Brain Behavior Exam 4 Orenda Johnson Learning and Memory Engram o It s a physical representation of a memory o In Lashley s experiment of looking for the engram he trained rats and then cut or lesioned certain areas of the cortex When cutting the cortex there was no significant effect on performance Lesions on the other hand did affect performance The bigger the lesion the greater the impairment Location didn t matter o His critical mistakes in looking for the engram were assuming that Memory is in discrete regions of cortex All memories are physiologically the same o A type of long term memory that is important for remembering events and knowing facts o The hippocampus nearby cortical areas and medial diencephalon are Explicit memory important with this type of memory Implicit memory o A type of long term memory that is important for Skills and habits located in the striatum motor areas of cortex and cerebellum Emotional associations located in the amygdala Conditioned reflexes located in the cerebellum Differences between o Short term working memory Small capacity Fades quickly unless rehearsed Once forgotten it s gone The dorsolateral prefrontal cortex is important for working memory o Long term memory Infinite capacity Lasts indefinitely Could be forgotten and then later remembered with Henry Molaison appropriate cues o Doctors removed much of his temporal lobe including the hippocampus This resulted in anterograde amnesia o He lost declarative explicit memory and spatial memory o He retained his procedural implicit memory and working memory though Hippocampus and memory o It s active during the formation of memories and during recall o Important for the consolidation of declarative explicit memory transferring from STM LTM o Spatial memory increased activity in the hippocampus when doing a spatial task like imagining the best route to take Other brain regions that are important for memory o Cerebellum Learning a conditioned response Motor learning skills and other cognitive stuff If damaged you can t spontaneously elaborate on memories Damage causes semantic dementia which is a loss of factual o Parietal lobe o Temporal lobe knowledge o Prefrontal cortex Learning reward and punishment Also works has to do with working memory Hebbian synapse a synapse that increases in effectiveness due to repeated and persistent activity in presynaptic and postsynaptic neurons o In other words when an axon successfully stimulates a cell it will be even more successful in the future The synapse gets strengthened Long term potential LTP o It s a burst of stimulation from axons o Glutamate receptors are necessities This includes AMPA and NMDA receptors In terms of LTP o Cooperativity simultaneous stimulation by two or more axons results in LTP more strongly than repeated stimulation by 1 axon o Specificity only active synapses become strengthened o Associativity pairing a weak input with a strong input enhances a future response to the weak input o Classical conditioning depends on the associative nature of LTP because of how an unimportant stimulus acquires properties of an important one through pairing Example conditioning an eye to blink in response to a tone Presynaptic changes that occur in LTP o Stimulation of the postsynaptic cell releases a retrograde transmitter that feeds back to the presynaptic cell It increases presynaptic release of neurotransmitter and the production of GAP 43 which facilitates the growth of axons Postsynaptic changes that occur in LTP o Ionotropic glutamate receptors open channels in postsynaptic neurons to let in one or more kinds of ions Evidence of a functional connection between LTP and actual learning o Abnormal NMDA receptors impair learning o Drugs that block LTP block retention of learned material o Drugs that facilitate LTP facilitate learning o LTP increases certain proteins and blocking those proteins weakens memories Alzheimer s Disease and Other Dementias Impairment in memory Decreased ability to relate function at home work or social Symptoms of dementia o Cognitive settings o Non cognitive Delusions Suspicions Hallucinations Agitation Depression The 4 A s of dementia o Amnesia the loss of memory working memory first o Agnosia loss of ability to recognize objects o Apraxia loss of knowledge about how to do things o Aphasia loss of speech Symptoms of Alzheimer s Disease AD o Problems with explicit and implicit memory Better procedural than declarative memory o Gradual progression to more serious memory loss and Language problems Confusion Depression Hallucinations Loss of appetite o Sun downing a disturbance in the circadian rhythm o End stage is usually coma and death is usually caused by an infection Types of AD o Early onset Found in people under 40 years old Only about 1 10 of people with AD A mutation of the gene for APP on chromosome 21 can cause it Mutations of the gene for presenilin can increase risk o Late onset Found in people over 60 years old Found in 5 of people between 65 74 years old Found in 50 of people over 85 years old Mutations in the gene for Apolipoprotein ApoE4 which probably helps break down beta amyloid increases risk by itself Half of patients have no known relative with AD so health lifestyle and age are factors o Early onset AD has a stronger genetic contribution Characteristics of an Alzheimer s Disease brain o Brain atrophy Loss of neurons Loss of spines and synapses o Proteins fold abnormally clump and interfere with neuronal activity Plaques Tangles o Found outside of cells o Formed by beta amyloid aka A beta o Found inside of cells o Formed by an abnormal form of the intracellular protein Tau Treatment options for AD o Drugs that stimulate Acytylcholine receptors or prolong Ach release o Partial NMDA receptor antagonists to slow excitotoxic damage of Ach neurons o NSAIDs to reduce inflammation that could be caused by plaques o Antioxidants Curcumin found in turmeric reduces amyloid deposits and tau hyper phosphorylation o Immunization to produce antibodies against beta amyloid Resulted in life threatening side effects though so research was stopped Korsakoff s Syndrome o Caused by a prolonged thiamine vitamin B1 deficiency Usually in alcoholics or someone with a poor diet o Symptoms Similar to damage to the prefrontal cortex Apathy and confusion Retrograde and anterograde amnesia Having better implicit than explicit memory Difficulty reasoning through memories For example which event happened first Confabulation
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