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McCall, MA, Gregg, RG, Behringer, RR, Brenner, M, Delaney, CL, Galbreath, EJ, Zhang, CL, Pearce, RA, Chiu, SY and Messing, A (1996) Targeted deletion in astrocyte intermediate filament (Gfap) alters neuronal physiology. Proc. Natl. Acad. Sci. U.S.A. 93:6361-6
Glial fibrillary acidic protein (GFAP) is a member of the family of intermediate filament structural proteins and is found predominantly in astrocytes of the central nervous system (CNS). To assess the function of GFAP, we created GFAP-null mice using gene targeting in embryonic stem cells. The GFAP-null mice have normal development and fertility, and show no gross alterations in behavior or CNS morphology. Astrocytes are present in the CNS of the mutant mice, but contain a severely reduced number of intermediate filaments. Since astrocyte processes contact synapses and may modulate synaptic function, we examined whether the GFAP-null mice were altered in long-term potentiation in the CA1 region of the hippocampus. The GFAP-null mice displayed enhanced long-term potentiation of both population spike amplitude and excitatory post-synaptic potential slope compared to control mice. These data suggest that GFAP is important for astrocyte-neuronal interactions, and that astrocyte processes play a vital role in modulating synaptic efficacy in the CNS. These mice therefore represent a direct demonstration that a primary defect in astrocytes influences neuronal physiology.
Animals; Astrocytes/ultrastructure; Glial Fibrillary Acidic Protein/genetics; Hippocampus/cytology; Hippocampus/physiology; Hippocampus/ultrastructure; Homozygote; Long-Term Potentiation; Mice; Mice, Inbred C57BL; Microscopy, Electron; Neurons/physiology; Neurons/ultrastructure; Schwann Cells/ultrastructure; Sequence Deletion; Synaptic Transmission