Download 1 - U-System

1. NMDA receptors and LTP in learning and memory
- long term potentiation  LTP; a neuron is given a brief, but rapid series of stimuli  leaves
neuron potentiated (highly responsive to new input of same type); LTP occurs in hippocampal
neurons
- LTP depends on activation of NMDA receptors
- NMDA receptor binds glutamate (and with depolarization to remove the Mg2+) produces a
prolonged facilitation of transmission
- Once Mg2+ block removed and glutamate is bound to the NMDA receptor  calcium flows
into the postsynapse  activates NOS (nitrous oxide synthase)  NO to presynapse  more
release of glutamate from presynapse  LTP  learning in hippocampus
- learning impairments may result form chemical deficiencies in the brain and drugs may
impair/improve learning
- drugs that block NMDA synapses also block LTP in the hippocampus, and those same drugs
block the kind of learning dependent on the hippocampus
- protein synthesis is critical in formation of long-term memories (LTP); drugs inhibiting
protein synthesis impair long-term storage of memory, although they do not impair short-term
retention; protein synthesis modifies the properties of neurons to store information
2. Role of acetylcholine (Ach) in learning and memory/neural changes associated with
aging
- Ach muscarinic receptors in brain
- changes occur at Ach synapses to produce a change in the resting activity of certain neurons or
a change in the responsiveness at certain synapses; changes in Ach synapses are the results from
increased protein synthesis
- scopolamine blocks Ach synapses  deficiencies in memory tasks
- physostigimine prolongs effects of Ach at synapses  improves memory but has side effects
(restlessness, sweating, excessive salivation)
- providing Ach dietary precursors (choline, lecithin) provides no significant benefits; senility
and other memory failures associated with massive depletion of Ach synapses
- normal aging  memory impairment is common; degree of memory loss correlates with
decline in brain Ach levels; Alzheimer’s patients have more serve memory dysfunctions and
more decline in brain Ach level
Other NTs and their synapses
- in old age brain suffers a decline in norepinephrine, serotonin, and dopamine (as well as
Ach); norepinephrine and dopamine synapses in the prefrontal cortex are major contributors
to memory
- ideal performance requires balance between ability to focus attention and to shift one’s focus
from time to time; autism has focused attention (ignoring shifting) and ADD/schizophrenia
shifts attention (cannot focus)
3. above, #1
4. Memory in young and old brain
- infant amnesia  we don’t remember much from our first five years, but we still can establish
procedural memories (tying shoes, walking, eating with a fork), even if we don’t form factual
memories that will last long
- infants have memory problems because hippocampus is slow to mature; old people have
memory related troubles because hippocampus is deteriorating
- prefrontal cortex also deteriorates with old age, due in part to declining number of dopamine
and norepinephrine synapses in prefrontal cortex
- memory may vary due to the rise and fall of levels of glutamate, Ach, and other chemicals
- LTP depends on entry of calcium ions into postsynaptic neurons; in aged humans  calcium
channels become leaky resulting in higher than normal resting levels of calcium within neurons
 calcium that enters during a train of stimuli (tetanus) produces less effect than in younger
individuals
5. Important structures for learning and memory abilities
- limbic system plays a role in deciding what is worth remembering and limbic damage causes
problems with this process
- damage to the hippocampus produces amnesia and the ability to input new information
- new memories are encoded by the prefrontal cortex (which handles our working memory)
and the parahippocampal gyri (which consolidate our memory); memory is mostly likely
stored in cortical areas
- encoding takes place in the left hemisphere, while retrieving/recognizing takes place in the
right hemisphere
Amnesia
- deficit in long-term memory including retrograde and anterograde amnesia; trouble learning
facts, but no trouble learning new skills
- amnesia is usually caused by bilateral damage in one of two specific places – the medial
temporal lobe (including subcortical structures, such as the amygdala and the hippocampus) or
the diencephalon adjacent to the midline
- medial temporal lobe is surgically damaged  loss of ability to form new memories of facts
and events (anterograde); patients are aware of their deficit; hippocampus plays a major role
- hippocampus receives its inputs adjacent entorhinal cortex (anterior part of
parahippocampal gyrus), which in turn receives inputs from widespread cortical areas,
including multimodal association areas
- information is processed in the hippocampus though a one-way entorhinal  dentate gyrus 
hippocampus proper  subiculum pathway (perforant path) and then returned to multimodal
association cortex, either via the entorhinal cortex or through the limbic system; damage along
this one-way path through the hippocampus disrupts the whole process  amnesia
- unilateral medial temporal damage causes less severe memory deficit; left damage causes
verbal memory problems and right damage causes spatial memory problems
- diencephalic damage  anterograde amnesia; retrograde amnesia; less aware of deficit;
possible damage to mammillary bodies
- combined bilateral damage to both hippocampal limbic circuits (mammillary bodies,
mamillothalamic tracts, anterior nuclei) and amygdala (to DM of thalamus) causes amnesia
6. Different types of memory abilities
- working memory  memory for temporary information (current score of a game); patients
with amnesia have trouble with working memory
- declarative memory  involved in learning new facts, what is going on right now, and what
happened last year
- procedural memory  involved in learning new skills and how to perform acquired skills
such as driving or swinging a golf club; difficult to put into words