SUMMARY

PART I
In part I of this thesis we investigated the effects of stress on hippocampal synaptic plasticity in both mice mand rats. The stressful situations used were: exposure of animals to acute (1 hour) or chronic stress (21 days) and in vitro exposure of hippocampal slices to elevated levels of corticosterone (20 minutes).

The following results were obtained:

Chapter 2

• Incubating slices with 100 nM corticosterone reduced the maximal slope of the fEPSP.
  Primed burst potentiation of the fEPSP was impaired after corticosterone treatment. Primed burst
  potentiation of the population spike was not impaired.
• Theta burst potentiation of both fEPSP and population spike was not impaired.
  Exposing mice briefly to a stressor impaired primed burst potentiation of the fEPSP.
  

Chapter 3

• Long-term potentiation of the fEPSP was impaired in both CA1 and dentate gyrus after exposure to chronic stress when recorded under conditions where plasma corticosterone levels are low.
  Long-term potentiation of the fEPSP was impaired in the CA1 area after in vitro exposure to high levels of corticosterone. No further decrease was observed after corticosterone treatment in stressed rats.
• Long-term potentiation in the dentate gyrus was not affected by in vitro exposure to high levels of corticosterone in both control and stressed rats.
  

PART II
In part II we investigated the effects of short term exposure to corticosterone and chronic stress on dendritic morphology and spine density of hippocampal CA1 neurons. Two different substrates of the hippocampal formation were used: organotypic slice cultures and acute slices.

The following results were obtained:

Chapter 4

• Hippocampal organotypic slice cultures contain both mineralocorticoid and glucocorticoid receptors.
• Exposing organotypic slice cultures to 100 nM of corticosterone induced atrophy of the CA1 pyramidal apical dendritic tree.
  Atrophy of apical dendrites was induced in slices when imaged ≥ 2 hours following incubation with 30 nM corticosterone.
• The effects of corticosterone on dendritic length could be prevented with the GR antagonist RU486.
  

Chapter 5

• Rats exposed to 21 days of unpredictable stress showed increased apical dendritic length of CA1 pyramidal cells.
• Exposure of slices from control animals to elevated corticosterone levels resulted in hypertrophy of CA1 apical dendrites.
• Exposing slices of stressed animals to 20 minutes of 100 nM corticosterone reversed the hypertrophy.
• Treating control and stressed rats with the GR antagonist RU486 during the last 4 days of the stress experiment prevented the effects of acute corticosterone administration, but not the effects of exposure to chronic stress.