storing Information in the Nervous System Biochemical mechanisms of LTP are known to depend on changes in glutamate synapses primarily in the postsynaptic neuron This occurs at several types of receptor sites including the ionotropic receptors: –AMPA receptors. –NMDA receptors.

53 Fig. 13-21, p. 409

54 Storing Information in the Nervous System LTP in hippocampal neurons occurs as follows: –Repeated glutamate excitation of AMPA receptors depolarizes the membrane. –The depolarization removes magnesium ions that had been blocking NMDA receptors. –Glutamate is then able to excite the NMDA receptors, opening a channel for calcium ions to enter the neuron.

55 Storing Information in the Nervous System –Entry of calcium through the NMDA channel triggers further changes. –Activation of a protein that sets in motion a series of events occurs. –More AMPA receptors are built and dendritic branching is increased. These changes increase the later responsiveness of the dendrite to incoming glutamate.

56 Storing Information in the Nervous System Changes in presynaptic neuron can also cause LTP. Extensive stimulation of a postsynaptic cell causes the release of a retrograde transmitter that travels back to the presynaptic cell to cause the following changes: –Decrease in action potential threshold –Increase neurotransmitter release of –Expansion of the axons. –Transmitter release from additional sites.

57 Storing Information in the Nervous System LTP changes behavior by creating changes in multiple synapses and complex networks of neurons. Understanding the mechanisms of changes that enhance or impair LTP may lead to drugs that improve memory. –Example: Mice with genes that cause abnormalities in the NMDA receptor learn slowly and extra NMDA receptors result in faster learning.


Download ppt "Chapter 13: Biology of Learning and Memory. Learning, Memory, Amnesia, and Brain Functioning An early influential idea regarding localized representations."

Similar presentations


Ads by Google