Co-induction of long-term potentiation and long-term depression at a central synapse in the leech

Neurobiol Learn Mem. 2008 Jul;90(1):275-9. doi: 10.1016/j.nlm.2007.11.004. Epub 2008 Jan 7.

Abstract

Most studies of long-term potentiation (LTP) have focused on potentiation induced by the activation of postsynaptic NMDA receptors (NMDARs). However, it is now apparent that NMDAR-dependent signaling processes are not the only form of LTP operating in the brain [Malenka, R. C., & Bear, M. F. (2004). LTP and LTD: An embarrassment of riches. Neuron, 44, 5-21]. Previously, we have observed that LTP in leech central synapses made by the touch mechanosensory neurons onto the S interneuron was NMDAR-independent [Burrell, B. D., & Sahley, C. L. (2004). Multiple forms of long-term potentiation and long-term depression converge on a single interneuron in the leech CNS. Journal of Neuroscience, 24, 4011-4019]. Here we examine the cellular mechanisms mediating T-to-S (T-->S) LTP and find that its induction requires activation of metabotropic glutamate receptors (mGluRs), voltage-dependent Ca(2+) channels (VDCCs) and protein kinase C (PKC). Surprisingly, whenever LTP was pharmacologically inhibited, long-term depression (LTD) was observed at the tetanized synapse, indicating that LTP and LTD were activated at the same time in the same synaptic pathway. This co-induction of LTP and LTD likely plays an important role in activity-dependent regulation of synaptic transmission.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Calcium Channels / physiology
  • Ganglia, Invertebrate / cytology*
  • Ganglia, Invertebrate / physiology*
  • Hirudo medicinalis
  • Interneurons / physiology
  • Long-Term Potentiation / physiology*
  • Long-Term Synaptic Depression / physiology*
  • Mechanoreceptors / physiology
  • Models, Animal
  • Neuronal Plasticity / physiology
  • Protein Kinase C / physiology
  • Receptors, Metabotropic Glutamate / physiology
  • Synaptic Transmission / physiology*

Substances

  • Calcium Channels
  • Receptors, Metabotropic Glutamate
  • Protein Kinase C