Memory, learning, and neuroplasticity Flashcards
Learning and memory
Learning is the process of acquiring new information, and memory is the ability to store, consolidate, and retrieve that information. Long-term memory: declarative - things you can tell others, hippocampus dependent. Nondeclarative - things that you know that you can show by doing, hippocampus independent.
Hippocampus
Centrally involved in declarative memory or the consolidation of “what” information and the transfer of “what” information from short-term memory to long-term memory. The hippocampus is also involved in spatial memory. Long-term memory is stored in the entire brain - visual parts in visual areas, etc. and brain brings them back together. Hippocampus is doorway through which memory must be consolidated.
HM, the hippocampus, and anterograde amnesia
Amnesia is something that informed us about memory. Retrograde amnesia - not remembering the head injury, anterograde amnesia - can’t form new declarative memories. HM had seizures, destroying tissue in temporal lobe, didn’t have electrocorticography, taking out medial temporal lobe and hippocampus. No new declarative memories. Tells us hippocampus is involved in forming declarative memories but not in storage (could retrieve old memories), told us it’s involved in consolidation of memories. Could do procedural memory tasks (mirrored that of other people), highlighting that different neural systems underlie different components of memory.
The extended hippocampus
The hippocampal complex is involved in memory. Lesions of hippocampus and neighboring cortex impaired memory much more than just lesioning the hippocampus. Have to remove whole complex to get full HM effect.
Hippocampus and space
Involved in spatial memory too. Place, grid cells. London taxi drivers (MRI), complicated city to drive, have to understand complex things but bus drivers follow set route. Taxi drivers had bigger hippocampal volume. More years of experience as cab drivers had higher volume, so learning spatial orientation drives hippocampal volume.
Pathways to hippocampus
Damage to the pathways to hippocampus also associated with severe anterograde amnesia. Dorsomedial thalamus and mammillary bodies. Korsakoff’s syndrome - anterograde amnesia, alcoholism, thiamine deficiency, anorexia too - secondary to nutritional deficits, affecting mammilary bodies. Hippocampus critical for consolidation, but memories are stored in the cortex.
Types of declarative memory
Episodic (an event), semantic (knowledge)
Stages of memory
Incoming information goes to sensory buffers (iconic information ex., noise screened out, consciousness, current awareness), encoding into short-term memory (STM/working memory - hippocampal dependent but not as much). Then into long-term (hippocampus) You can lose long-term memory - it’s adaptive. Consolidation is short to long term. Reconsolidation - when retrieving a memory, you recreate it, why memories are so malleable. Memory trace - persistent change in the brain that reflects the storage of a memory.
Conditioning
Part of non-declarative. Ventral striatum dopamine signaling central to reward conditioning. Emotion of memory mediated through other portions of the brain. Ventral striatum is Pavlovian center of the brain. Eventually the ventral striatum fires to CS instead of UCS, ventral striatum important for reinforcement learning. Amygdala central to fear conditioning. If things don’t mean much, we don’t remember. Amygdala activity modulates declarative memory, electrical stimulation of amygdala alters memory, both norepinephrine injected into amygdala and epineprhine/cortisol released from adrenal glands during times of distress enhances memory. Injecting beta-blockers (propanolol) blocks emotional modulation of memory.
Treating trauma through targeting reconsolidation
Reconsolidation: return of a memory trace to stable long-term storage after it has been temporarily made changeable during the process of recall. Every time you have a memory, the memory is reconsolidated. Among individuals with PTSD, administration of beta-adrenergic antagonist propranolol (blocks epinephrine) during trauma recall reduces symptoms. Can we block memory reconsolidation? Initial memory formation and reconsolidation involves protein synthesis. Injecting a protein synthesis inhibitor (anisomycin) into the rat amygdala blocks reconsolidation of conditioned fear response. Dissociation between declarative and emotional memory. Tougher to block memories in humans than in rats.
Synaptic plasticity
Memory is about using it, can involve more neurotransmission, can get larger postsynaptic membrane, enlargement of pre or post synaptic neuron, interneurons modulate amount of neurotransmission. If circuit used more often, more synapses there. Full neural pathways forming. Extraordinary scenario of neurons remodeling.
Experience modulates synaptic plasticity
Enriched environments most strongly modulate basal dendrites (environment has less of an effect on apical dendrites - apical come off axon and form connections with other neurons, the basal ones are responsive to incoming info and are very plastic). Animals (multiple levels of analysis) in enriched environments have heavier, thicker cortices, more dendritic branches/spines, larger cortical synapses, enhanced neurogenesis in the hippocampus, enhanced recovery from brain damage.
LTP and memory consolidation
Presynaptic and postsynaptic neurons that repeatedly activate together form a stronger and more stable synaptic connection. Hebbian synapse - a synapse that is strengthened when it successfully drives the postsynaptic cell. Cells that fire together wire together. Using neuronal resource to recall something enhances the synaptic connections between them. LTP is a stable and enduring increase in the effectiveness of synapses following repeated string stimulation (the cellular mechanism of memory).
NMDA and AMPA in LTP
LTP occurs in hippocampus and other brain regions. The most studied form of LTP occurs at synapses that use excitatory neurotransmitter glutamate. LTP is critically dependent on a glutamate receptor subtype called the NMDA receptor. Treatment with drugs that block NMDA receptors prevent new LTP, but it does not affect synaptic changes that have already been established. AMPA receptors are fast-acting ionotropic receptors that are also involved in LTP. AMPA operated on at baseline, repeated activation of AMPA (when they become active, bumps magnesium out of AMPA, and now NMDA can be factored in), now Ca flow into NMDA. Once brain starts to fire in a particular way relevant for LTP and memory, have opening of NMDA (facilitating LTP, accentuating things). NMDA increases conductance of AMPA, facilitates release of nitric oxide which goes back and binds to the presynaptic terminal to facilitate more release of glutamate (one of few times you get gas neuromodulation). This all makes the connection stronger. Hebbian synapses are made stronger via the glutamatergic mechanisms. Presynaptic neurons that fire out of synchrony don’t rampu up LTP, firing in unison does. Desynchronized output gets trimmed out more often. Brain will strengthen synchronous outputs. Increased transmission, receptor size, etc.
