Spontaneous recovery of deficits in spatial memory and cholinergic potentiation of NMDA in CA1 neurons during chronic lithium treatment

Hippocampus. 1992 Jul;2(3):279-86. doi: 10.1002/hipo.450020307.

Abstract

The therapeutic action of lithium in affective disorders is still unclear. One effect of lithium is to deplete membrane inositol and consequently to exhaust the phosphoinositide (PI) pathway. Under chronic lithium treatment, rats showed persistent performance deficits in an active avoidance task and in a visually cued maze. The same treatment, however, resulted in only a transient deficit in the performance of rats in a spatial memory task. Lithium treatment caused a similarly transient deficit in the ability of acetylcholine to potentiate responses to N-methyl-D-aspartate (NMDA) in neurons of the hippocampal slice. The authors propose that the development of compensatory mechanisms may account for the lack of severe memory impairments during lithium treatment. It is suggested that the effects of lithium on the PI pathway are not sufficient to explain the behavioral consequences of chronic lithium treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / pharmacology*
  • Animals
  • Avoidance Learning / drug effects
  • Avoidance Learning / physiology
  • Chlorides / pharmacology*
  • Drug Synergism
  • Evoked Potentials / drug effects
  • Hippocampus / drug effects
  • Hippocampus / physiology*
  • In Vitro Techniques
  • Learning / physiology
  • Lithium / pharmacology*
  • Lithium Chloride
  • Male
  • Memory / drug effects
  • Memory / physiology*
  • Motor Activity / drug effects
  • N-Methylaspartate / pharmacology*
  • Neurons / drug effects
  • Neurons / physiology*
  • Pyramidal Tracts / drug effects
  • Pyramidal Tracts / physiology*
  • Rats
  • Rats, Wistar
  • Space Perception / drug effects
  • Space Perception / physiology*
  • Tetrodotoxin / pharmacology

Substances

  • Chlorides
  • Tetrodotoxin
  • N-Methylaspartate
  • Lithium
  • Lithium Chloride
  • Acetylcholine