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Distribution of P2X receptors on astrocytes in juvenile rat hippocampus
Author(s) -
Kukley Maria,
Barden Julian A.,
Steinhäuser Christian,
Jabs Ronald
Publication year - 2001
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.1091
Subject(s) - biology , ionotropic effect , purinergic receptor , astrocyte , receptor , metabotropic receptor , neuroscience , hippocampal formation , microbiology and biotechnology , hippocampus , neuroglia , glutamate receptor , central nervous system , biochemistry
Recent evidence suggested that ATP acting via ionotropic (P2X) and metabotropic (P2Y) purinergic receptors might be involved in signaling between glial cells and within glial–neuronal networks. In contrast to their neuronal counterpart, the identity of P2X receptors in CNS glial cells is largely unknown. In the present study, antibodies recognizing the subunits P2X 1 –P2X 7 were applied together with the astroglial marker S100β and nuclear labeling with Hoechst 33342 to investigate semiquantitatively the distribution of the whole set of P2X receptors in astrocytes of the juvenile rat hippocampus. Expression of P2X 1 –P2X 4 , P2X 6 , and P2X 7 subunits was observed in astrocytes of various hippocampal subregions, but the cells were completely devoid of P2X 5 protein. S100β‐positive cells expressing subunits P2X 3 –P2X 7 occurred evenly in the different subfields, while P2X 1 ‐ and P2X 2 ‐positive astrocytes were distributed more heterogeneously. The staining pattern of P2X subunits also differed at the subcellular level. Antibodies against P2X 2 and P2X 4 labeled both astroglial cell bodies and processes. Immunoreactivity for P2X 1 and P2X 6 was mainly confined to somatic areas of S100β‐positive cells, whereas the subunit P2X 3 was primarily localized along astroglial processes. Knowledge of the distribution of P2X receptors might provide a basis for a better understanding of their specific role in cell–cell signaling. GLIA 36:11–21, 2001. © 2001 Wiley‐Liss, Inc.