We conducted a study that bears on this issue, although it did not originally aim to do so. We wanted to compare the effects of light anesthesia on conscious and unconscious memory, so we played lists of fictitious names to volunteers who were awake, lightly sedated with a small dose of propofol (a general anesthetic agent), or more deeply sedated with propofol. Participants remained conscious. With the smaller dose, they were drowsy but able to talk and respond to commands to open their eyes or raise their hand. With the larger dose, they were less responsive but still raised their hand to command. When the effects of propofol had worn off, participants listened to names and were asked to select those which were famous or those which they remembered hearing during the experiment. In laboratory studies, the tendency to mistake previously heard fictitious names for famous names—the false fame effect—occurs despite divided attention at study (Jacoby et al. 1989). Conscious, recognition memory is more sensitive to manipulations of attention at study. Therefore we predicted that memory for the names presented during sedation would show up on the fame judgment task but not on the recognition test.
Another aim of the study was to assess the coherent frequency, an EEG measure of auditory evoked responding, as an index of depth of anesthesia (Andrade et al. 1996). To do this, we compared coherent frequency with an objective measure of cognitive function, performance on a within-list recognition test. Participants listened to a list of unrelated words and responded to repeated words by raising their right thumb. Repeats occurred after varying numbers of intervening words, therefore good performance required attention and rehearsal of recently heard words, i.e., working memory.
The recognition and fame judgment tasks revealed memory only for names presented before propofol was administered. Neither task showed any evidence for learning during propo-fol infusion. With the smaller dose of propofol, performance on the within-list recognition test was impaired compared with performance when awake, but it was still reasonably good; participants identified approximately half the repeated words. Thus participants had preserved working-memory function but no long-term learning during light propofol sedation. Following Caseley-Rondi (1996), we explained these data by suggesting that executive or frontal functions are needed to integrate or bind complex stimuli—in this case the fictitious names—before they can be encoded in memory (Andrade 1996).
Flohr's theory explains our data without recourse to assumptions about frontally mediated integration of stimuli. He proposes that NMDA cell assemblies function as Hebbian synapses, becoming more reactive with use through post-synaptic changes known as long-term potentia-tion, the cellular mechanism underlying fear conditioning and other types of learning (e.g., McKernan and Shinnick-Gallagher 1997). Flohr suggests that NMDA synapses also form transient assemblies which organize themselves into the higher-order representations underlying normal conscious cognition and working memory. Calcium ions are a secondary messenger in both types of plasticity. They promote transient changes by increasing transmitter release from the presynaptic membrane (by increasing synthesis of nitric oxide, which is released into the synaptic cleft) and more permanent changes by altering protein synthesis in the postsynaptic membrane. The more Ca2+ that passes through the ion channel of the NMDA receptor, the longer the duration of the synaptic change. Therefore long-term memory formation requires more Ca2+, and generally more activity in the NMDA receptor complex, than awareness and attention. This explains the coincident loss of awareness and loss of memory for particular stimuli in conditions such as agnosia, and the amnesic effects of dissociative anesthetics (see Flohr 1992).
A stronger prediction can also be made: For any anesthetic, there will be a dose that preserves awareness and working-memory function but prevents long-term learning. The data from our volunteer study support this prediction, as does Harborne et al.'s (1996) finding that a sub-anesthetic dose of ketamine impaired verbal learning and memory but had little effect on attention and measures of frontal function. The various demonstrations of learning during clinical anesthesia contradict it, unless one assumes that all patients with implicit memory for intraoperative events were at least momentarily conscious during surgery. An alternative, ad hoc explanation of the clinical data is that when words are presented during anesthesia, stored representations of those words are temporarily activated in a way that alters performance on the memory tests but is not dependent on formation of NMDA-mediated cell assemblies.
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