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This Article Full Text Full Text (PDF) All Versions of this Article: 107/4/1223    most recent 00363.2009v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Behringer, E. J. Articles by Buchholz, J. N. PubMed PubMed Citation Articles by Behringer, E. J. Articles by Buchholz, J. N.

Maturation and long-term hypoxia alters Ca²⁺-induced Ca²⁺ release in sheep cerebrovascular sympathetic neurons

¹Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, California; ; ²Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina Florianópolis, Santa Catarina, Brazil; and ; ³Department of Biological Sciences, Carter Hall, Alabama A&M University, Normal, Alabama

Submitted 6 April 2009 ; accepted in final form 24 July 2009

The contribution of sympathetic nerves arising from the superior cervical ganglia (SCG) toward the growth and function of cerebral blood vessels is pertinent throughout maturation as well as in response to cardiovascular stress imposed by high-altitude long-term hypoxia (LTH). The function of SCG sympathetic neurons is dependent on intracellular Ca²⁺ concentration ([Ca²⁺]_i) signaling, which is strongly influenced by a process known as Ca²⁺-induced Ca²⁺ release (CICR) from the smooth endoplasmic reticulum (SER). In this study, we used the sheep SCG neuronal model to test the hypotheses that maturation decreases CICR and high-altitude LTH depresses CICR in fetal SCG neurons but not in those of the adult. We found that the contribution of CICR to electric field stimulation (EFS)-evoked [Ca²⁺]_i transients was greatest in SCG cells from normoxic fetuses and was abolished by LTH. The decline in CICR was associated with a reduction in sarco(endo)plasmic reticulum Ca²⁺-ATPase (SERCA) function in fetal SCG cells during LTH, reducing SER Ca²⁺ levels below the threshold needed for the coupling of Ca²⁺ influx and CICR. With respect to the maturation from the fetus to adult, the decrease in CICR may reflect both a reduction in the levels of ryanodine receptor isoforms 2 and 3 and SERCA function. In response to LTH and in contrast to the fetus, CICR function in adult SCG cells is maintained and may reflect alterations in other mechanisms that modulate the CICR process. As CICR is instrumental in the function of sympathetic neurons within the cerebrovasculature, the loss of this signaling mechanism in the fetus may have consequences for the adaptation to LTH in terms of fetal susceptibility to vascular insults.

function of superior cervical ganglia; sympathetic development; electric field stimulation-evoked calcium transients; intracellular calcium stores; intracellular calcium release