Epilepsy Research
Volume 27, Issue 2 , Pages 111-118, May 1997

Post-ictal depression transiently inhibits induction of LTP in area CA1 of the rat hippocampal slice

  • Deborah S Barr

      Affiliations

    • Department of Pharmacology, Duke University Medical Center, Durham, NC 27 710, USA
  • ,
  • Kendall L Hoyt

      Affiliations

    • Neurology Research Laboratory, Veterans Administration Medical Center, 508 Fulton St., Bldg 16, Rm 25, Durham, NC 27 705, USA
  • ,
  • Scott D Moore

      Affiliations

    • Neurology Research Laboratory, Veterans Administration Medical Center, 508 Fulton St., Bldg 16, Rm 25, Durham, NC 27 705, USA
    • Department of Psychiatry, Duke University Medical Center, Durham, NC 27 710, USA
  • ,
  • Wilkie A Wilson

      Affiliations

    • Department of Pharmacology, Duke University Medical Center, Durham, NC 27 710, USA
    • Neurology Research Laboratory, Veterans Administration Medical Center, 508 Fulton St., Bldg 16, Rm 25, Durham, NC 27 705, USA
    • Corresponding Author InformationCorresponding author.

Received 8 July 1995; accepted 4 January 1997.

Abstract 

We tested the effects of electrographic seizures (EGSs) elicited in a remote site (area CA3) on the induction of long-term potentiation (LTP) in area CA1 of the rat hippocampal slice. Induction of LTP was inhibited only when the LTP-inducing stimulus was delivered during the period of post-ictal depression (5–10 min period of field response depression) following an evoked EGS. It was not inhibited during the tonic firing phase of the EGS. The time course for the recovery of the ability to induce LTP after an EGS matched the recovery of field responses from post-ictal depression. Moreover, the magnitude of LTP was inversely proportional to the duration of post-ictal depression. Delaying the onset of depression with the adenosine A1 receptor antagonist 8-cyclopentyltheophylline (CPT) permitted LTP induction at a time point when it would normally be suppressed. Finally, the inhibitory effects of post-ictal depression on LTP induction were not restricted to electrically evoked EGSs, as LTP could not be induced during the depressed phase following a spontaneous EGS elicited in 10 mM K+ medium. These results demonstrate that the inhibition of LTP induction following epileptiform activity in vitro is in part a consequence of post-ictal depression of responses.

Keywords:  Amnesia, Epilepsy, LTP, Hippocampus

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PII: S0920-1211(97)01027-9

Epilepsy Research
Volume 27, Issue 2 , Pages 111-118, May 1997