Postsynaptic Regulation of Long-Term Facilitation in Aplysia

Curr Biol. 2008 Jun 24;18(12):920-5. doi: 10.1016/j.cub.2008.05.038.

Abstract

Repeated exposure to serotonin (5-HT), an endogenous neurotransmitter that mediates behavioral sensitization in Aplysia[1-3], induces long-term facilitation (LTF) of the Aplysia sensorimotor synapse [4]. LTF, a prominent form of invertebrate synaptic plasticity, is believed to play a major role in long-term learning in Aplysia[5]. Until now, LTF has been thought to be due predominantly to cellular processes activated by 5-HT within the presynaptic sensory neuron [6]. Recent work indicates that LTF depends on the increased expression and release of a sensory neuron-specific neuropeptide, sensorin [7]. Sensorin released during LTF appears to bind to autoreceptors on the sensory neuron, thereby activating critical presynaptic signals, including mitogen-activated protein kinase (MAPK) [8, 9]. Here, we show that LTF depends on elevated postsynaptic Ca2+ and postsynaptic protein synthesis. Furthermore, we find that the increased expression of presynaptic sensorin resulting from 5-HT stimulation requires elevation of postsynaptic intracellular Ca2+. Our results represent perhaps the strongest evidence to date that the increased expression of a specific presynaptic neuropeptide during LTF is regulated by retrograde signals.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Aplysia / physiology*
  • Calcium / metabolism
  • Calcium / pharmacology*
  • Excitatory Postsynaptic Potentials / physiology*
  • Gene Expression Regulation*
  • Long-Term Potentiation / drug effects*
  • Long-Term Potentiation / physiology
  • Neuropeptides / metabolism
  • Neuropeptides / pharmacology*
  • Serotonin / metabolism
  • Signal Transduction
  • Synapses / physiology

Substances

  • Neuropeptides
  • sensorin A protein, Aplysia
  • Serotonin
  • Calcium