PSYC 362 Chapter 12 Learning Objectives

PSYC 362 Special Topics in Biological Psychology

Consolidation of new memories and retrieval of older memories. Consolidation is the process in which the brain forms a more or less permanent physical representation of a memory. Retrieval is the process of accessing stored memories–in other words, the act of remembering. Until the memory is consolidated, it is particularly fragile. New memories may be disrupted just by engaging in another activity, and even older memories are vulnerable to intense experiences such as emotional trauma or electroconvulsive shock treatment (a means of inducing convulsions, usually in treating depression). Researchers divide memory into two stages, short-term memory and long-term memory. Long-term memory, at least for some kinds of learning, can be divided into two stages that have different durations and occur in different locations.

Explain how the brain is involved in the different types of memory.

Researchers have used PET scans to confirm that the hippocampus also retrieves memories in humans. The prefrontal area is also active during learning and retrieval, and some researchers think that it directs the search strategy required for retrieval. The prefrontal area is active during effortful attempts at retrieval, whereas the hippocampus is activated during successful retrieval. Increasing dopamine levels by injecting the dopamine precursor levodopa improves memory in humans. In humans, learning can be increased by dopamine-enhancing stimulation. Dopamine affects consolidation of long-term memory, rather than improving short-term memory. The hippocampal area is not the permanent storage site for memories. According to most researchers, the hippocampus stores information temporarily in the hippocampal formation; then, over time, a more permanent memory is consolidated elsewhere in the brain. Thus, all memories are not stored in a single area, nor is each memory disrupted throughout the brain. Rather, different memories are in different cortical areas, apparently according to where the information they are based on was processed.

Diagram the neural involvement in processing of information that is stored in memory.

Learning is a form of neural plasticity that changes behavior by remodeling neural connections. Specialized neural mechanisms have evolved to make the most of this capability. Long-term potentiation (LTP) is a persistent strengthening of synapses that results from the simultaneous activation of presynaptic neurons and postsynaptic neurons. LTP has been studied mostly in the hippocampus, but it also occurs in several other areas, including the visual, auditory, and motor cortex. LTP appears to be a chrematistic of much of neural tissue, at least in the areas most likely to be involved in learning. Long-term depression (LTD) is a decrease in the strength of synapses that occurs when stimulation of presynaptic neurons is insufficient to activate the postsynaptic neurons. LTD is believed to be the mechanism the brain uses to modify memories and to clear old memories to make room for new information.

Describe the changes that occur in the brain as learning proceeds.

The hippocampus can acquire learning “on the fly” while the event is in progress, but a longer time is needed for long-term storage of declarative memories in the cortex. Many researchers now believe that the hippocampus transfers information to the cortex during times when the hippocampus is less occupied, even during sleep. Human EEG and PET studies showed the hippocampus repeatedly activating the cortical areas that participated in the daytime learning, and this reactivation was accompanied by significant tasks improvement the next morning without further practice. Even a daytime nap is enough to evoke this kind of activity in the hippocampus and improve subsequent performance. During sleep, more than 100 genes increase their activity, and many of those have been identified as major players in protein synthesis, synaptic modification, and memory consolidation.

Explain what happens to memories when we sleep.

Although we usually associated aging with brain cell loss, significant deficits occur only in the midbrain, basal forebrain (lower frontal lobes), and some prefrontal areas. Some parts of the prefrontal cortex and hippocampus also decline in volume, likely due to a decrease in synaptic density. These areas, of course, are critical for learning, memory, and cognitive functioning. Deficits occur at the molecular level as well. 17 genes in the dentate gyrus of the hippocampus that undergo changed levels of expression with aging. Some elderly people seem immune to the effects of aging on learning and cognition. Certainly, a part of this is genetic, but there have been many research efforts to identify environmental interventions that could benefit the rest of the population. Consumption of flavonoids (nutrients found in cocoa, tea, grapes, and apples) enhances functioning in the hippocampal association and is associated with better language and episodic memory and slower cognitive decline in the elderly.

Examine how memory changes during aging.

Substantial loss of memory and other cognitive abilities (usually, but not necessarily, in the elderly) is referred to as dementia. The most common cause of dementia is Alzhemier’s disease, a disorder characterized by progressive brain deterioration and impaired memory and other cognitive abilities. Alzheimer’s is primarily a disorder of the aged, although it can strike early in life. The earliest and most severe symptom is usually impaired declarative memory. Initially, the person is indistinguishable from a normally aging individual, though the symptoms may start earlier the person has trouble remembering events from the day before, mislays items, forgets names, and must search for the right word in a conversation. Later, the person repeats questions and tells the same story again during a conversation. As time and the diseases progress, the person eventually fails to recognize acquaintances and even family members. Alzheimer’s disease is not just a learning disorder but a disorder of the brain, so ultimately most behaviors suffer. Alzheimer’s is fatal, and it is the sixth leading cause of death in the United States. If all the dementias were counted together, they would rank as the third leading cause of death behind heart disease and cancer. There are two notable characteristics of the Alzhemier’s brain, though they are not unique to the disease. Plaques are clumps of amyloid beta (AB), a type of protein, that cluster among axon terminals and interfere with neural transmission. Leads to the accumulation of the protein tau to form neurofibrillary tangles inside neurons; tangles are associated with the death of brain cells. Development of plaques and tangles progresses through the brain in a predictable succession of stages, beginning with the medial cortex and progressing to the limbic areas, particularly the hippocampus, and then to the neocortex, the outer layers of cortex responsible for our highest functions. Progressive variation in two significant factors in those areas: the relative level of expression of inflammatory genes and the balance between proteins that promote or inhibit the aggregation (accumulation and clumping) of plaques and tangles. Alzheimer’s accounts for 60% to 80% of all cases of dementia. Second is vascular dementia, also called vascular cognitive impairments, at 5% to 10%. It is caused by loss of blood supply to a part of the brain, by stroke; in memory-related areas, this produces Alzheimer’s-like symptoms, and in other areas, the result can include confusion, motor problems, and language impairment. The third most common type of dementia is fronto-temporal dementia. It is most often caused by the accumulation of tau, or of the protein TDP43. It differs from Alzheimer’s in its greater language impairment and alter onset of memory problems. A less common (underdiagnosed) form of dementia is Korsakoff syndrome, brain deterioration that is almost always caused by chronic alcoholism. The damage is due to deficiency in thiamine (vitamin B1), which is needed to produce energy from sugar. Alcohol reduces thiamine absorption in the stomach, and the situation is made worse because the alcoholic tends to forgo food in favor of alcohol. Korsakoff syndrome impairs declarative memory, especially anterograde without affecting nondeclarative forms. Thiamine therapy can relive the symptoms of Korsakoff syndrome somewhat if the disorder is not too advanced, but the brain damage itself is irreversible. The hippocampus and temporal lobes are unaffected in Korsakoff syndrome, but the mammillary bodies and the medial thalamus are reduced in size, and structural and functional abnormalities occur int eh frontal lobes. Some Korsakoff patients show a particularly interesting characteristic in their behavior, called spontaneous confabulation; they fabricate stories and facts to make up for those missing from their memories.

Contrast the impacts of normal aging and disorders on memory.