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The Journal of Neuroscience, January 5, 2011 31(1):97 104 97 Neurobiology of Disease Knockout of Zn Transporters Zip-1 and Zip-3 Attenuates Seizure-Induced CA1 Neurodegeneration Jing IAN,1 Taiping

City, Missouri 67235, USA. Jean et al.: Neurobiology of Disease [Online First] Departments of 1Neurology, 2Neuroscience, and 3Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, and 4Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Missouri 67235, USA. Abstract A recent report in the journal Nature Medicine found that mice lacking zap3, a single nucleotide polymorphism in the gene encoding zip3, could be induced to develop a mouse model of epilepsy. These mice are sensitive to the toxic effects of quinine and demonstrate abnormal neuronal morphology and neuronal migration, deficits that resemble those seen in human patients with epilepsy. To determine the biological significance of zip3 genotype, we used a model mouse model of mouse modeling. Zip3 deficient mice (ZDP3) demonstrate impaired seizure threshold, an abnormally large cell population, and enhanced sensitivity to seizures. In addition, zap3 knockout mice produce a significant number of immature and senescent neurons and experience spontaneous seizures. The results support the hypothesis that zap3 genotype influences seizure susceptibility and epilepsy pathogenesis. Introduction Epilepsy is a disabling brain disorder that is characterized by seizure frequency that is both severe and unpredictable (1–3). The pathophysiology of epilepsy is not fully understood and the cellular mechanisms associated with its onset and progression are poorly understood (4–7). Although neuropeptides and hormones can be implicated in the pathogenesis of epilepsy, no single pathway is thought to be the sole mechanism or a necessary and sufficient condition for its development and progression (8). Therefore, it has been postulated that a single genetic alteration may represent a possible molecular event or set point that defines an individual's susceptibility to developing epilepsy (9). Epilepsy involves abnormal synaptic function and is marked by a wide variety of neurologic pathology and symptoms (9–12). Although some studies have shown a role for specific brain areas in the pathogenesis of epilepsy, additional studies are required to provide greater insight into the neural circuit underlying this complex disease. A key challenge in deciphering the complex neuropsychology underlying epilepsy is to determine the genetic basis for such abnormalities.

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Knockout of zn transporters is a genetic technique used to suppress or eliminate the function of zinc transporters in an organism.

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The purpose of knockout of zn transporters is to study the role and function of zinc transporters in an organism, and their impact on various biological processes.

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