Impaired delay eyeblink classical conditioning in individuals with anterograde amnesia resulting from anterior communicating artery aneurysm rupture.

Myers, Catherine E.; DeLuca, John; Schultheis, Maria T.; Schnirman, Geoffrey; Ermita, Brandon R.; Diamond, Bruce J.; Warren, Stacey G.; Gluck, Mark A.

doi:10.1037/0735-7044.115.3.560

Cited by 17 publications

(7 citation statements)

References 109 publications

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“…This is consistent with existing data showing that patients with ACoA aneurysm also show impairment learning other behavioral tasks, including eye blink conditioning (Myer, Bryant, DeLuca, & Gluck, 2002; Myers, Deluca, Hopkins, & Gluck, 2006; Myers et al, 2001): Performing both of the acquisition phase of the acquired equivalence task and the eye blink conditioning task relies on associative learning processes.…”

Section: Discussionsupporting

confidence: 91%

“…Patients with ACoA aneurysm have amnesia (O’Connor & Lafleche, 2004), executive dysfunction (Simard, Rouleau, Brosseau, Laframboise, & Bojanowsky, 2003), and other cognitive deficits (Bondi, Kaszniak, Rapcsak, & Butters, 1993; DeLuca, 1993; Diamond, DeLuca, & Kelley, 1997; Mavaddat, Sahakian, Hutchinson, & Kirkpatrick, 1999). We argue that ACoA amnesia results from basal forebrain damage that disrupts learning in the hippocampal region (Myers et al, 2001; Myers et al, 2002). Cholinergic treatments are used to treat patients with ACoA aneurysm (Benke, Koylu, Delazer, Trinka, & Kemmler, 2005), which is consistent with a dysfunction to the cholinergic system in these patients.…”

Section: Introductionmentioning

confidence: 93%

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A neural model of hippocampal–striatal interactions in associative learning and transfer generalization in various neurological and psychiatric patients

Moustafa

Kéri

Herzallah

et al. 2010

Brain and Cognition

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Building on our previous neurocomputational models of basal ganglia and hippocampal-region function (and their modulation by dopamine and acetylcholine, respectively), we show here how an integration of these models can inform our understanding of the interaction between the basal ganglia and hippocampal region in associative learning and transfer generalization across various patient populations. As a common test bed for exploring interactions between these brain regions and neuromodulators, we focus on the acquired equivalence task, an associative learning paradigm in which stimuli that have been associated with the same outcome acquire a functional similarity such that subsequent generalization between these stimuli increases. This task has been used to test cognitive dysfunction in various patient populations with damages to the hippocampal region and basal ganglia, including studies of patients with Parkinson's disease (PD), schizophrenia, basal forebrain amnesia, and hippocampal atrophy. Simulation results show that damage to the hippocampal region-as in patients with hippocampal atrophy (HA), hypoxia, mild Alzheimer's (AD), or schizophrenia-leads to intact associative learning but impaired transfer generalization performance. Moreover, the model demonstrates how PD and anterior communicating artery (ACoA) aneurysm-two very different brain disorders that affect different neural mechanisms-can have similar effects on acquired equivalence performance. In particular, the model shows that simulating a loss of dopamine function in the basal ganglia module (as in PD) leads to slow acquisition learning but intact transfer generalization. Similarly, the model shows that simulating the loss of acetylcholine in the hippocampal region (as in ACoA aneurysm) also results in slower acquisition learning. We argue from this that changes in associative learning of stimulus-action pathways (in the basal ganglia) or changes in the learning of stimulus representations (in the hippocampal region) can have similar functional effects.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 93%

A neural model of hippocampal–striatal interactions in associative learning and transfer generalization in various neurological and psychiatric patients

Moustafa

Kéri

Herzallah

et al. 2010

Brain and Cognition

Self Cite

View full text Add to dashboard Cite

show abstract

“…Lesions of medial septum, which modulates hippocampal activity through cholinergic projections, disrupt the acquisition delay eyeblink conditioning in rabbits (Allen et al 2002). Humans with damage to the basal forebrain structures including the medial septum, as a result of anterior communicating artery aneurism rupture, also show impaired delay eyeblink conditioning compared with matched controls (Myers et al 2001). In fact, patients with medial septum damage showed no appreciable learning across 70 training trials.…”

Section: Discussionmentioning

confidence: 99%

Parallel acquisition of awareness and differential delay eyeblink conditioning

Weidemann

Antees²

2012

Learn. Mem.

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There is considerable debate about whether differential delay eyeblink conditioning can be acquired without awareness of the stimulus contingencies. Previous investigations of the relationship between differential-delay eyeblink conditioning and awareness of the stimulus contingencies have assessed awareness after the conditioning session was finished using a post-experimental questionnaire. In two experiments, the point at which contingency awareness developed during the conditioning session was estimated from a button-press measure of expectancy of the unconditioned stimulus (US). In both experiments, knowledge of the stimulus contingencies and acquisition of differential delay eyeblink conditioning developed approximately in parallel. In Experiment 1 it was shown that predicting the US facilitated eyeblink conditioning compared with predicting the eyeblink response. In Experiment 2, a masking task was used that slowed down the emergence of awareness, and it was shown that differential conditioning only occurred in participants who were able to predict the US. The current findings challenge the hypothesis that differential delay eyeblink conditioning is entirely mediated by a functionally and neurally distinct nondeclarative learning system.

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“…It would appear that disruption of the septo-hippocampal system impairs delay learning much more than does simply removing the hippocampus, consistent with a presumed modulatory role. Patients with anterior communicating artery (AcoA) aneurysm rupture were studied with standard delay eyeblink conditioning (Myers et al 2001). These patients exhibit an anterograde amnesia syndrome similar to that shown by patients with hippocampal-medial temporal lobe damage.…”

Section: Delay Conditioningmentioning

confidence: 99%

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Christian¹,

Thompson²

2003

Learn. Mem.

564

473

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Classical conditioning of the eyeblink reflex to a neutral stimulus that predicts an aversive stimulus is a basic form of associative learning. Acquisition and retention of this learned response require the cerebellum and associated sensory and motor pathways and engage several other brain regions including the hippocampus, neocortex, neostriatum, septum, and amygdala. The cerebellum and its associated circuitry form the essential neural system for delay eyeblink conditioning. Trace eyeblink conditioning, a learning paradigm in which the conditioned and unconditioned stimuli are noncontiguous, requires both the cerebellum and the hippocampus and exhibits striking parallels to declarative memory formation in humans. Identification of the neural structures critical to the development and maintenance of the conditioned eyeblink response is an essential precursor to the investigation of the mechanisms responsible for the formation of these associative memories. In this review, we describe the evidence used to identify the neural substrates of classical eyeblink conditioning and potential mechanisms of memory formation in critical regions of the hippocampus and cerebellum. Addressing a central goal of behavioral neuroscience, exploitation of this simple yet robust model of learning and memory has yielded one of the most comprehensive descriptions to date of the physical basis of a learned behavior in mammals.

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Impaired delay eyeblink classical conditioning in individuals with anterograde amnesia resulting from anterior communicating artery aneurysm rupture.

Cited by 17 publications

References 109 publications

A neural model of hippocampal–striatal interactions in associative learning and transfer generalization in various neurological and psychiatric patients

A neural model of hippocampal–striatal interactions in associative learning and transfer generalization in various neurological and psychiatric patients

Parallel acquisition of awareness and differential delay eyeblink conditioning

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

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