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The blockade of oxytocinergic receptors in the CeA modify VP plasma levels and mRNA expression induced by hypertonic BVE in the rat.
Author(s) -
Margatho Lisandra O,
Elias Carol F,
Elias Lucila LK,
AntunesRodrigues Jose
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.993.3
Subject(s) - endocrinology , medicine , oxytocin , vasotocin , vasopressin , supraoptic nucleus , chemistry , in situ hybridization , receptor , hypothalamus , magnocellular cell , messenger rna , neuropeptide , biology , biochemistry , gene
We investigated the effects of oxytocin (OT) and the oxytocinergic antagonist vasotocin (OVT) injection in the central amygdala (CeA) in the regulation of vasopressin (VP) mRNA expression in the hypothalamus and VP plasma levels in response to hypertonic blood volume expansion (hyper BVE). Male Wistar rats with cannulas unilaterally in the CeA were subjected to BVE (2 ml/100 g bw) over 1 minute. OT, OVT or vehicle was injected into the CeA 20 min before the BVE. Five min after BVE rats were decapitated and the blood was collected for VP plasma determination. Another group was perfused 40 min after BVE. Brain sections of the paraventricular (Pa) and the supraoptic (SON) nuclei were collected for in situ hybridization using a 35S‐labeled VP probe. OT injection in the CeA increased plasma VP levels after hyper BVE and reduced VP mRNA in the PaLM. OVT reduced plasma AVP levels following a reduction VP mRNA in the PaLM and SON. Our data suggest that OT in the CeA may modulate the physiological mechanisms involved in plasma AVP release but the time course of the hormonal release has been shown dissociated from the genomic AVP expression in the PaLM. We hypothesize that the blockade of OT CeA receptors with OVT may activate an inhibitory input to vasopressinergic magnocellular neurons in the hypothalamus leading to the decrease in plasma AVP levels that can be strongly correlated with the reduction in the genomic AVP mRNA.