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Previous Article | Next Article
Volume 17, Number 23, Issue of December 1, 1997 pp. 8927-8936
Knock-Out Mice Reveal a Critical Antiepileptic Role for Neuropeptide Y
Received June 3, 1997; revised Sept. 9, 1997; accepted Sept. 11, 1997.
Scott C. Baraban1, Gunther Hollopeter3, Jay C. Erickson3, Philip A. Schwartzkroin1, 2, and Richard D. Palmiter3 Departments of 1 Neurological Surgery, 2 Physiology/Biophysics, and 3 Biochemistry, Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195
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.
Key words: anticonvulsant; homologous recombination; electrophysiology; epilepsy; mouse; hippocampus; neuropeptide Y
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