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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