Experimental study reveals age-dependent decline of calcium signaling in olfactory bulb astrocytes, indicating receptor downregulation during postnatal brain maturation.
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 Ca 2+ signals that were sensitive to the mGluR 5 antagonist MTEP. Adenosine-evoked Ca 2+ transients were inhibited by the A 2A antagonist ZM241385 in most astrocytes and by the A 2B antagonist PSB603 in a small number of astrocytes. Both the fraction of astrocytes that respond to stimulation of mGluR 5 and A 2A/B receptors with Ca 2+ 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.
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Mohammadpour et al. (2026) studied this question.
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