Journal of Neuroscience, Vol 5, 3295-3301, Copyright © 1985 by Society for Neuroscience
Pharmacological properties of gamma-aminobutyric acid-, glutamate-, and aspartate-induced depolarizations in cultured astrocytes
H Kettenmann and M Schachner
Differentiated glial fibrillary acidic protein-positive astrocytes in
homogeneous cultures of early postnatal rat cerebral hemispheres respond by
membrane depolarization to gamma-aminobutyric acid (GABA), glutamate, and
aspartate with a threshold concentration of approximately 10(-5) M. The
GABA-induced depolarization is antagonized by two blockers of the neuronal
GABAA receptor, picrotoxin and bicuculline, but is not affected by the
uptake blockers beta-alanine or nipecotic acid. An agonist of the GABAA
receptor, muscimol, produces a dose-response curve similar to that of GABA,
whereas the agonist of the GABAB receptor, baclofen, did not alter the
membrane potential. When repetitive pulses of GABA are given to one cell,
its responsiveness depends on the time interval between pulses. Within 30
sec after termination of the first pulse the cell remains unresponsive to
the second pulse. With increased time intervals between the pulses,
reactivity toward GABA recovers. Five minutes after the first pulse the
cell regains 75% of its initial depolarization peak. Aspartate results in a
depolarization similar in size and time course to that induced by
glutamate. The glutamate agonists, quisqualate and ibotenate, and kainate
are less potent than glutamate. N-Methyl-D-aspartate has no effect on the
membrane potential of astrocytes. The pharmacological features of the
glutamate response are therefore similar to those of the receptor mediating
neuronal glutamate transport.
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