Abstract
Hypothalamic paraventricular nucleus (PVN) is a major source of arginine vasopressin (AVP). Our previous work has proven that: (1) pain stimulation enhances PVN synthesis and secretion of AVP; (2) AVP in periaqueductal gray (PAG) plays a role in antinociception; (3) pain stimulation increases AVP concentration in PAG tissue. The present study was to investigate AVP source in PAG during pain modulation of the rat. The results showed that: (1) pain stimulation elevated AVP concentration in both PVN and PAG perfusion liquid, in which the peak of AVP concentration in PVN perfusion liquid occurred earlier than that in PAG perfusion liquid; (2) PVN cauterization weakened pain stimulation-induced PAG releasing AVP, in which the inhibitive effect of bilateral PVN cauterization showed stronger than that of unilateral PVN cauterization; (3) microinjection of l-glutamate sodium into PVN, which excited local neurons, increased AVP concentration in PAG perfusion liquid in a dose-dependent manner. The data suggest that AVP in PAG, which relates with pain modulation, comes from PVN.
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