Knock-out mice reveal a critical antiepileptic role for neuropeptide Y

Scott C. Baraban, Gunther Hollopeter, Jay C. Erickson, Philip A Schwartzkroin, Richard D. Palmiter

Research output: Contribution to journalArticlepeer-review

262 Scopus citations


Neuropeptide Y (NPY) inhibits excitatory synaptic transmission in the hippocampus and is implicated in control of limbic seizures. In the present study, we examined hippocampal function and the response to pharmacologically induced seizures in mutant mice lacking this peptide. In slice electrophysiology studies, no change in normal hippocampal function was observed in NPY-deficient mice compared with normal wild-type littermates. Kainic acid (KA) produced limbic seizures at a comparable latency and concentration in NPY-deficient mice compared with littermates. However, KA- induced seizures progressed uncontrollably and ultimately produced death in 93% of NPY-deficient mice, whereas death was rarely observed in wild-type littermates. Intracerebroventricular NPY infusion, before KA administration, prevented death in NPY-deficient mice. These results suggest a critical role for endogenous NPY in seizure control.

Original languageEnglish (US)
Pages (from-to)8927-8936
Number of pages10
JournalJournal of Neuroscience
Issue number23
StatePublished - 1997
Externally publishedYes


  • Anticonvulsant
  • Electrophysiology
  • Epilepsy
  • Hippocampus
  • Homologous recombination
  • Mouse
  • Neuropeptide Y

ASJC Scopus subject areas

  • Neuroscience(all)


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