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This study examined priming in perceptual identification of orthographically illegal nonwords in control subjects and patients with global amnesia. Subjects studied a list of orthographically illegal nonwords and then performed a perceptual identification task in which half of the stimuli were from the prior study list and half were new (unstudied) stimuli. Priming was reflected in enhanced identification accuracy of studied compared to unstudied nonwords. Amnesic patients showed significant and normal priming despite impaired recognition memory performance. Because the experimental stimuli were dissimilar to real words in terms of orthography and phonology, it is unlikely that this priming effect was mediated by activation of pre-existing representations of orthographically or phonologically similar words, morphemes, or syllables. These results demonstrate that intact perceptual priming in amnesia is not limited to stimuli that are premorbidly represented in long-term knowledge, nor to novel stimuli that conform to the rules that characterize familiar items. Further, because the experimental stimuli comprised novel letter assemblies, the results suggest that amnesic patients can show normal priming for new perceptual associations. These findings demonstrate that processes spared in amnesia can support the creation and subsequent retrieval of novel stimulus representations. (JINS, 1995, I, 425–433.)
Memory comprises the recording, retention and retrieval of knowledge. All that we know, except for what is genetically predetermined, is acquired through experience. Such knowledge includes the events we remember, the facts we know, and the skills we master. Memory is not a unitary faculty, but rather an ensemble of multiple forms of learning that differ in their uses, their operating characteristics, and the neural networks that mediate their processing (Gabrieli, 1998). A memory system may be defined as a particular neural network that mediates a specific form of mnemonic processing. Neurological and psychiatric diseases result in characteristic mnemonic deficits that reflect which memory systems are injured by a particular disease.
Levels of analysis: cells and systems
Learning and memory reflect experience-induced plasticity in the brain. An experience leaves a memory trace composed of an enduring alteration in the cellular organization of the brain called an engram. Experience-induced plasticity can be examined at many levels of analysis, including molecular events at the cellular and synaptic level, reorganization of local neuronal circuits, and large-scale alterations in the functional neural architecture of memory systems.
Cellular mechanisms of memory
Little is known about neural plasticity in the human brain, but findings from in vitro and invertebrate models offer suggestions about the cellular bases of human memory. Studies of the marine snail Aplysia have revealed links between learning and alterations in neurotransmitter release. Aplysia have a gill withdrawal reflex that is triggered when the gill is touched by a rod. Repeated stimulation leads to habituation such that the gills are no longer withdrawn in response to the rod. Short-term habituation has been linked to decreased presynaptic transmitter release. Repeated stimulation with a highly noxious stimulus, such as an electric shock, can lead to sensitization, an intensification of the withdrawal response. Short-term sensitization involves increased neurotransmitter release from a facilitating interneuron (Kandel & Schwartz, 1982). Modulation of neurotransmitter release may underlie short-term changes in functional connectivity between neurons.
Long-term memory processes, in contrast, require messenger RNA and protein synthesis (Davis & Squire, 1984) to establish structural changes in synaptic connectivity as a record of experience.
This study examined the distinction between identification
and production processes in repetition priming for 16 patients
with Alzheimer's disease (AD) and 16 healthy old control
participants (NC). Words were read in three study phases. In
three test phases, participants (1) reread studied words, along
with unstudied words, in a word-naming task (identification
priming); (2) completed 3-letter stems of studied and unstudied
words into words in a word-stem completion task (production
priming); and (3) answered yes or no to having
read studied and unstudied words in a recognition task (explicit
memory). Explicit memory and word-stem completion priming were
impaired in the AD group compared to the NC group. After correcting
for baseline slowing, word-naming priming magnitude did not
differ between the groups. The results suggest that the distinction
between production and identification processes has promise
for explaining the pattern of preservation and failure of
repetition priming in AD. (JINS, 2001, 7,
Cowan argues that the true short-term memory (STM) capacity limit is about 4 items. Functional neuroimaging data converge with this conclusion, indicating distinct neural activity patterns depending on whether or not memory task-demands exceed this limit. STM for verbal information within that capacity invokes focal prefrontal cortical activation that increases with memory load. STM for verbal information exceeding that capacity invokes widespread prefrontal activation in regions associated with executive and attentional processes that may mediate chunking processes to accommodate STM capacity limits.
Priming for line drawings of real and nonreal objects
was examined in an object decision task for 16 patients
with Alzheimer's disease (AD) and 16 normal elderly
control (NC) participants. In two study phases, participants
decided if objects were real or nonreal. In an implicit
test phase, real/nonreal decisions were made for studied
and unstudied objects, and priming was measured as the
difference in decision speed or accuracy between studied
and unstudied objects. In an explicit test phase, yes/no
recognition was measured for real and nonreal objects.
AD patients had impaired explicit memory for real and nonreal
objects and intact repetition priming for real objects.
By the latency measure, both AD and NC groups showed priming
for nonreal objects but in opposite ways. Classification
decisions about studied relative to nonstudied nonreal
objects were slower for the AD patients, whereas such decisions
were faster for the NC participants. Classification decisions
of both groups were less accurate for repeated nonreal
objects. These results support the claim that AD patients
with mild cognitive impairment show normal perceptual priming.
The AD inhibition for studied nonreal objects is discussed
in terms of the decision conflict that occurs when recollection
of source is not available to counter the influence of
familiarity. (JINS, 1998, 4, 435–446.)
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