Impairment of Long-Term Associative Memory in Aging Snails (Lymnaea stagnalis)

Age-dependent impairment in learning and memory functions occurs in many animal species, including humans. Although cell death contributes to age-related cognitive impairment in pathological forms of aging, learning and memory deficiencies develop with age even without substantial cell death. The mo...

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Veröffentlicht in:Behavioral neuroscience 2007-12, Vol.121 (6), p.1400-1414
Hauptverfasser: Hermann, Petra M, Lee, Arden, Hulliger, Sara, Minvielle, Michelle, Ma, Bonita, Wildering, Willem C
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container_end_page 1414
container_issue 6
container_start_page 1400
container_title Behavioral neuroscience
container_volume 121
creator Hermann, Petra M
Lee, Arden
Hulliger, Sara
Minvielle, Michelle
Ma, Bonita
Wildering, Willem C
description Age-dependent impairment in learning and memory functions occurs in many animal species, including humans. Although cell death contributes to age-related cognitive impairment in pathological forms of aging, learning and memory deficiencies develop with age even without substantial cell death. The molecular and cellular basis of this biological aging process is not well understood but seems to involve a decline in the aging brain's capacity for experience-dependent plasticity. To aid in resolving this issue, we used a simple snail appetitive classical conditioning paradigm in which the underlying molecular, cellular, and neural network functions can be directly linked to age-associated learning and memory performance (i.e., the Lymnaea stagnalis feeding system). Our results indicate that age does not affect the acquisition of appetitive memory but that retention and/or consolidation of long-term memory become progressively impaired with advancing age. The latter phenomenon correlates with declining electrophysiological excitability in key neurons controlling the feeding behavior. Together, these results present the Lymnaea feeding system as a powerful paradigm for investigations of cellular and molecular foundations of biological aging in the brain.
doi_str_mv 10.1037/0735-7044.121.6.1400
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Although cell death contributes to age-related cognitive impairment in pathological forms of aging, learning and memory deficiencies develop with age even without substantial cell death. The molecular and cellular basis of this biological aging process is not well understood but seems to involve a decline in the aging brain's capacity for experience-dependent plasticity. To aid in resolving this issue, we used a simple snail appetitive classical conditioning paradigm in which the underlying molecular, cellular, and neural network functions can be directly linked to age-associated learning and memory performance (i.e., the Lymnaea stagnalis feeding system). Our results indicate that age does not affect the acquisition of appetitive memory but that retention and/or consolidation of long-term memory become progressively impaired with advancing age. The latter phenomenon correlates with declining electrophysiological excitability in key neurons controlling the feeding behavior. 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subjects Action Potentials - physiology
Age Factors
Aging
Analysis of Variance
Animal
Animal Feeding Behavior
Animals
Apoptosis
Association Learning - physiology
Associative Memory
Behavior, Animal
Behavioral psychophysiology
Biological and medical sciences
Brain
Cerebellum - cytology
Classical Conditioning
Correlation analysis
Electrical Activity
Feeding Behavior - drug effects
Feeding Behavior - physiology
Freshwater
Fundamental and applied biological sciences. Psychology
Learning
Long Term Memory
Lymnaea stagnalis
Memory
Memory Disorders - physiopathology
Mollusks
Neurons - drug effects
Neurons - physiology
Physiological Aging
Psychology. Psychoanalysis. Psychiatry
Psychology. Psychophysiology
Snails
Snails - physiology
Sucrose - pharmacology
Sweetening Agents - pharmacology
Time Factors
title Impairment of Long-Term Associative Memory in Aging Snails (Lymnaea stagnalis)
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