Abstract
AimsVasopressin (AVP) and oxytocin (OT) are considered to be related to gastric functions and the regulation of stress response. The present study was to study the role of vasopressinergic and oxytocinergic neurons during the restraint water-immersion stress.MethodsTen male Wistar rats were divided into two groups, control and RWIS for 1h. The brain sections were treated with a dual immunohistochemistry of Fos and oxytocin (OT) or vasopressin (AVP) or OT receptor or AVP 1b receptor (V1bR).Results(1) Fos-immunoreactive (Fos-IR) neurons dramatically increased in the hypothalamic paraventricular nucleus (PVN), the supraoptic nucleus (SON), the neucleus of solitary tract (NTS) and motor nucleus of the vagus (DMV) in the RWIS rats; (2) OT-immunoreactive (OT-IR) neurons were mainly observed in the medial magnocellular part of the PVN and the dorsal portion of the SON, while AVP-immunoreactive (AVP-IR) neurons mainly distributed in the magnocellular part of the PVN and the ventral portion of the SON. In the RWIS rats, Fos-IR neurons were indentified in 31% of OT-IR neurons and 40% of AVP-IR neurons in the PVN, while in the SON it represented 28%, 53% respectively; (3) V1bR-IR and OTR-IR neurons occupied all portions of the NTS and DMV. In the RWIS rats, more than 10% of OTR-IR and V1bR-IR neurons were activated in the DMV, while lower ratio in the NTS.ConclusionRWIS activates both oxytocinergic and vasopressinergic neurons in the PVN and SON, which may project to the NTS or DMV mediating the activity of the neurons by OTR and V1bR.
Highlights
Restraint water-immersion stress (RWIS) is considered to be a mixture of physical and psychological stressor, and this stimulation in conscious rats induces behavioral responses, hypothermia and vagally-mediated gastric hypercontractility, gastric acid hypersecretion and gastric mucosal lesions within a few hours [1,2]
After different durations of RWIS, neuronal activation, demonstrated by Fos-immunoreactivity (Fos-IR), was found significantly increased in specific brain areas, such as the medullary visceral zone [dorsal motor nucleus of the vagus (DMV), nucleus of solitary tract (NTS), area postrema (AP) and nucleus ambiguous (NA)] and the hypothalamus [paraventricular nucleus (PVN) and supraoptic nucleus (SON)] [3,4]. These results suggest the neuronal hyperactivity of the NTS, DMV and AP may be one of the primary central mechanisms of the gastric dysfunctions induced by the RWIS, while the neuronal hyperactivity of PVN and SON may be one of the higher central mechanisms
Previous studies indicate that the abnormalities of gastric functions induced by RWIS are not due to the hyperactivity of the hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic adrenamedullary system, but due to the hyperactivity of vagal parasympathetic efferents, which largely originating in the DMV and partly in the NA [3,5,6,7,8,9]
Summary
Restraint water-immersion stress (RWIS) is considered to be a mixture of physical and psychological stressor, and this stimulation in conscious rats induces behavioral responses (anxiety, scrabble, outrage and cry), hypothermia and vagally-mediated gastric hypercontractility, gastric acid hypersecretion and gastric mucosal lesions within a few hours [1,2]. After different durations of RWIS, neuronal activation, demonstrated by Fos-immunoreactivity (Fos-IR), was found significantly increased in specific brain areas, such as the medullary visceral zone [dorsal motor nucleus of the vagus (DMV), nucleus of solitary tract (NTS), area postrema (AP) and nucleus ambiguous (NA)] and the hypothalamus [paraventricular nucleus (PVN) and supraoptic nucleus (SON)] [3,4] These results suggest the neuronal hyperactivity of the NTS, DMV and AP may be one of the primary central mechanisms of the gastric dysfunctions induced by the RWIS, while the neuronal hyperactivity of PVN and SON may be one of the higher central mechanisms. Whether the hyperactivity of the higher centre of the anterior hypothalamus relieves the inhibition of gastric motility mediated by the primary nerve centre during the RWIS? If so, what are the neurotransmitters released by the anterior hypothalamus neurons?
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