Classical conditioning of the eyeblink response in the delay paradigm in adults aged 18–83 years.

Woodruff-Pak, Diana S.; Thompson, Richard F.

doi:10.1037/0882-7974.3.3.219

Cited by 151 publications

(163 citation statements)

References 28 publications

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“…These findings provided evidence that this age-related deleterious process occurs much earlier and that some cognitive abilities exhibit a dramatic decline between 8 and 11 months of age, consistent with one human study (28). From our survey of the literature, it appears that very few reports of animal studies have described changes in learning and memory during this period.…”

Section: Discussionsupporting

confidence: 66%

Reversal of age-related learning deficits and brain oxidative stress in mice with superoxide dismutase/catalase mimetics

Liu

Liu²,

Bi³

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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336

215

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Oxidative stress has been implicated in cognitive impairment in both old experimental animals and aged humans. This implication has led to the notion that antioxidant defense mechanisms in the brain are not sufficient to prevent age-related increase in oxidative damage and that dietary intake of a variety of antioxidants might be beneficial for preserving brain function. Here we report a dramatic loss of learning and memory function from 8 to 11 months of age in mice, associated with marked increases in several markers of brain oxidative stress. Chronic systemic administration of two synthetic catalytic scavengers of reactive oxygen species, Eukarion experimental compounds EUK-189 and EUK-207, from 8 to 11 months almost completely reversed cognitive deficits and increase in oxidative stress taking place during this time period in brain. In particular, increase in protein oxidation was completely prevented, whereas increase in lipid peroxidation was decreased by Ϸ50%. In addition, we observed a significant negative correlation between contextual fear learning and levels of protein oxidation in brain. These results further support the role of reactive oxygen species in age-related learning impairment and suggest potential clinical applications for synthetic catalytic scavengers of reactive oxygen species.A ging in humans, as well as in experimental animals, is associated with a slow deterioration of cognitive performance and, in particular, of learning and memory (1-5). In humans, recent studies (6) have indicated the importance of impaired learning and memory processes, because 12% of humans with mild cognitive impairment will develop Alzheimer's disease as opposed to 2% of the general population. Oxidative damage has long been proposed to be critically involved in several pathological manifestations of aging (7,8). Numerous studies (9 -12) have indeed reported increases in protein oxidation and lipid peroxidation in various regions of aged mammalian brains. These findings have led to the notion that antioxidant defense mechanisms in the brain are not sufficient to prevent age-related increase in oxidative damage and that dietary intake of a variety of antioxidants might be beneficial for preserving brain function. In agreement with this idea, synthetic catalytic molecules that exhibit both superoxide dismutase (SOD) and catalase activity significantly increase the mean and maximum lifespan in Caenorhabditis elegans (13) and alleviate lethal oxidative pathologies in mice with genetically deleted . The present studies tested, in wild-type mice, the effects of such molecules on age-related learning and memory impairment, and on markers of oxidative damage in the brain. We found that C57BL͞6N Sim mice exhibit a dramatic decrease in learning and memory function between 8 and 11 months of age, accompanied by a marked increase in brain oxidative damage. Chronic treatment of mice with two recently developed SOD͞catalase mimetics over a 3-month period almost completely reversed the age-related decline in cognitive functi...

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Section: Discussionsupporting

confidence: 66%

Reversal of age-related learning deficits and brain oxidative stress in mice with superoxide dismutase/catalase mimetics

Liu

Liu²,

Bi³

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

336

215

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“…Woodruff-Pak and Thompson (1988) found similar results in their younger participants trained on delay conditioning (learning progressed from 40% to 80% CRs over the first 72 trials). Therefore, rapid rates of learning were expected in the age group we examined (the mean age of the normal control participants was in the mid-40s; Patient B.R.…”

Section: Conditioningsupporting

confidence: 63%

Cerebellar cortical degeneration disrupts discrimination learning but not delay or trace classical eyeblink conditioning.

Fortier¹,

Disterhoft²,

McGlinchey-Berroth³

2000

Neuropsychology

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The authors investigated classical eyeblink conditioning in a relatively rare patient, B.R., with extensive cerebellar cortical atrophy and marked sparing of the dentate nucleus. Patient B.R.'s ability to acquire and extinguish simple associations (delay and trace conditioning tasks) as well as her ability to acquire more complex associations (temporal and simple discrimination tasks) were examined. There are 2 primary findings from this study. First, B.R. showed normal acquisition and extinction in delay and trace conditioning. Second, she demonstrated a complete inability to learn associative discriminations, even in the case of a simple 2-tone discrimination within the context of a delay paradigm. The latter finding was unexpected because of the sparing of her deep cerebellar nuclei. These data suggest that the cerebellar cortex, or pathways traversing cerebellar cortex, play an important role in classical eyeblink discrimination learning.

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“…Several studies have shown impaired conditioning with increasing age (Bellebaum & Daum, 2004;Knuttinen, Power, Preston, & Disterhoft, 2001;LaBar, Cook, Torpey, & Welsh-Bohmer, 2004;Solomon, Pomerleau, Bennett, James, & Morse, 1989;Woodruff-Pak & Thompson, 1988). In the present study, the age (61 years) of one member of the trace group fell in a range that has previously shown impairment relative to younger subjects (Bellebaum & Daum, 2004;LaBar et al, 2004).…”

Section: Discussionmentioning

confidence: 58%

The role of awareness in delay and trace fear conditioning in humans

Knight

Nguyen

Bandettini

2006

Cognitive, Affective, & Behavioral Neuroscience

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Expression of conditional fear without awareness has been previously demonstrated during delay conditioning, a procedure in which the conditioned stimulus (CS) and unconditioned stimulus (UCS) overlap. However, less is known about the role of awareness in trace fear conditioning, where an interval of time separates the CS and UCS. The present study assessed skin conductance response (SCR) and UCS expectancy during delay and trace conditioning. UCS predictability was varied on a trial-bytrial basis by presenting perithreshold auditory CSs. Differential UCS expectancies were demonstrated only on perceived delay and trace trials. Learning-related SCRs were observed during both perceived and unperceived delay CSs. In contrast, differential SCRs were demonstrated only for perceived trace CSs. These data suggest that awareness is necessary for conditional responding during trace, but not delay, fear conditioning.

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Classical conditioning of the eyeblink response in the delay paradigm in adults aged 18–83 years.

Cited by 151 publications

References 28 publications

Reversal of age-related learning deficits and brain oxidative stress in mice with superoxide dismutase/catalase mimetics

Reversal of age-related learning deficits and brain oxidative stress in mice with superoxide dismutase/catalase mimetics

Cerebellar cortical degeneration disrupts discrimination learning but not delay or trace classical eyeblink conditioning.

The role of awareness in delay and trace fear conditioning in humans

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