Acute stress facilitates trace eyeblink conditioning in C57BL/6 male mice and increases the excitability of their CA1 pyramidal neurons

  1. Craig Weiss1,3,
  2. Evgeny Sametsky1,
  3. Astrid Sasse2,
  4. Joachim Spiess2, and
  5. John F. Disterhoft1
  1. 1Department of Physiology and Institute for Neuroscience, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA 2Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, 37075 Goettingen, Germany

Abstract

The effects of stress (restraint plus tail shock) on hippocampus-dependent trace eyeblink conditioning and hippocampal excitability were examined in C57BL/6 male mice. The results indicate that the stressor significantly increased the concentration of circulating corticosterone, the amount and rate of learning relative to nonstressed conditioned mice, and the excitability of CA1 hippocampal pyramidal neurons. Behaviorally, there was no effect of the stressor on control mice that received unpaired presentations of the tone and periorbital shock, i.e., neither stressed nor nonstressed control mice showed an increase in conditioned responding that was above baseline levels. Biophysically, the stressor significantly decreased the amplitude of the post-burst afterhyperpolarization (AHP) and decreased spike frequency accommodation relative to cells from nonstressed control mice. The effect was significant for mice that were stressed either 1 h or 24 h earlier. The results suggest that the stressor increases the excitability of hippocampal pyramidal neurons and that the mechanism underlying this increase may contribute to the more rapid acquisition of hippocampally dependent eyeblink conditioning.

Footnotes

  • Article and publication are at http://www.learnmem.org/cgi/doi/10.1101/lm.89005.

    • Accepted January 11, 2005.
    • Received November 12, 2004.
| Table of Contents