In vivo stimulus-induced vasodilation occurs without IP3 receptor activation and may precede astrocytic calcium increase
Autor: | Tyler Steed, Ju Chen, David A. Boas, Eliezer Masliah, Vishnu B. Sridhar, Jianxia Cui, Sergey L. Gratiy, Gabriel A. Silva, Anders M. Dale, Christopher L. MacDonald, Lidia Reznichenko, Kimberly L. Weldy, Qun Cheng, Gaute T. Einevoll, Krystal Nizar, Hana Uhlirova, Anna Devor, Thomas Ibsa Beka, Peifang Tian, Payam A. Saisan, Sava Sakadzic |
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Jazyk: | angličtina |
Rok vydání: | 2013 |
Předmět: |
Male
medicine.medical_specialty Time Factors chemistry.chemical_element Action Potentials Vasodilation Calcium Calcium in biology Article chemistry.chemical_compound Mice Adenosine Triphosphate Internal medicine medicine Premovement neuronal activity Animals Inositol 1 4 5-Trisphosphate Receptors Inositol Cycloleucine Receptor Egtazic Acid Mice Knockout Neurons Mice Inbred ICR Chemistry General Neuroscience Dextrans Inositol trisphosphate receptor Electric Stimulation Endocrinology Neuroprotective Agents Astrocytes Hypercalcemia Female Intracellular Fluorescein-5-isothiocyanate Signal Transduction |
Zdroj: | Journal of Neuroscience |
Popis: | 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 (IP3) 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 IP3-dependent pathway—is lacking. Further, our results in wild-type (WT) mice indicate thatin vivoonset 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 IP3R2-KO animals. |
Databáze: | OpenAIRE |
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