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Identification of mouse type‐2‐like astrocytes: Demonstration of glutamate and GABA transmitter activated responses
Author(s) -
Magoski N. S.,
Walz W.,
Juurlink B. H. J.
Publication year - 1992
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490330112
Subject(s) - depolarization , glutamate receptor , biophysics , astrocyte , chemistry , membrane potential , neuroglia , microbiology and biotechnology , biology , neuroscience , biochemistry , central nervous system , receptor
We have identified mouse type‐2‐like astrocytes and examined some of their electrophysiological properties. Cultures were prepared from P4 mouse neopallia. We demonstrate that mouse type‐2‐like astrocytes can be identified using the following criteria: presence of glial fibrillary acidic protein (GFAP), presence of chondroitin sulfate polysaccharide, and presence of γ‐aminobutyric acid (GABA). A2B5‐binding is not a sufficient criterion to identify O2A lineage cells in mouse neopallial glial cultures since the monoclonal antibody A2B5 binds not only to O2A lineage cells but also to a subpopulation of large, flat type‐1‐like astrocytes. Mouse type‐2‐like astrocytes have resting membrane potentials of −76.2 ± 2.1 mV—i.e., similar to that of mouse type‐1‐like astrocytes. The input resistance of 44.2 ± 0.5 MΩ is an order of magnitude greater than that of type‐1‐like astrocytes suggesting the type‐2‐like astrocytes are not extensively electrically coupled either to each other or to type‐1‐like astrocytes. Glutamate application caused an 8.8 ± 1.7 mV depolarization of type‐2‐like astrocytes. Application of glutamate to barium treated astrocytes caused a fast depolarization with a peak amplitude of 21.4 ± 1.8 mV; the cells repolarized from this peak by about 10 mV and upon removal of glutamate returned to its pre‐glutamate value. Application of GABA caused a transient depolarization of 14.0 ± 1.7 mV. The presence of barium resulted in a steady‐state GABA‐induced depolarization of 10.3 ± 2.0 mV. Neither SITS nor β‐alanine interfered with the amplitude of the glutamate and GABA responses. © 1992 Wiley‐Liss, Inc.