Age-related deficits in synaptic plasticity rescued by activating PKA or PKC in sensory neurons of Aplysia californica

Andrew T. Kempsell, Lynne A. Fieber

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Brain aging is associated with declines in synaptic function that contribute to memory loss, including reduced postsynaptic response to neurotransmitters and decreased neuronal excitability. To understand how aging affects memory in a simple neural circuit, we studied neuronal proxies of memory for sensitization in mature vs. advanced age Aplysia californica (Aplysia). L-Glutamate- (L-Glu-) evoked excitatory currents were facilitated by the neuromodulator serotonin (5-HT) in sensory neurons (SN) isolated from mature but not aged animals. Activation of protein kinase A (PKA) and protein kinase C (PKC) signaling rescued facilitation of L-Glu currents in aged SN. Similarly, PKA and PKC activators restored increased excitability in aged tail SN. These results suggest that altered synaptic plasticity during aging involves defects in second messenger systems.

Original languageEnglish (US)
Article number173
JournalFrontiers in Aging Neuroscience
Volume7
Issue numberSEP
DOIs
StatePublished - 2015

Keywords

  • Long term potentiation
  • Marine invertebrate
  • Pedal ganglion
  • Pleural ganglion
  • Short term memory

ASJC Scopus subject areas

  • Aging
  • Cognitive Neuroscience

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