Abstract
The physiological and molecular mechanisms of age-related memory loss are complicated by the complexity of vertebrate nervous systems. This study takes advantage of a simple neural model to investigate nervous system aging, focusing on changes in learning and memory in the form of behavioral sensitization in vivo and synaptic facilitation in vitro. The effect of aging on the tail withdrawal reflex (TWR) was studied in Aplysia californica at maturity and late in the annual lifecycle. We found that short-term sensitization in TWR was absent in aged Aplysia. This implied that the neuronal machinery governing nonassociative learning was compromised during aging. Synaptic plasticity in the form of short-term facilitation between tail sensory and motor neurons decreased during aging whether the sensitizing stimulus was tail shock or the heterosynaptic modulator serotonin (5-HT). Together, these results suggest that the cellular mechanisms governing behavioral sensitization are compromised during aging, thereby nearly eliminating sensitization in aged Aplysia.
Highlights
Brain aging is associated with the progressive decline of neurophysiological processes and an increased prevalence of memory impairments
This study investigated whether behavioral sensitization in tail withdrawal reflex (TWR) undergoes age-related declines that involve changes in synaptic facilitation between SNs and MNs known to be involved in the reflex circuit
The results indicate that aging of the neural circuit for TWR resulted in learning failure, including the ability to sensitize TWR in intact animals, and related impairment of synaptic facilitation of the SN-MN circuit underlying TWR
Summary
Brain aging is associated with the progressive decline of neurophysiological processes and an increased prevalence of memory impairments. In the rodent hippocampus, aging is associated with a decrease in synapses in the dentate gyrus and area CA1, a decrease in NMDA-receptor-evoked responses at perforant path synapses onto dentate gyrus granule cells, and changes in Ca2+ regulation in area CA1 [6]. As these changes in synaptic structure and function accumulate during aging, cellular analogs of learning and memory, including long-term potentiation (LTP) and longterm depression (LTD), are disrupted. Altered synaptic plasticity in aged hippocampal networks results in age-related memory loss including reduced performance in spatial memory tasks [8, 9]
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