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Janelle Leboutillier

PSYB64: Introduction to Physiological Psychology Lecture 9: Learning and Memory (Chapter 12) Chapter Exclusions  Not responsible for: o Classical conditioning in vertebrates pages 348 to 351 o Biochemical factors in long term memory pages 366 to 368 o You need to know LTP pages 358 to 361 only to the extent it is covered in lecture Overview  Learning o Types of Learning o Using Invertebrates to Study Learning o Classical Conditioning in Vertebrates  Memory o Types of Memory o Brain Mechanisms in Memory o Effects of Stress and Aging Learning  A relatively permanent change in behavior due to experience  Types of Learning o Associative and nonassociative learning o Habituation and Sensitization  Types of nonassociative learning that do not involve forming a connection between two elements or events o Classical Conditioning  Is a type of associative learning that does involve forming a connection between two elements or events. Remember your Intro Psych  Habituation occurs when an organism reduces its response to a repeated stimulus. Often habituation occurs to unchanging, harmless stimuli as a means of focusing our attention on relevant stimuli. o An example is when you do not notice trucks and cars driving by outside while you are studying  Sensitization occurs when an exposure to a strong stimulus actually heightens an organism’s overall level of response to other environmental stimuli o An example is when you blackout (a strong sensory stimulus) causing sensitization (learning to intensify your response to all stimuli)  Classical Conditioning o Pavlov and the canine digestive system. o Classical conditioning occurs when an organism learns that stimuli may act as signals that predict the occurrence of other important events. o Typically, classical conditioning involves the pairing of an unconditioned stimulus (UCS), which elicits an innate unconditioned response (UCR), with a neutral stimulus called the conditioned stimulus (CS) that is not innately associated with the UCS and UCR. o The UCS and CS pairing may only need to occur once for some types of learning such as conditioned taste aversions, but often require multiple pairings in order to form an association between the CS and the UCR. o When the unconditioned response behavior can be elicited by presenting the CS in absence of the UCS then the response is called a conditioned response (CR) Learning  Using Invertebrates to Study Learning (very simple neural network) o Sea slug Aplysia californica o Habituation in Aplysia  Gill withdrawal reflex  Reduced activity at synapse between sensory and motor neurons o Sensitization in Aplysia  A stimulus gains the ability to influence more than one neural pathway  Increased neurotransmitter release by sensory neuron o Classical Conditioning in Aplysia  Sequential activation of sensory neurons by CS and UCS leads to greater neurotransmitter release. The Dissection of Aplysia (Figure 12.3)  Major anatomical features involved with learned responses  Siphon = excretes waste  Mantle = sensitive area near gill  Gill = fully extended or withdrawn The Dissection of Aplysia (Figure 12.3)  Many learned responses involve neurons in the abdominal ganglion  P9 is the largest nerve serving the tail. Habituation and Sensitization in Aplysia (Figure 12.4) Habituation and Sensitization in Aplysia (Figure 12.4)  The Aplysia demonstrates habituation of the gill-withdrawal reflex in response to repeated stimulation of the sensory receptors in the siphon (Figure 12.4a)  As shown in Figure 12.4b, the habituation behaviour was a direct result of the release of less neurotransmitter at the synapse between the sensory and motor neurons  Sensitization in Aplysia: following an electric shock stimulates to the head or tail, there is an increase in the gill- withdrawal reflex in response to touching the siphon Structural Changes in Synapses Result from Learning (Figure 12.5)  Bailey and Chen (1983) counted the number of axon terminals found on sensory neurons following sensitization and habituation  Habituation reduced the number of terminals, whereas sensitization increased the number of terminals. In animals undergoing sensitization, the motor neuron dendrites also showed signs of modification.  Habituation reduces the # of terminals whereas sensitization increases the #  The animals that had undergone sensitization training showed the highest numbers of terminals, 2,800, compared with 1,300 for the control animals and only 800 in the animals that had undergone habituation training  In sensitized animals, the dendrites of the motor neurons were also modified to accommodate the increased number of presynaptic elements  These structural changes appear to involve actin, a protein that makes up the microfilaments of the cytoskeleton Classical Conditioning in Aplysia (Figure 12.6)  Touching the siphon (CS−) is not paired with shock and serves as a control  (b) Touching the mantle (CS+) is always followed by shock to the tail (UCS)  (c) After several pairings of touching the mantle (CS+) followed by shock (UCS), touching the mantle alone now triggers gill withdrawal (CR)  In the circled area in (b), the mantle shelf sensory neurons are sequentially activated, first by touching the mantle shelf and then by input from inter-neurons serving the tail  This sequence produces increased presynaptic facilitation, leading to the recording of greater postsynaptic potentials in the motor neuron than those recorded prior to training Atkinson-Shiffrin Model of Memory (Figure 12.11)  According to the information processing model proposed by Atkinson and Shiffrin, information is processed in a sequence of steps  The sensory memory holds large quantities of information for several seconds.  Short-term memory holds limited quantities of information for limited periods of time  Long-term memory can hold unlimited amounts of information for unlimited periods of time  Information that does not move to the next stage for processing will be permanently lost  Information Processing Model  Provides a helpful framework for thinking about memory and predicting the participation of different brain structures Types of Long-Term Memory (Figure 12.12) Memory  Brain Mechanisms in Memory  Early Efforts to Locate Memory Functions o Lashley – engram o Penfield– Recordings during surgery  Noted experiental responses to temporal lobe stimulation  Temporal Lobe and Memory o H.M.’s anterograde amnesia o The delayed nonmatching to sample (DNMS) test Karl Lashley Observed the Results of Brain Lesions on Maze-Learning Performance (Figure 12.13)  Lashley trained rats to run a maze and then performed brain lesions on them  (b) As larger amounts of cortex were damaged, errors in running the maze increased Trapped in the Eternal Now : Introducing HM  HM  Henry, but know as HM  Suffered from epileptic seizures since the age of 16  Condition became steadily worse and could not be controlled by medication  Had to stop work at age 27  Symptoms indicated that the seizures began in the medial basal regions of both temporal lobes  1953 neurologist removed this tissue, including much of the amygdala and HC bilaterally  Upon recovery, H.M. seizures were milder and could be controlled by medication  He suffered moderate retrograde amnesia (loss of memory for events that occurred shortly before brain damage, i.e. he had difficulty retrieving memories that had formed during the 10 years before the operation) and severe anterograde amnesia (loss of LT memories for events that happened after brain damage) Anterograde Amnesia (Figure b below)  Loss of memories for events that happened after brain damage  Inability to retain new material for more than a brief period Retrograde Amnesia (See Fig a below)  Loss of memory for events that occurred shortly before brain damage  Not rare after damage Surgical Removal of Temporal Lobe Tissue in Patient H.M. (Figure 12.14)  To control life-threatening seizures, patient H. M. underwent surgery that removed the hippocampus, amygdala, and part of the association cortex from both temporal lobes  These MRI scans compare a typical control participant with patient H. M.  You can see that H. M. has some hippocampus (H) but no entorhinal cortex (EC). In this image, (V) r
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