Neuroscience and Behavioral Physiology

, Volume 31, Issue 3, pp 305–310

The Effects of Forelimb Deafferentation on the Post-Natal Development of Synaptic Plasticity in the Hippocampus

Authors

  • I. E. Kudryashov
    • Russian Academy of SciencesInstitute of Higher Nervous Activity and Neurophysiology
  • I. V. Kudryashova
    • Russian Academy of SciencesInstitute of Higher Nervous Activity and Neurophysiology
Article

DOI: 10.1023/A:1010338702708

Cite this article as:
Kudryashov, I.E. & Kudryashova, I.V. Neurosci Behav Physiol (2001) 31: 305. doi:10.1023/A:1010338702708

Abstract

The effects of partial deafferentation of the forelimb on the development of long-term potentiation in the hippocampus of rats aged 13–18 days were studied. Long-term potentiation in hippocampus field CA1 was of greater amplitude and duration in control rats at 16–18 days of post-natal ontogenesis than in adult animals. Partial deafferentation by section of the median nerve in the forelimb on the 13th day of life led to the disappearance of this excess at 16–18 days. The peak in synaptic plasticity occurred later in operated animals – on day 17 – and was much less marked than in controls. The decreases in the amplitude and duration of long-term potentiation in hippocampal field CA1 in operated animals provides evidence for a decrease in the sensitivity and/or number of NMDA receptors. This suggests that partial deafferentation of one limb may lead not to a decrease but to an increase in spike and synaptic activity in the hippocampus, which in normal conditions may affect the maturation of the plastic properties of synaptic transmission associated with the expression and positions of NMDA receptors. The level of long-term potentiation in sham-operated rats was significantly greater than in controls of the same age. This significant increase in NMDA-dependent long-term potentiation may be explained by a decrease in the level of activation due to anesthesia. It is suggested that the decrease in the spike activity of cells receiving signals from the median nerve may be compensated for by activation of other specific and non-specific inputs.

Copyright information

© Plenum Publishing Corporation 2001