Disruption of human eyeblink conditioning after central cholinergic blockade with scopolamine.

Solomon, Paul R.; Groccia-Ellison, MaryEllen; Flynn, Deirdre; Mirak, Jennifer; Edwards, Keith R.; Dunehew, Allen R.; Stanton, Mark E.

doi:10.1037/0735-7044.107.2.271

Cited by 73 publications

(41 citation statements)

References 40 publications

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“…Sub-seizure electrical stimulation of the hippocampus during delay eyeblink conditioning disrupts the acquisition, but not the expression of eyeblink CRs (Salafia et al 1979). Systemic injection of the cholinergic antagonist scopolamine, which alters hippocampal neuronal activity, severely disrupts delay eyeblink conditioning in rabbits (Moore et al 1976) and in humans (Solomon et al 1993). Lesions of medial septum, which modulates hippocampal activity through cholinergic projections, disrupt the acquisition delay eyeblink conditioning in rabbits (Allen et al 2002).…”

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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Section: Discussionmentioning

confidence: 99%

Parallel acquisition of awareness and differential delay eyeblink conditioning

Weidemann

Antees²

2012

Learn. Mem.

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“…Drug effects on acquisition are legion. In general, drugs that enhance acetylcholine (ACh) function enhance acquisition, and drugs that impair ACh function impair acquisition, either via actions on nicotinic or muscarinic receptor systems or via acetylcholinesterase (e.g., Solomon et al 1993;Woodruff-Pak and Ewers 2000;see above). Drugs that impair functions of certain types of calcium channels, for example, nimodipine, enhance acquisition and retention of eyeblink conditioning (Deyo et al 1989;Straube et al 1990;Solomon et al 1995;Woodruff-Pak et al 1997), consistent with the putative AHP mechanism operative in hippocampal pyramidal neurons (see above).…”

Section: Modulatory Effects On Eyeblink Conditioningmentioning

confidence: 99%

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

Christian¹,

Thompson²

2003

Learn. Mem.

565

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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“…Previous animal studies have demonstrated a retardation in classical conditioning of the eye-Bahro/Molchan/Sunderland/Herscovitch/ Schreurs blink response, a relatively simple form of learning and memory, after scopolamine administration [4][5][6]. Several human eyeblink conditioning studies have also shown that scopolamine produces a retardation in classical eyeblink conditioning [7,8]. The major influence of scopolamine in the central nervous system is on the cholinergic pathways to the hippocampus and neocortex.…”

Section: Introductionmentioning

confidence: 99%

The Effects of Scopolamine on Changes in Regional Cerebral Blood Flow during Classical Conditioning of the Human Eyeblink Response

Bahro

Molchan²,

Sunderland³

et al. 1999

Neuropsychobiology

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We examined the effects of scopolamine on the functional anatomy of classical conditioning of the human eyeblink response. Ten healthy young normal female volunteers (mean age ± SEM: 26.7 ± 0.9 years) were administered 0.4 mg scopolamine intravenously 1 h before regional cerebral blood flow (rCBF) was measured with positron emission tomography (PET) and H₂¹⁵O. Scans occurred during three sequential phases: (1) explicitly unpaired presentations of the unconditioned stimulus (airpuff to the right eye) and conditioned stimulus (binaural tone), (2) paired presentations of the two stimuli (associative learning) and (3) explicitly unpaired presentation of the stimuli (extinction phase). Scopolamine impaired acquisition of the conditioned eyeblink response (54.7 ± 4.9%) relative to 18 untreated subjects from two previous PET studies. Regions that showed significant relative increases in rCBF during conditioning included the right lateral occipital cortex, the right inferior occipital cortex, the right lateral temporo-occipital cortex, the left medial temporo-occipital cortex, the posterior cingulate, the right cerebellum/brain stem area and the medial cerebellum. Significant relative decreases in rCBF were measured in the thalamus, the left putamen/insula area, the right putamen and the left and middle cerebellar cortex. The data partially replicate previous findings in unmedicated young volunteers of conditioning-specific rCBF changes in the cingulate cortex, the cerebellar cortex, the insula and the lateral temporo-occipital cortex. Our finding of decreased rCBF in the thalamus and increased rCBF in the occipital cortex may be attributable to effects of scopolamine per se rather than conditioning. Our data lend further support to the notion that classical conditioning involves distributed changes in multiple systems within the central nervous system.

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Disruption of human eyeblink conditioning after central cholinergic blockade with scopolamine.

Cited by 73 publications

References 40 publications

Parallel acquisition of awareness and differential delay eyeblink conditioning

Parallel acquisition of awareness and differential delay eyeblink conditioning

Neural Substrates of Eyeblink Conditioning: Acquisition and Retention

The Effects of Scopolamine on Changes in Regional Cerebral Blood Flow during Classical Conditioning of the Human Eyeblink Response

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