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Perinatal 192 IgG-Saporin as Neuroteratogen.

Abstract
The immunotoxin 192 IgG-saporin selectively destroys basal forebrain cholinergic neurons that provide cholinergic input to the hippocampus, entire cortical mantle, amygdala, and olfactory bulb. Perinatal immunotoxic lesions by 192 IgG-saporin induce long-lasting cholinergic depletion mimicking a number of developmental disorders reported in humans. The perinatal injection of 192 IgG-saporin induces several brain modifications, which are observed in neocortex and hippocampus at short and long term. These plastic changes involve both structural (alterations in brain volume, neuronal morphology, and neurogenesis) and molecular (modulations of the levels of neurotransmitters and other proteins related to neurodegeneration) levels. Moreover, the perinatal injection of 192 IgG-saporin may interact with the brain plastic capacity to react to other injuries. Perinatal 192 IgG-saporin lesions allowed investigating the role of the basal forebrain cholinergic system in modulating behavioral functions in developing as well as adult rats. After perinatal cholinergic depletion, rats display reduced ultrasonic vocalizations as neonates, learning and exploratory deficits as juveniles, altered discriminative abilities, impulsive and perseverative behaviors, and memory deficits as adults. Overall, these findings underline the importance of cholinergic system integrity for the development of specific structural and functional features.
AuthorsLaura Petrosini, Paola De Bartolo, Debora Cutuli, Francesca Gelfo
JournalCurrent topics in behavioral neurosciences (Curr Top Behav Neurosci) 2016 Vol. 29 Pg. 111-123 ISSN: 1866-3370 [Print] Germany
PMID26695170 (Publication Type: Journal Article, Review)
Chemical References
  • 192 IgG-saporin
  • Antibodies, Monoclonal
  • Immunotoxins
  • Ribosome Inactivating Proteins, Type 1
  • Teratogens
  • Saporins
Topics
  • Animals
  • Antibodies, Monoclonal (toxicity)
  • Brain (drug effects)
  • Disease Models, Animal
  • Humans
  • Immunotoxins (toxicity)
  • Neurodevelopmental Disorders (chemically induced)
  • Rats
  • Ribosome Inactivating Proteins, Type 1 (toxicity)
  • Saporins
  • Teratogens (pharmacology)

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