Patterns of memory failure after scopolamine treatment: Implications for cholinergic hypotheses of dementia

Beatty, William W.; Butters, Nelson; Janowsky, David S.

doi:10.1016/s0163-1047(86)90772-7

Cited by 234 publications

(127 citation statements)

References 38 publications

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“…As previously noted, the B-list intrusion rate after scopolamine injection was 2-8 times higher than this rate in the other study conditions, but we could not justify performing a post hoc focused contrast analysis, as this was not a specific a priori hypothesis we had set out to demonstrate in this study. Although significant levels of prior-item and extra-list intrusions were not seen in previous studies using scopolamine in short-term memory tasks such as the Brown-Peterson paradigm (Beatty et al, 1986;Troster et al, 1989), Frith et al (1984) found that scopolamine increased current-list intrusion errors during immediate serial free recall of verbal items. Though they tested a different memory process, short-term list item memory, compared to our study of long-term memory for novel paired associates, it is nonetheless interesting to note that Beatty et al (1986) and Troster et al (1989) both observed that the rates of extra-list intrusions (but not prior-item intrusions), though not reaching statistical significance, were at least 2 times greater, and the percentage of perseverative responses were always higher in the Brown-Peterson paradigm under scopolamine.…”

Section: Discussionmentioning

confidence: 81%

“…In addition, short-term memory phenomena such as the recency component of a serial position curve (Crow & Grove-White, 1973;Frith et al, 1984) and digit span (Beatty et al, 1986;Drachman, 1978) are also spared. Recently, studies have shown that scopolamine may impact recognition memory processes by affecting both recollection and familiarity (Mintzer & Griffiths, 2001Sherman, Atri, Hasselmo, Stern, & Howard, 2003).…”

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confidence: 99%

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Blockade of Central Cholinergic Receptors Impairs New Learning and Increases Proactive Interference in a Word Paired-Associate Memory Task.

Atri¹,

Sherman²,

Norman³

et al. 2004

Behavioral Neuroscience

137

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Experimental data and computational models suggest that blockade of muscarinic cholinergic receptors impairs paired-associate learning and increases proactive interference (E. DeRosa & M. E. Hasselmo, 2000; M. E. Hasselmo & J. M. Bower, 1993). The results presented here provide evidence in humans supporting these hypotheses. Young healthy subjects first learned baseline word pairs (A-B) and, after a delay, learned additional overlapping (A-C) and nonoverlapping (D-E) word pairs. As predicted, when compared with subjects who received the active placebo glycopyrrolate (4 g/kg) and subjects who were not injected, those who received scopolamine (8 g/kg) showed (a) overall impairment in new word paired-associate learning, but no impairment in cued recall of previously learned associates; and (b) greater impairment in learning overlapping (A-C) compared with nonoverlapping (D-E) paired associates.Acetylcholine may play an important role in the encoding of new information. Numerous studies demonstrate that blockade of muscarinic acetylcholine receptors by systemic administration of the drug scopolamine interferes with the encoding of new verbal information, but has little effect on retrieval of previously stored information

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Section: Discussionmentioning

confidence: 81%

mentioning

confidence: 99%

Blockade of Central Cholinergic Receptors Impairs New Learning and Increases Proactive Interference in a Word Paired-Associate Memory Task.

Atri¹,

Sherman²,

Norman³

et al. 2004

Behavioral Neuroscience

137

View full text Add to dashboard Cite

show abstract

“…For a similar reason, we have not yet attempted to replicate the apparent sparing of implicit memory in the presence of scopolamine [117]. Despite this absence of an effect on recency and digit span, scopolamine has been shown to clearly impair recall performance on the Brown -Peterson task, which tests the free recall of a consonant trigram after performance of a distractor task for short periods [30,118]. This suggests a difference in mechanism for the short-term memory of a Brown -Peterson task versus the shortterm memory involved in recency.…”

Section: Discussionmentioning

confidence: 99%

Free recall and recognition in a network model of the hippocampus: simulating effects of scopolamine on human memory function

Hasselmo

Wyble

1997

Behavioural Brain Research

309

263

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“…Muscarinic blockade with drugs such as scopolamine in humans also causes deficits on DMS and N-back tasks [34][35][36] and on the Brown-Peterson task when letter trigrams that involve novel combinations of well-known elements are used [37]. However, scopolamine injections do not lead to impairments on simple measures of short-term memory such as digit span [38] and the recency component of a serial position curve [39], suggesting a lack of effect on working memory for highly familiar stimuli such as words or numbers.…”

Section: Cholinergic Manipulations Working Memorymentioning

confidence: 99%

Mechanisms underlying working memory for novel information

Hasselmo

Stern

2006

Trends in Cognitive Sciences

223

185

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We describe a theory that brain mechanisms underlying working memory for novel information include a buffer in parahippocampal cortices. Computational modelling indicates that mechanisms for maintaining novel information in working memory could differ from mechanisms for maintaining familiar information. Electrophysiological data suggest that the buffer for novel information depends on acetylcholine. Acetylcholine activates single-cell mechanisms that underlie persistent spiking of neurons in the absence of synaptic transmission, allowing maintenance of information without prior synaptic modification. fMRI studies and lesion studies suggest that parahippocampal regions mediate working memory for novel stimuli, and effects of cholinergic blockade impair this function. These intrinsic mechanisms in parahippocampal cortices provide an important alternative to theories of working memory based on recurrent synaptic excitation. Keywordsacetylcholine; entorhinal cortex; sustained activity; fMRI; scopolamine Research has demonstrated the existence of multiple memory systems, including working memory, which is defined as a limited capacity system for the temporary storage and manipulation of information for cognitive tasks [1,2]. Many initial fMRI studies of working memory in humans used highly familiar stimuli such as letters and words, and focused primarily on a system which includes prefrontal cortex (PFC) and parietal cortex [1][2][3]. However, electrophysiological and lesion studies in animals, and recent imaging studies suggest that temporal lobe structures play a critical role in working memory [4][5][6]. Here we present the theory that working memory for novel information differs from working memory for familiar information, proposing that novel stimuli require additional cellular mechanisms within the entorhinal and perirhinal cortex; whereas prefrontal and parietal systems are sufficient for maintaining familiar stimuli in working memory. It is critical to note that we are not proposing a double dissociation between the systems, but instead we suggest that the prefrontal-parietal system alone is insufficient for maintaining information that has no prior representation in the brain. We hypothesize that cholinergic activation of these single neuron mechanisms results in persistent spiking activity without excitatory synaptic transmission between neurons (see Figure 1 and Box). This theory provides an alternative to many physiological models of working memory, which use recurrent excitation between neurons to maintain persistent spiking [7]. Critically, models based on recurrent excitation can only maintain information consistent with previously formed representations (i.e. familiar information).In this article, we evaluate experimental data [6,[8][9][10] and computational modelling [11][12][13] that support the proposal that working memory for novel stimuli requires additional cellular mechanisms activated by acetylcholine in the entorhinal cortex and other parahippocampal cortices that differ substantial...

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Patterns of memory failure after scopolamine treatment: Implications for cholinergic hypotheses of dementia

Cited by 234 publications

References 38 publications

Blockade of Central Cholinergic Receptors Impairs New Learning and Increases Proactive Interference in a Word Paired-Associate Memory Task.

Blockade of Central Cholinergic Receptors Impairs New Learning and Increases Proactive Interference in a Word Paired-Associate Memory Task.

Free recall and recognition in a network model of the hippocampus: simulating effects of scopolamine on human memory function

Mechanisms underlying working memory for novel information

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