Activation of the medial septal area attenuates LTP of the lateral perforant path and enhances heterosynaptic LTD of the medial perforant path in aged rats

Kevin Pang, Megan J. Williams, David S. Olton

Research output: Contribution to journalArticlepeer-review

29 Scopus citations

Abstract

Age-related memory impairments may be due to dysfunction of the septohippocampal system. The medial septal area (MSA) provides the major cholinergic projection to the hippocampus and is critical for memory. Knowledge of the neurobiological mechanisms by which the cholinergic system can attenuate age-related memory loss can facilitate the development of effective cognitive enhancers. At present, one of the best neurobiological models of memory formation is long-term potentiation/long-term depression (LTP/LTD). In previous studies, intraseptal infusion of the muscarinic agonist oxotremorine, which excites MSA neurons, improved memory in aged rats. The present study examined LTP and LTD in aged Fisher 344 rats following intraseptal infusion of oxotremorine. LTP and LTD were assessed using the slope of the EPSP recorded from the hilar region of the dentate gyrus. Induction of LTP was blocked in the lateral perforant path, but not in the medial perforant path, following intraseptal infusions of oxotremorine. The generation and amplitude of heterosynaptic LTD was enhanced in the medial perforant path, but not in the lateral perforant path. The results provide evidence that pharmacological activation of the MSA can modulate LTP and LTD in the hippocampus of aged rats. The implications of these results with respect to memory and synaptic plasticity in the hippocampus are discussed.

Original languageEnglish (US)
Pages (from-to)150-160
Number of pages11
JournalBrain Research
Volume632
Issue number1-2
DOIs
StatePublished - Dec 31 1993
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Molecular Biology
  • Neuroscience(all)
  • Developmental Biology

Keywords

  • Acetylcholine
  • Aging
  • Hippocampus
  • Long-term depression
  • Long-term potentiation
  • N-methyl-d-aspartate
  • Opioid peptide

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