Ch 11: Learning, Memory & Amnesia Part 2

Amnesia after Concussion Concussions are the #1 cause of amnesia Posttraumatic amnesia (PTA) Coma: pathological state of unconsciousness Can last seconds to weeks… After regaining consciousness, there is a period of confusion Usually there is permanent retrograde amnesia for events just prior to the blow to the head & permanent retrograde amnesia for the subsequent period of confusion With amnesia, there are sometimes surviving memories for isolated events: islands of memory

Memory Consolidation The fact that concussions disrupt recent memories more than older ones suggests that the older ones have been strengthened Hebb’s theory of consolidation Memories are stored in STM by reverberating in closed circuits If this is disrupted ex: by a blow to the head, the memory can be lost But normally the recirculating STM will cause structural changes in the synapse, providing stable place to store it as LTM Electroconvulsive shock (ECS) used to study consolidation by interrupting this reverberation Mixed results; doesn’t explain long gradients of amnesia; consolidation can continue potentially indefinitely

Hippocampus & Consolidation Standard consolidation theory Memories are temporarily stored in the hippocampus until they are transferred to cortical storage Multiple-trace theory Hippocampus & other memory storage areas store the memories as long as they exist but over time, they become more resistant to disruption Each time a similar experience occurs, the original memory is recalled & creates a new engram (change in the brain that stores a memory), which is linked to the original engram, making it stronger Accounts for long gradients of retrograde amnesia

Reconsolidation Theory that each time a memory is retrieved from LTM, it is temporarily held in STM and is once again susceptible to amnesia until it is reconsolidated Some evidence suggests not all types of memories are susceptible to reconsolidation

Neuroanatomy of Object-Recognition Memory Lesion studies to determine neuroanatomy of memory Object-recognition memory tested with delayed nonmatch-to-sample test Rhinal cortex: cortical area adjacent to the hipppocampus & amygdala; one of the 3 major temporal lobe structures Lesions of this area caused serious deficit in object recognition memory 2 areas: entorhinal cortex & perirhinal cortex Hippocampal lesions only caused moderate deficits Pyramidal cells of the CA1 region seem to be the key to hippocampal involvement in this kind of memory

Hippocampus & Spatial Memory While hippocampal lesions have little/no effect on general memory, they consistently impair memory of spatial location Many hippocampal neurons are place cells Neurons that respond only when a subject is in specific locations Grid cells: neurons in the rhinal cortex that have an array of evenly spaced place fields

Hippocampus & Spatial Memory Birds that cache food have larger hippocampi than other species Cognitive map theory There are several systems in the brain each specialized in memory for different kinds of info; the hippocampus is for spatial memory There are criticisms of this theory

Where are memories stored? While the hippocampus & rhinal cortex are involved in memory, memories are not necessarily stored there Memories are stored diffusely in the brain Can survive the destruction of one specific area Memories become more resistant to disruption over time Memories appear to be stored in the brain areas that participated in the original experience that created the memory

Where are memories stored? So far we’ve discussed 4 brain areas with some memory storage Hippocampus (spatial) Perirhinal cortex (object) Mediodorsal nucleus (Korsakoff’s) Basal forebrain (Alzheimer’s) 5 more to discuss Inferotemporal cortex Amygdala Prefrontal cortex Cerebellum Striatum

Inferotemporal Cortex Involved in visual perception of objects & thought to participate with the perirhinal cortex in storing memories of visual patterns In general, areas of 2ndary sensory cortex play a role in storing sensory memories

Amygdala Role in memory for the emotions tied to an experience Ex: the fear that goes along with a foot shock Doesn’t seem to store the memory itself It is involved in strengthening emotionally significant memories stored elsewhere Explains why you are better at remembering emotion-provoking experiences

Prefrontal Cortex Damage to this area does not cause major amnesia & patients often perform well on traditional memory tests However, damage to the PFC does seem to impair 2 episodic memory abilities The order of events Working memory (ability to maintain relevant memories while a task is being completed)

Cerebellum & Striatum Implicit memories of sensorimotor learning presumed to be stored in the sensorimotor circuit associated with first experiencing them Cerebellum involved in Pavlovian conditioning Striatum stores memories of consistent relationships between stimuli & responses; habit formation Both also seem to be involved in non-motor memories

Synaptic Mechanisms of L&M Long-term potentiation (LTP) Based on Hebb’s hypothesis about reverberation & STM to LTM Facilitation of synaptic transmission following high- frequency electrical stimulation applied to presynaptic neurons Can last for a long time (months) after multiple stimulations Only develops if both the pre & postsynaptic neurons fire One of the most widely studied phenomena in neuroscience

LTP 3 part process Induction Maintenance Expression High-frequency stimulation induces LTP (learning) Maintenance Changes responsible for storing LTP (memory) Expression Changes that allow it to be expressed during the test (recall) NMDA receptors (glutamate) play a large role in LTP Still more questions than answers

Infantile Amnesia We remember essentially nothing from our infancy But we do show there are implicit memories for experiences from this time When kids are later shown pictures of themselves with preschool classmates, they remember almost none of them; however, they do exhibit a skin conductance response associated with seeing familiar individuals