Learning and memory Flashcards
What is learning and what is memory?
[learning is a change in behavior as a result of experience; memory is the retention of that experience over time]
how is memory distinguished?
[most common distinction is between episodic and procedural memory. Episodic (declarative) is our common sense version of memory, what happened in sequence, as well as dates, the ability to draw the structure of DNA, your cat’s name, etc. Procedural is how things are done. This includes motor learning (e.g., how to ride a bicycle) and also include rules in language such as syntax. HM, the famous patient without a hippocampus, had both. What he lacked was the ability to convert short-term episodic into long-term episodic memory. Procedural memory is associated with basal ganglia among other brain regions so people with Parkinson’s will often see decrements in procedural memory as the disorder progresses.
how is episodic memory divided?
[it is usually divided into short-term and long-term; short-term is the retention of events for a few sec with a phone number being the classic example; long-term is retention over longer periods; Several areas of brain are associated with short-term memory including pre-frontal cortex, inferotemporal cortex, and hippocampus; conversion of short-term into long-term memory is called consolidation and requires hippocampus]
What is the difference between associative and non-associative learning?
[Non-associative learning does not pair (‘associate’) independent events in time, the 2 big examples being habituation and sensitization. Habituation is the loss of response associated with repetition of an innocuous stimulus; sensitization is the heightened responsiveness to repetition of a painful or upsetting stimulus. Associative learning is the association of independent events in time (contiguity; the close temporal relation is critical). Associative learning is divided into classical and operant learning]
What’s the difference between classical and operant learning?
[Classical learning is the temporal association (contiguity) between two stimuli that yields a conditioned response. E.g., Pavlov’s dogs: pairing presentation of meat with ringing a bell (CS, conditioned stimulus) causes the dog to salivate to the ringing of the bell alone. The meat is the unconditioned stimulus (UCS), the bell is the conditioned stimulus. Operant conditioning is the pairing of a behavior with its consequences. If pressing a bar delivers a food pellet to a hungry rat, the operant is the bar press, delivery of the pellet is the reinforcer, which increases the probability of that behavior (versus punishers, which decrease the probability of that behavior).
What is Hebb’s rule?
[The idea that a synaptic input associated with a post-synaptic event (action potential) will be strengthened as a result of causing that post-synaptic event. Easy to see the transparency in classical conditioning in which one has a cell/circuit in which the bell’s influence was originally weak, but becomes strong as a result of being paired with the meat. Cells that fire together wire together]
What is long-term potentiation (LTP)?
[A physiological phenomenon that matches learning and implementation of Hebb’s rule. Originally documented in the hippocampus, it is the strengthening of a synaptic input by delivering a high-frequency (‘tetanic’) train of electrical stimulation. This ‘experience’ strengthens subsequent EPSPs associated with that synapse by increasing the number of AMPA glutamate receptors at that synapse. Further, if one pairs activating a 2nd weak synapse with the tetanic stimulation, that weak synapse is now also strengthened, forming a basis for understanding conditioning (‘associative’ learning). Induction of LTP requires not only the tetanic stimulation, but also activation of NMDA receptors as they allow an influx of Ca++. This Ca++ is critical as it phosphorylates latent AMPA receptors, inserting them into the membrane and bringing them ‘online’. LTP is often broken into short-term and long-term. Short-term does not need protein synthesis (the Ca++ influx simply brings available AMPA receptors online), but long-term does. Although more complicated, the tetanic stimulation initiates the synthesis of new AMPA receptors that can then be inserted into the cell membrane making that post-synaptic cell even more responsive to signals (glutamate) being released from the pre-synaptic cell. LTP is long-term… in vivo, it endures for weeks if not months.]
What are NMDA receptors?
[A type of ionotropic mixed cation glutamate receptor that pass Na+, K+ and (importantly) Ca++ through its channel. It also has a voltage-dependence; at ‘rest’ (-60 mV) the channel is blocked by a Mg++ ion. This block is relieved by depolarization, implying other depolarizing channels (e.g., those from nearby AMPA receptors) must also be active. The AMPA receptors respond to glutamate by cause graded depolarizations. As those graded depolarizations are added together, the area becomes less negative (~-45 mV ) which causes the Mg++ ion to be removed from the NMDA channel and allows greater influx of Na+ moving the cell closer to threshold. As such, it is referred to as a ‘coincidence’ detector. Activation of NMDA receptors has proven to be critical for LTP because the passage of Ca++ through the channel activates phosphorylating agents that are responsible for bringing latent AMPA receptors online]
What is amnesia?
[loss of memory, and/or inability to form new memories. Most common cause is concussion, a traumatic brain injury associated with temporary unconsciousness. Amnesia is divided into retrograde and anterograde. In retrograde amnesia, one cannot recall what happened prior to the injury. This is usually a gradient, with the most recent events the most likely to be forgotten (this happens on soap operas all the time). In anterograde amnesia, one cannot recall what happens following the injury. Concussion is retrograde dominant… the interpretation being that memory is labile, the conversion from a short-term version to a long-term version takes time, and the injury disrupted that process. Anterograde amnesia dominates early Alzheimer’s disease, the patient cannot form new memories. This is a failure of memory consolidation, the conversion of memory from short-term into long-term. There is consensus that memory consolidation depends on the hippocampus]
What is an engram?
[the term for a memory trace. Memory is not stored in any single place, it is a distributed property across broad areas of cortex. It is not clear how memories are retrieved. Whereas some argue that retrieval depends on the hippocampus, HM had no hippocampus, and was perfectly capable of recollecting incidents in the years prior to his surgery.]
What is the medial temporal lobe system?
[the main declarative memory system whose star structure is the hippocampus. On-going experience passes from broad areas of cortex into the entorhinal cortex and into the hippocampal circuits, converting short-term experience (memory) into a more permanent version. These signals then return to entorhinal cortex, and are then broadly distributed across cortex (long-term memory). The hippocampus is thus critical for converting short-term into long-term memory. In addition, the hippocampus seems to hold a cognitive ‘map’ of our world, and is apparently plastic (changeable). A study of experienced London cab drivers indicated they had larger than average hippocampi, and the structures seemed to shrink after they got out of the biz.]
What is the medial diencephalic system?
[a series of structures associated with declarative memory and when damaged, will yield anterograde amnesia. The main structures are the mammillary bodies, the fornix and the mediodorsal nu of thalamus. Damage here is usually associated with chronic alcoholism. Such patients suffer intellectual impairment (with which medial temporal lobe damage may or may not be associated) and confabulation in which they invent stories when questioned, rather than just indicating they don’t know or remember.]
What is the role of the neostriatum in memory?
[It seems to be involved in procedural memory, how things are done. People with Parkinson’s and Huntington’s Chorea both appear to have procedural memory impairment, whereas those that have damage to the hippocampus do not. HM exhibited a normal learning curve in the mirror drawing task on day 1. On day 2, despite his denials that he’d ever done the task, he showed significant savings, and performed within the range of normal. People with Parkinson’s and especially Huntington’s chorea are especially impaired in that task.]
What is Alzheimer’s disease?
[A devastating progressive disease accompanied by significant atrophy of the medial temporal lobe (including hippocampus) if not the entire neocortex. It is characterized by profound memory loss. Initially, the person cannot remember events that just happened or events of that day (anterograde amnesia; failure to convert short-term into long-term memory). As the disease progresses, the patient will not remember events from years past (retrograde amnesia). Most devastating, is the patient fails to recognize even their spouse or other family members. Procedural memory seems spared. It is a dementia (loss of mental faculties) as well as a primary amnesia. Confirmatory diagnosis remains based on post-mortem findings, typically exhibiting severe brain atrophy (expansion of sub-arachnoid space), and presence of senile plaques (extracellular deposits of beta-amyloid deposits) and tangles (intracellular accumulation of hyperphosphorylated tau proteins, clogging axon transport). Clinically one is diagnosed with probable or possible Alzheimer’s. The hippocampus and entorhinal cortex seem always among the first structures to show wasting. There is no cure. Drugs that boost acetylcholine efficiency or block NMDA receptors are of modest benefit. Much of what we know about causal relations suggest a link between inability to sequester cholesterol and Alzheimer’s. For example, Lipitor, the major cholesterol-lowering drug may be of benefit in lowering Alzheimer’s risk].
