Basal and apical synapses of CA1 pyramidal cells employ different LTP induction mechanisms.

  1. J E Haley,
  2. E Schaible,
  3. P Pavlidis,
  4. A Murdock, and
  5. D V Madison
  1. Department of Molecular and Cellular Physiology, Stanford University School of Medicine, California 94305, USA.

Abstract

Nitric oxide (NO) production has been widely reported to be required for the induction of long-term potentiation (LTP) in hippocampal CA1 cells. Of the two constitutive isoforms of NO synthase, the endothelial form (eNOS) has been implicated in the induction of LTP in these cells. The distribution of eNOS within CA1 cells is not uniform, however, being present in the cell bodies and apical dendrites but absent from the basal dendrites. Using extracellular and intracellular recording techniques, we demonstrate that LTP induction in stratum radiatum synapses (onto apical dendrites) is dependent on NO production, being attenuated by pretreatment with a NOS inhibitor. LTP induced in stratum oriens synapses (onto basal dendrites) is, however, resistant to NOS inhibitors. Both forms of LTP require the activation of N-methyl-D-aspartate (NMDA) receptors because induction of LTP in both stratum radiatum and stratum oriens is blocked by AP5. Thus, it appears that synapses onto apical and basal dendrites of CA1 cells use different cellular mechanisms of LTP induction.

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