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GABA‐induced Ca 2+ transients in astrocytes are mediated by GABA B receptors. (A) GABA‐induced Ca 2+ transients are slightly enhanced in the presence of the GABA A receptor antagonist, <t>gabazine</t> (5 μM). Note that these experiments were performed in the presence <t>of</t> <t>TTX,</t> D‐APV, and NBQX to isolate direct GABAergic Ca 2+ responses in astrocytes with minimal neuronal influence. (B) Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application. (C) GABA‐induced Ca 2+ transients are strongly reduced in the presence of the GABA B antagonist, CGP 55845 (10 μM). Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application, showing a significant difference in the presence of the GABA B receptor inhibitor, CGP 55845. Statistical significance was determined by the Wilcoxon test for paired data sets. The error probability p was ** p < 0.01; *** p < 0.001.
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gaba a receptor antagonist sr 95531  (Toronto Research Chemicals)
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GABA‐induced Ca 2+ transients in astrocytes are mediated by GABA B receptors. (A) GABA‐induced Ca 2+ transients are slightly enhanced in the presence of the GABA A receptor antagonist, <t>gabazine</t> (5 μM). Note that these experiments were performed in the presence <t>of</t> <t>TTX,</t> D‐APV, and NBQX to isolate direct GABAergic Ca 2+ responses in astrocytes with minimal neuronal influence. (B) Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application. (C) GABA‐induced Ca 2+ transients are strongly reduced in the presence of the GABA B antagonist, CGP 55845 (10 μM). Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application, showing a significant difference in the presence of the GABA B receptor inhibitor, CGP 55845. Statistical significance was determined by the Wilcoxon test for paired data sets. The error probability p was ** p < 0.01; *** p < 0.001.
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GABA‐induced Ca 2+ transients in astrocytes are mediated by GABA B receptors. (A) GABA‐induced Ca 2+ transients are slightly enhanced in the presence of the GABA A receptor antagonist, <t>gabazine</t> (5 μM). Note that these experiments were performed in the presence <t>of</t> <t>TTX,</t> D‐APV, and NBQX to isolate direct GABAergic Ca 2+ responses in astrocytes with minimal neuronal influence. (B) Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application. (C) GABA‐induced Ca 2+ transients are strongly reduced in the presence of the GABA B antagonist, CGP 55845 (10 μM). Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application, showing a significant difference in the presence of the GABA B receptor inhibitor, CGP 55845. Statistical significance was determined by the Wilcoxon test for paired data sets. The error probability p was ** p < 0.01; *** p < 0.001.
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gabazine  (Tocris)
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GABA‐induced Ca 2+ transients in astrocytes are mediated by GABA B receptors. (A) GABA‐induced Ca 2+ transients are slightly enhanced in the presence of the GABA A receptor antagonist, <t>gabazine</t> (5 μM). Note that these experiments were performed in the presence <t>of</t> <t>TTX,</t> D‐APV, and NBQX to isolate direct GABAergic Ca 2+ responses in astrocytes with minimal neuronal influence. (B) Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application. (C) GABA‐induced Ca 2+ transients are strongly reduced in the presence of the GABA B antagonist, CGP 55845 (10 μM). Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application, showing a significant difference in the presence of the GABA B receptor inhibitor, CGP 55845. Statistical significance was determined by the Wilcoxon test for paired data sets. The error probability p was ** p < 0.01; *** p < 0.001.
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Image Search Results


GABA‐induced Ca 2+ transients in astrocytes are mediated by GABA B receptors. (A) GABA‐induced Ca 2+ transients are slightly enhanced in the presence of the GABA A receptor antagonist, gabazine (5 μM). Note that these experiments were performed in the presence of TTX, D‐APV, and NBQX to isolate direct GABAergic Ca 2+ responses in astrocytes with minimal neuronal influence. (B) Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application. (C) GABA‐induced Ca 2+ transients are strongly reduced in the presence of the GABA B antagonist, CGP 55845 (10 μM). Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application, showing a significant difference in the presence of the GABA B receptor inhibitor, CGP 55845. Statistical significance was determined by the Wilcoxon test for paired data sets. The error probability p was ** p < 0.01; *** p < 0.001.

Journal: The European Journal of Neuroscience

Article Title: GABA B Receptors Mediate Intracellular Calcium Release in Astrocytes of the Prefrontal Cortex

doi: 10.1111/ejn.70187

Figure Lengend Snippet: GABA‐induced Ca 2+ transients in astrocytes are mediated by GABA B receptors. (A) GABA‐induced Ca 2+ transients are slightly enhanced in the presence of the GABA A receptor antagonist, gabazine (5 μM). Note that these experiments were performed in the presence of TTX, D‐APV, and NBQX to isolate direct GABAergic Ca 2+ responses in astrocytes with minimal neuronal influence. (B) Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application. (C) GABA‐induced Ca 2+ transients are strongly reduced in the presence of the GABA B antagonist, CGP 55845 (10 μM). Average amplitudes of GABA‐induced Ca 2+ transients normalized to the control application, showing a significant difference in the presence of the GABA B receptor inhibitor, CGP 55845. Statistical significance was determined by the Wilcoxon test for paired data sets. The error probability p was ** p < 0.01; *** p < 0.001.

Article Snippet: The reagents D‐2‐amino‐5‐phosphonovaleric acid (D‐APV; antagonist of NMDA receptors; #D‐145; working concentration: 100 μM), 2,3‐dioxo‐6‐nitro‐1,2,3,4‐tetrahydrobenzo[f]quinoxaline‐7‐sulfonamide (NBQX; antagonist of AMPA/kainate receptors; #N‐186; working concentration: 10 μM), tetrodotoxin (TTX; inhibiting voltage‐gated sodium channels; #T‐550; working concentration: 0.5 μM), and gabazine (antagonist of GABA A and Glycine receptors, #G‐215; working concentration: 5 μM) were purchased from Alomone Labs (Jerusalem, Israel).

Techniques: Control