What resolves this contention: Mechanistic conflict: one line of evidence concl…

What resolves this contention: Mechanistic conflict: one line of evidence concludes that astrocytic Ca2+ is dispensable for synaptic transmission based on IP3R2 KO, while another shows that IP3R2-independent TRPA1-mediated microdomain Ca2+ in astrocytes is required for basal D-serine supply and thus LTP. / IP3R2 is the key astrocytic IP3R driving Gq-linked GPCR-mediated Ca2+ increases in hippocampal astrocytes, and removal of IP3R2-dependent astrocytic Ca2+ does not significantly affect excitatory neuronal synaptic activity or ambient glutamate levels. / Independent TRPA1 channel-mediated Ca2+ flux in astrocytes (not dependent on IP3R2) maintains basal astrocytic Ca2+ and drives constitutive D-serine release that supports Schaffer collateral–CA1 LTP; pharmacological or genetic block of astrocyte TRPA1 impairs LTP.