Chapter 14 - Chapter 14 Chapter 14 Relational Learning and...

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Unformatted text preview: Chapter 14 Chapter 14 Relational Learning and Amnesia Human Anterograde Amnesia Human Anterograde Amnesia Anterograde amnesia ­ difficulty in learning new information, due to head injury or certain degenerative brain diseases; pure form is rare Retrograde amnesia – inability to remember events that occurred prior to brain damage Korsakoff’s syndrome – permanent anterograde amnesia caused by brain damage resulting from chronic alcoholism or malnutrition (due to thiamine deficiency); also have confabulations (reporting of memories that did not occur, without the intention to deceive) Anterograde amnesia can be caused by damage to temporal lobes – e.g. patient H.M. – bilateral removal of medial temporal lobe to alleviate epilepsy; resulted in severe anterograde amnesia Human Anterograde Amnesia Human Anterograde Amnesia – Basic description Results from study with H.M. 1. 2. 3. These results are too simple; anterograde amnesia is actually much more complex Learning consists of at least 2 stages: The hippocampus is not the location of long­term memory (LTM); nor is it necessary for the retrieval of LTM The hippocampus is not the location for short­term memory (STM) The hippocampus is involved in converting STM into LTM STM – immediate memory for events, which may or may not be consolidated into LTM; can only hold a limited amount of info LTM – relatively stable memory of events that occurred in the more distant past, as opposed to STM; no limit on amount of info Consolidation – the process by which STM are converted into LTM Simple model of memory process Simple model of memory process Sensory info enters STM Rehearsal keeps that info in STM Eventually, info will move into LTM via consolidation Human Anterograde Amnesia Human Anterograde Amnesia Spared learning abilities – Still capable of: Perceptual learning – e.g. recognize broken drawings; also faces and melodies Stimulus­response learning – Can acquire a classical conditioned eyeblink response Motor learning – Mirror drawing task – subjects required to trace the outline of a figure while looking at the figure in a mirror Human Anterograde Amnesia Human Anterograde Amnesia Declarative and nondeclarative memories – Although patients can learn other tasks, they cannot recall ever learning them – Learning and memory involve different processes – 2 major categories of memories Declarative memories – memory that can be verbally expressed, such as memory for events, facts, or specific stimuli; this is impaired with anterograde amnesia Nondeclarative memories – memory whose formation does not depend on the hippocampal formation; a collective term for perceptual, stimulus­ response, and motor memory; not affected by anterograde amnesia; these control behavior; cannot always be described in words Human Anterograde Amnesia Human Anterograde Amnesia Failure of relational learning – Verbal learning is disrupted in anterograde amnesia e.g. H.M. did not learn any new words after his surgery (biodegradable = “two grades”) – Episodic memories – most complex form of declarative memory; memory of a collection of perceptions of events organized in time and identified by a particular context e.g. explain what you did this morning after waking up – The hippocampal formation enables us to learn the relationship b/t the stimuli that were present at the time of an event (i.e. context) and then events themselves Human Anterograde Amnesia Human Anterograde Amnesia Anatomy of anterograde amnesia – Damage to the hippocampus or to regions that supply its inputs and receive its outputs causes anterograde amnesia – The most important input to the hippocampal formation is the entorhinal cortex, which receives inputs from the limbic cortex either directly or via the perirhinal cortex or the parahippocampal cortex – How does the hippocampus form new declarative memories? Hippocampus receives info about what is going on from sensory and motor assc. cortex and from some subcortical regions It processes this info and then modifies the memories being consolidated by efferent connections back to these regions Experiences that lead to declarative memories activate the hippocampal formation – Patient R.B., suffered brain damage that lead to anterograde amnesia; after autopsy, found that field CA1 of the hippocampal formation was completely destroyed Limbic cortex Limbic cortex Human Anterograde Amnesia Human Anterograde Amnesia Anatomy of anterograde amnesia – Damage to other subcortical regions that connect with the hippocampus can cause memory impairments Limbic cortex of the medial temporal lobe – Semantic memories – a memory of facts and general info; different from episodic memory – Destruction of hippocampus alone disrupts episodic memory only; must have damage to limbic cortex of medial temporal lobe to also impair semantic memory (and thus all declarative memory) Fornix and mammillary bodies – Patients with Korsakoff’s syndrome suffer degeneration of the mammillary bodies – Most of the efferent axons of the fornix terminate in the mammillary bodies – Damage to any part of the neural circuit that includes the hippocampus, fornix, mammillary bodies and anterior thalamus cause memory impairments Human Anterograde Amnesia Human Anterograde Amnesia Role of the medial temporal lobe in spatial memory – Individuals with anterograde amnesia are unable to consolidate info about the location of rooms, corridors, buildings, roads, and other important items in their env’t – Bilateral medial temporal lobe lesions produce the most profound impairment on spatial memory, but enough damage to only the R hemisphere is sufficient – R hippocampal formation is activated when a person is remembering or performing a navigational task – Damage to this area also impairs ability to learn spatial arrangement of objects Human Anterograde Amnesia Human Anterograde Amnesia Role of the medial temporal lobe in memory retrieval – The hippocampal formation and its related structures also play a role in memory retrieval – Anterograde amnesia is usually accompanied by retrograde amnesia; brain damage can either cause loss of memories or loss of access to memories – However, if damage is only limited to field CA1, patients do not show additional retrograde amnesia – Semantic dementia – loss of semantic memories caused by progressive degeneration of the neocortex of the lateral temporal lobes Impairment for meaning of words, and functions of common objects Human Anterograde Amnesia Human Anterograde Amnesia Confabulation – May be a result of disruption of the normal functions of the prefrontal cortex – Frontal lobes may be involved in distinguishing b/t real and imaginary memories; may do this by helping us to distinguish items with general familiarity from specific items we have encountered before Relational learning in lab animals Relational learning in lab animals Lab animals with hippocampal formation lesions do not sow impairment in stimulus­response learning, but with relational learning tasks Remembering places visited – Radial maze task – food placed at end of each arm, rats did not go down arm that they had already collected food from; lesions to hippocampus, fornix, or entorhinal cortex impaired this task; animals must remember which arm they have collected from that exact day (as opposed to another testing day) Relational learning in lab animals Relational learning in lab animals Spatial perception and learning – Lab animals with hippocampal lesions show problems with navigational tasks just as humans do – Morris water maze task – requires rat to find a particular location in the water drum, by means of visual cues external to the apparatus; if rats wit hippocampal lesions are released from same position every testing time, they perform fine (e.g. S­R learning), but if they are started from a different place, they cannot complete the task correctly (e.g. relational learning) Relational learning in lab animals Relational learning in lab animals Spatial perception and learning – Hippocampal lesions disrupt performance of homing pigeons – Hippocampal formation of animals that normally store seeds or food in hidden caches and later retrieve them is larger than that in animals without this ability Role of hippocampal formation in memory consolidation – Brain activity in the hippocampus is increased in mice learning a spatial task; however, after 25 days of testing, the activity there decreases, suggesting that the hippocampus is involved in consolidating spatial memories for only a limited time Relational learning in lab animals Relational learning in lab animals Place cells in the hippocampal formation – When recording the activity of individual neurons in the hippocampus of an animals moving around its env’t, some neurons fired at a high rate only when the rat was in a particular location – The suggests evidence that different neurons have different spatial receptive fields (i.e. they responded when the animals were in different locations) – these neurons were named place cells – When placed on a circular platform that is rotated slowly within a larger chamber, rats will ignore local cues and orient themselves to face a cue card; the place cells however, oriented themselves to the local cues – When animals encounter new env’ts, they learn the layout and “maps” become established in their hippocampus; an animal’s location within each env’t is encoded by the pattern of firing of these neurons – Place cells are guided by both visual stimuli and internal stimuli (e.g. proprioceptive feedback) – Hippocampus receives spatial info via the entorhinal cortex Relational learning in lab animals Relational learning in lab animals Role of LTP in relational learning – When place cells become active when an animal is present in a particular location, this causes changes in the excitability of neurons in the hippocampal formation – Knockout mice for NMDA receptors specific for the field CA1: no establishment of LTP in field CA1, smaller and less focused spatial receptive fields, and learn Morris water maze task much slower – NMDA mediated LTP appears to be required for the consolidation of spatial receptive fields in field CA1 pyramidal cells but not their short­ term establishment Modulation of hippocampal functions – Hippocampal formation receives input from ACh, NE, DA, and5­HT neurons – They appear to control the information­processing functions of the hippocampal formation – 5­HT has suppressive effect on establishment of LTP in hipp. form. Relational learning in lab animals Relational learning in lab animals Modulation of hippocampal functions (con’t) – NE has a facilitator effect, particularly on synapses of terminals of entorhinal neurons of the dentate gyrus – DA had excitatory effects on LTP and memory­related functions of the hippocampal formation Synaptic plasticity is induced by simultaneous depolarization of hippocampal neurons and activation of DA receptors on these neurons – ACh neurons from medial septum project to hippocampus via fornix; activity of these neurons is responsible for hippocampal theta rhythms (medium amplitude, medium frequency waves) that influence the establishment of LTP in the hippocampus If theta activity is disrupted, animals show deficits in learning tasks that are affected by hippocampal lesions Theta behaviors – exploration or investigation Nontheta behaviors – alert immobility, drinking, self­directed behaviors ...
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