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Inconsistent with this hypothesis, intact stimulus-induced vasodilation was observed in inositol 1,4,5-triphosphate (IP\n                    <jats:sub>3<\/jats:sub>\n                    ) type-2 receptor (R2) knock-out (KO) mice, in which the primary mechanism of astrocytic calcium increase\u2014the release of calcium from intracellular stores following activation of an IP\n                    <jats:sub>3<\/jats:sub>\n                    -dependent pathway\u2014is lacking. Further, our results in wild-type (WT) mice indicate that\n                    <jats:italic>in vivo<\/jats:italic>\n                    onset of astrocytic calcium increase in response to sensory stimulus could be considerably delayed relative to the simultaneously measured onset of arteriolar dilation. Delayed calcium increases in WT mice were observed in both astrocytic cell bodies and perivascular endfeet. Thus, astrocytes may not play a role in the initiation of blood flow response, at least not via calcium-dependent mechanisms. Moreover, an increase in astrocytic intracellular calcium was not required for normal vasodilation in the IP\n                    <jats:sub>3<\/jats:sub>\n                    R\n                    <jats:sub>2<\/jats:sub>\n                    -KO animals.\n                  <\/jats:p>","DOI":"10.1523\/jneurosci.3285-12.2013","type":"journal-article","created":{"date-parts":[[2013,5,8]],"date-time":"2013-05-08T12:38:10Z","timestamp":1368016690000},"page":"8411-8422","source":"Crossref","is-referenced-by-count":220,"title":["<i>In vivo<\/i>\n                    Stimulus-Induced Vasodilation Occurs without IP\n                    <sub>3<\/sub>\n                    Receptor Activation and May Precede Astrocytic Calcium 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