Classical Eyeblink Conditioning in Normal and Autistic Children

Sears, Lonnie; Steinmetz, Joseph E.

doi:10.1007/0-306-46896-4_7

Cited by 6 publications

(11 citation statements)

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“…The eyeblink conditioning paradigm offers a number of advantages as a behavioral test of a rodent model of autism [3,41,48]. There is an enormous body of empirical research on the behavioral and neurobiological mechanisms of eyeblink conditioning gathered over the past 60 years in both humans [54] and animals models [55].…”

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confidence: 99%

Discrimination learning and reversal of the conditioned eyeblink reflex in a rodent model of autism

Stanton

Peloso

Brown

et al. 2007

Behavioural Brain Research

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Offspring of rats exposed to valproic acid (VPA) on Gestational Day (GD) 12 have been advocated as a rodent model of autism because they show neuron loss in brainstem nuclei and the cerebellum resembling that seen in human autistic cases [20,37]. Studies of autistic children have reported alterations in acquisition of classical eyeblink conditioning [40] and in reversal of instrumental discrimination learning [9]. Acquisition of discriminative eyeblink conditioning depends on known brainstem-cerebellar circuitry whereas reversal depends on interactions of this circuitry with the hippocampus and prefrontal cortex. In order to explore behavioral parallels of the VPA rodent model with human autism, the present study exposed pregnant Long-Evans rats to 600 mg/kg VPA on GD12 [cf. 37] and tested their offspring from PND26-31 on discriminative eyeblink conditioning and reversal. VPA rats showed faster eyeblink conditioning, consistent with studies in autistic children [40]. This suggests that previously reported parallels between human autism and the VPA rodent model with respect to injury to brainstem-cerebellar circuitry [37] are accompanied by behavioral parallels when a conditioning task engaging this circuitry is used. VPA rats also showed impaired reversal learning, but this likely reflected "carry-over" of enhanced conditioning during acquisition rather than a reversal learning deficit like that seen in human autism. Further studies of eyeblink conditioning in human autism and in various animal models may help to identify the etiology of this developmental disorder. KeywordsEyeblink Conditioning; Gestational Valproate Exposure; Discrimination Reversal; Cerebellum; Hippocampus; Development The purpose of this article is to use a developmental rodent model of eyeblink conditioning to gather evidence bearing on the hypothesis that early gestational injury to the brainstem plays a role in the etiology of autism [3,37,39]. Evidence for this hypothesis arises from a disparate set of findings that show remarkable convergence [39]. The first clues came from reports of an association between autism and early gestational exposure to thalidomide and misoprostol [27]. Knowledge concerning the teratology of thalidomide permits inferences concerning the timing of thalidomide exposure based on the presence of craniofacial defects (ear anomolies). When thalidomide cases involving exposure specifically between 20-24 days post-conception were considered, autism occurred at a staggering rate (~30%, [39]). It was subsequently

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confidence: 99%

Discrimination learning and reversal of the conditioned eyeblink reflex in a rodent model of autism

Stanton

Peloso

Brown

et al. 2007

Behavioural Brain Research

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“…Eye-blink conditioning (EBC) is a model system for studying neural correlates of learning and memory (Sears and Steinmetz 2000;Stanton and Freeman 1994;Woodruff-Pak andSteinmetz 2000a, 2000b). Data collected from human and animals (monkeys, rabbits, rats, cats, mice) show similar patterns of acquisition, retention, and extinction of EBC.…”

Section: Eye-blink Conditioningmentioning

confidence: 99%

“…The EBC task can be varied by changing the length of the trace or complexity of the conditioning stimuli, or by methods such as discrimination reversal conditioning (Sears and Steinmetz 2000). There is evidence that delay EBC (when the CS and US overlap and coterminate) can be acquired and retained independently of the forebrain and independently of awareness, whereas trace EBC [which occurs when a short empty interval called the interstimulus interval (ISI) separates the CS and US] cannot (Manns and Clark 2002).…”

Section: Eye-blink Conditioningmentioning

confidence: 99%

“…Although EBC has been well studied in adults, considerably less work has been done in human infants and children. The developmental aspects of the conditioned response have not been systematically studied using either a cross-sectional or a longitudinal approach (Sears and Steinmetz 2000). From limited published data on normal infants and Standardized visual display of brightly colored objects unconditional stimulus (US; typically a brief air puff to the Soft band to secure the infant's head eyelid area).…”

Section: Eye-blink Conditioningmentioning

confidence: 99%

“…Continued, next page children, Sears and Steinmetz (2000) described the developmental process. Between infancy and early childhood, the acquisition rate for the conditioned eye-blink response dramatically increases from 28% at 1 month to levels near 80% at 5 months, and near 70% for 4-to 6-year-olds.…”

Section: Eye-blink Conditioningmentioning

confidence: 99%

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Comparable measures of cognitive function in human infants and laboratory animals to identify environmental health risks to children.

Sharbaugh

Viet

Fraser

et al. 2003

Environ Health Perspect

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The importance of including neurodevelopmental end points in environmental studies is clear. A validated measure of cognitive function in human infants that also has a homologous or parallel test in laboratory animal studies will provide a valuable approach for large-scale studies. Such a comparable test will allow researchers to observe the effect of environmental neurotoxicants in animals and relate those findings to humans. In this article, we present the results of a review of post-1990, peerreviewed literature and current research examining measures of cognitive function that can be applied to both human infants (0-12 months old) and laboratory animals. We begin with a discussion of the definition of cognitive function and important considerations in cross-species research. We then describe identified comparable measures, providing a description of the test in human infants and animal subjects. Available information on test reliability, validity, and population norms, as well as test limitations and constraints, is also presented.

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Effect of delay interval on classical eyeblink conditioning in 5‐month‐old human infants

Claflin

Stanton

Herbert

et al. 2002

Developmental Psychobiology

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Associative learning was evaluated in human infants with simple delay classical eyeblink conditioning. A tone conditioned stimulus (CS) was paired with an airpuff unconditioned stimulus (US) at three different delay intervals (250, 650, and 1,250 ms). Independent groups of healthy, full-term 5-month-old human infants were assigned to these three paired conditions and received two identical training sessions 1 week apart. The two longer delays resulted in associative conditioning, as confirmed by comparison with unpaired control groups. However, only at the 650-ms delay were associative eyeblinks adaptively timed to avoid the airpuff. The delay function at 5 months of age appears much sharper than is observed in adults. Together with the findings of A. H. Little, L. P. Lipsitt, and C. Rovee-Collier (1984), the present study suggests a downward shift in the optimal delay interval for associative eyeblink conditioning between 1 and 6 months of age. However, this delay remains longer than what is typically reported in adults.

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Classical Eyeblink Conditioning in Normal and Autistic Children

Cited by 6 publications

References 59 publications

Discrimination learning and reversal of the conditioned eyeblink reflex in a rodent model of autism

Discrimination learning and reversal of the conditioned eyeblink reflex in a rodent model of autism

Comparable measures of cognitive function in human infants and laboratory animals to identify environmental health risks to children.

Effect of delay interval on classical eyeblink conditioning in 5‐month‐old human infants

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