Neural lesioning with ribosome-inactivating proteins: suicide transport and immunolesioning

Trends Neurosci. 1992 Aug;15(8):285-90. doi: 10.1016/0166-2236(92)90078-m.

Abstract

Toxic lectins, plant proteins that inactivate ribosomes, irreversibly inhibit protein synthesis with high efficiency. After intraneural (subepineurial) microinjection, these agents are taken up by axons and are retrogradely transported to the perikarya, where they result in cell death. These 'suicide transport' toxins can produce pathway-specific lesions that are useful in several types of experiment, including cellular localization of neurotransmitter receptors. The toxins can be coupled to monoclonal antibodies to produce immunotoxins: reagents that can make highly selective lesions of specific types of neurons. Central or peripheral neurons that express the low-affinity NGF receptor are selectively destroyed by the immunotoxin 192 IgG-saporin. Development of other anti-neuronal immunotoxins should provide a variety of powerful selective lesioning tools.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Antibodies, Monoclonal
  • Brain Mapping / methods
  • Cell Death / drug effects
  • Immunotoxins / toxicity*
  • Lectins / toxicity*
  • N-Glycosyl Hydrolases*
  • Neurophysiology / methods*
  • Neurotoxins / toxicity*
  • Plant Proteins / pharmacokinetics
  • Plant Proteins / toxicity
  • Receptors, Nerve Growth Factor / antagonists & inhibitors
  • Receptors, Nerve Growth Factor / drug effects
  • Receptors, Neurotransmitter / antagonists & inhibitors
  • Receptors, Neurotransmitter / drug effects*
  • Ribosome Inactivating Proteins, Type 1
  • Ribosomes / drug effects*
  • Saporins

Substances

  • Antibodies, Monoclonal
  • Immunotoxins
  • Lectins
  • Neurotoxins
  • Plant Proteins
  • Receptors, Nerve Growth Factor
  • Receptors, Neurotransmitter
  • Ribosome Inactivating Proteins, Type 1
  • N-Glycosyl Hydrolases
  • Saporins