Developmental changes in Ca2+ signaling mediated by A2A adenosine and mGluR5 glutamate receptors in olfactory bulb astrocytes.

Astrocytes play pivotal roles in brain homeostasis and neuronal communication. Most astrocyte functions are orchestrated by intracellular Ca²⁺ signaling in response to neurotransmitters. Although astrocyte function has been widely studied, the ontogenetic development of their Ca²⁺ dynamics is not fully understood. This study investigated developmental changes in astrocyte Ca²⁺ signaling mediated by group I metabotropic glutamate receptors and adenosine receptors in the olfactory bulb. Stimulation with (R, S)-3,5-dihydroxyphenylglycine (DHPG), a group I mGluR agonist, evoked Ca2+ signals that were sensitive to the mGluR5 antagonist MTEP. Adenosine-evoked Ca2+ transients were inhibited by the A2A antagonist ZM241385 in most astrocytes and by the A2B antagonist PSB603 in a small number of astrocytes. Both the fraction of astrocytes that respond to stimulation of mGluR5 and A2A/B receptors with Ca2+ responses and the amplitude of the responses significantly decreased during the first four weeks of postnatal development. Our results show that olfactory bulb astrocytes create glutamatergic and adenosinergic Ca²⁺ signaling that is downregulated as the olfactory bulb matures.