In:
The Journal of Neuroscience, Society for Neuroscience, Vol. 33, No. 19 ( 2013-05-08), p. 8411-8422
Kurzfassung:
Calcium-dependent release of vasoactive gliotransmitters is widely assumed to trigger vasodilation associated with rapid increases in neuronal activity. Inconsistent with this hypothesis, intact stimulus-induced vasodilation was observed in inositol 1,4,5-triphosphate (IP 3 ) type-2 receptor (R2) knock-out (KO) mice, in which the primary mechanism of astrocytic calcium increase—the release of calcium from intracellular stores following activation of an IP 3 -dependent pathway—is lacking. Further, our results in wild-type (WT) mice indicate that in vivo 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 3 R 2 -KO animals.
Materialart:
Online-Ressource
ISSN:
0270-6474
,
1529-2401
DOI:
10.1523/JNEUROSCI.3285-12.2013
Sprache:
Englisch
Verlag:
Society for Neuroscience
Publikationsdatum:
2013
ZDB Id:
1475274-8
SSG:
12
