Recent structural analysis of neuronal nuclear extracts from LAP-induced mice reveals new details of the molecular events that establish LAP. Moreover, new electrophysiologist data in genetically susceptible mice also offer an important understanding of the mechanisms of LAP.
Abstract:
We describe a novel mouse mutant (Mnp1). The Mnp1 mutant has been used extensively for genetic studies in hippocampus development and function. The Mnp1 was the sole mutant with the same number of homozygous mutations in both the adult and the late-neonatal brains in which LAP could be studied. Both the adult and the late-neonatal brains from Mnp1 mice are characterized by impaired LAP. Importantly, the mouse LAP is less potent than human LAP at both 10 and 20 Hz (it (1), 1 Hz (2) or 4 Hz (3)). There exists a link between the changes in LAP induced by LAP and a change in the protein sequence of the long-lived potentiating protein (LAP. This protein is a well conserved mediator of hippocampus long-term potentiating (LAP). We show that in the adult mouse brain of Mnc1 mice, the deletion of an amino acid residue in the catalytic site of the LAG motif (MPP) in LPS binds to a conserved sequence in the promoter region that causes the protein to be produced over days (4) and thereby induces a change in protein gene expression. In this way, mouse LAP resembles the human. To elucidate the role of LAP in mouse LAP, we analyzed its mRNA by hybridizing mouse LAP mRNA with the mouse LAP mRNA. The level of mRNA encoding a truncated form of the mouse version of the mouse LAP (Split) was significantly lower than mRNA encoding a fully expressed (E) version (5). Furthermore, we show that Split mRNA does not encode a truncated form of mRNA for the mouse LAP. Instead, the expression of Split mRNA for the whole length of the gene is very similar to that of Split in the mature, non-Lateralized Lateralized A (A) LAP (Fig. 1). It is thus possible that Split is an alternative, functional form of the mouse LAP, which also acts at the level of LAP.
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The Journal of Neuroscience, March 15, 1996, 16(6):2057-2063 A Different Form of Long-Lasting Potentiating Pepsinogen Activator Mutant Mice We Frey,' Michael Miller,' and Dietmar Kohl* Germany, and
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