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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to test the possibility that sino-aortic baroreceptors may mediate the previously reported stress response in hypothalamic magnocellular neurosecretory cell activity in rats, effects of deafferentation of sino-aortic baroreceptors on plasma levels of vasopressin and oxytocin after fear-related emotional stress were studied in male rats 28-33 days after the surgery. An alpha 1-adrenergic receptor agonist, phenylephrine (1 mg/kg) injected i.p. under anesthesia increased arterial blood pressure in the rats that had received surgical operation of sino-aortic denervation (SAD) and in the rats of sham-operation control (SHAM). Reflex bradycardia after phenylephrine occurred in the SHAM but not in the SAD group. These results indicate that afferent signals originating from sino-aortic baroreceptors were effectively blocked by the SAD surgery. In the similarly prepared SAD group, plasma level of vasopressin was decreased and plasma level of oxytocin was increased significantly to the same extent as in the SHAM group after low-frequency shocks (0.05 Hz, 5 min) or environmental cue signals previously paired with shocks. It is therefore suggested that afferent neural signals originating from sino-aortic baroreceptors are not primarily involved in the suppressive vasopressin or the facilitatory oxytocin response to fear-related emotional stress in rats.
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PMID:Neurohypophysial responses to emotional stress after deafferentation of sino-aortic baroreceptors in rats. 131 20

The effects of intracerebroventricularly (i.c.v.) administered histaminergic receptor antagonists on plasma levels of vasopressin, oxytocin, prolactin and adrenocorticotrophic hormone (ACTH) after fear-related emotional stress were investigated in the male rat. Pyrilamine, a histaminergic H1-receptor antagonist did not significantly alter the suppressive vasopressin or the facilitative prolactin response to nonassociatively applied emotional stress. On the other hand, i.c.v. administered ranitidine, a histaminergic H2-receptor antagonist, blocked these responses to stress. Pyrilamine again did not significantly change the suppressive vasopressin response to the associatively applied emotional stress. However, the drug attenuated the prolactin response slightly but significantly. Ranitidine blocked the suppressive vasopressin and the facilitative prolactin responses to the associatively applied emotional stress, but the drug did not change the facilitative oxytocin or ACTH response to the stress. Suppression of motor activity during the associatively applied emotional stress was not significantly changed by either of these antagonists. These results suggest that histaminergic H2 receptors are selectively involved in the neural pathways which mediate the suppressive vasopressin and the facilitative prolactin responses to fear-related emotional stress.
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PMID:A histaminergic H2-receptor antagonist, ranitidine, blocks the suppressive vasopressin response to fear-related emotional stress in the rat. 136 4

The effects of various stressful conditions on the levels of oxytocin (OT) and vasopressin (VP) in plasma and cisternal cerebrospinal fluid (CSF) of male rats were investigated. Three experimental models were used: exposure to a novel environment for 5 min, immobilization for 15 min, and ether inhalation for 10 min resulting in anaesthesia. Novelty and immobilization induced a slight but significant increase in OT levels in the CSF immediately after the stress. The effect of ether was considerably more pronounced. The concentration of VP in the CSF was elevated only by ether stress. In plasma, the level of OT was increased immediately following immobilization and ether stress but not after novelty stress, whereas VP only showed a delayed response 20 min after immobilization. These results indicate a rapid preferential release of OT in the periphery in response to physical and pharmacological stress. In addition, they provide evidence that release of OT into the CSF is triggered by physical, pharmacological as well as emotional stress, while the central release of VP is rather resistant to emotional stress. The data suggest that OT is a stress hormone in the central nervous system.
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PMID:Differential effects of emotional and physical stress on the central and peripheral secretion of neurohypophysial hormones in male rats. 200 57

The effects of an opioid receptor antagonist, naloxone (NAL), were studied on the changes in pituitary hormone secretion induced by emotional stress. Male Wistar rats were trained with tone stimuli paired with electric footshocks and tested with the tone and environmental cue signals for emotional stress of fear acquired by learning as described previously (Onaka et al. 1988). Rats received s.c. injected NAL 30 min before testing at doses of 0, 0.2, 1.0, 5.0 and 25.0 mg/kg b.w. Half the rats were injected with 0.5 M NaCl (20 ml/kg b.w.) together with NAL. In these hypertonic rats plasma vasopressin level was slightly increased after NAL. The increment was statistically significant in control groups but not in experimental groups. However the suppression of vasopressin secretion by emotional stimuli was not changed by NAL. Plasma oxytocin levels were extremely high and not significantly different among experimental, unshocked control and untested control groups. NAL further increased the oxytocin level dose-dependently. NAL did not significantly change plasma adrenocorticotrophic hormone (ACTH) levels and hence did not modify the augmentative response in ACTH secretion to emotional stimuli. Plasma prolactin level was significantly elevated after emotional stimuli and NAL depressed the prolactin level in each of experimental and control groups. After NAL, the magnitude of the facilitatory response in prolactin secretion to emotional stimuli was decreased. Motor activity and its suppressive response to emotional stimuli were not influenced by NAL. In another half of rats under a normal osmotic condition the vasopressin response to emotional stimuli was not affected by NAL. NAL further augmented potentiation of oxytocin secretion after emotional stimuli dose-dependently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of naloxone on neuroendocrine responses to fear-related emotional stress. 216 20

In addition to corticotropin-releasing factor (CRF) and structurally related peptides, arginine vasopressin (AVP), oxytocin, angiotensin II, vasoactive intestinal polypeptide, peptide histidine isoleucinamide, epinephrine (E), and norepinephrine induce secretion of adrenocorticotropin (ACTH) from corticotropic cells in vitro. The apparent affinity and intrinsic ACTH-releasing activity of these substances are lower than those of CRF. These substances can also act synergistically with CRF. In this paper the role of catecholamines and AVP in the control of ACTH release is discussed. Infusion i.v. of E increases plasma ACTH and corticosterone to levels that are normally found during stress. E-induced stimulation of pituitary-adrenal activity is mediated by beta adrenoceptors and involves release of CRF, because it can be prevented by beta-adrenoceptor blockers and by destruction of CRF neurons (hypothalamic lesions), blockade of CRF release (chlorpromazine, morphine, and Nembutal), or administration of CRF antiserum. Although stress can cause a vast increase in plasma E, circulating E is not essential for the acute stress-induced release of ACTH because blockade of beta (or alpha) adrenoceptors, administration of chlorisondamine, or extirpation of the adrenal medulla and sympathectomy do not prevent the pituitary-adrenal response to stress. In contrast, circulating E plays a major role in the release of intermediate-lobe peptides during emotional stress. Studies of the role of AVP in pituitary-adrenal control by the use of pressor receptor (V1) antagonists are not valuable because of the ineffectiveness of such antagonists in blocking AVP-induced release of ACTH from corticotropic cells in vitro. Treatment of rats with an antiserum to AVP reduces the ACTH response to stress. We conclude that AVP has an important role in stress-induced activation of the pituitary-adrenal system, possibly by potentiating the effects of CRF.
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PMID:Role of epinephrine and vasopressin in the control of the pituitary-adrenal response to stress. 298 37

Stress induced oxytocin (OT) secretion was measured in female rats following treatment with various opiate antagonists selective for different types of opiate receptor. Naloxone (mu selective) and MR2266 BS (kappa selective) potentiated the OT response to an emotional stress (1 min. immobilization) whereas the delta selective antagonist ICI 154129 was without effect. Similarly, naloxone and MR2266 BS, but not ICI 154129, potentiated the response to a physical stress (i.p. hypertonic saline). A dose response comparison of the actions of naloxone and MR2266 BS revealed that naloxone was most effective in potentiating the immobilization response whereas MR2266 BS elicited greater responses than naloxone when administered prior to hypertonic saline. The results indicate that the opioid regulation of stress induced OT secretion is primarily mediated via mu and kappa opiate receptor types, the two types differentially regulating the OT response to two different stressors.
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PMID:Opioid control of oxytocin secretion: evidence of distinct regulatory actions of two opiate receptor types. 303 9

1. Oxytocin and vasopressin were assayed in samples of blood collected from conscious rabbits during suckling. The milk yields were determined from the weight gain of the litters.2. With normal milk yields (35-155 g), relatively high concentrations (31-375 muu./ml.) of oxytocin were present in the blood but vasopressin was detected in only one out of eight samples. It is concluded that the release of oxytocin by the milk-ejection reflex is essential for normal milk removal in the rabbit and that this hormone is released independently of vasopressin.3. When the milk yield did not exceed 15 g, an amount which could be removed by passive withdrawal from the mammary gland, vasopressin was detected in four out of five blood samples but none contained a detectable concentration of oxytocin. This result can be explained by the intervention of emotional stress which is known to block the milk-ejection reflex but which acts as a stimulus for the release of vasopressin.4. Emotional stress could inhibit the milk-ejection reflex either centrally by blocking the release of oxytocin, or peripherally by blocking the response of the mammary gland to circulating oxytocin. The absence of the hormone in blood during ineffectual suckling suggests that the block is central.
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PMID:Blood levels of oxytocin and vasopressin during suckling in the rabbit and the problem of their independent release. 549 14

1. The forebrain is a major organizer of the complex behavioural, physiological and neuroendocrine responses to environmental challenges of a stressful nature. 2. Combined physiological and neuroanatomical studies suggest that a specific forebrain-brain stem network, composed of connections between the central nucleus of the amygdala, the paraventricular nucleus of the hypothalamus, the mesencephalic cuneiform nucleus, the parabrachial nucleus and the dorsal motor nucleus of the vagus nerve, may be important for integrating behavioural and physiological responses. 3. Based on studies using bilateral electrolytic lesions of the central nucleus of the amygdala, it has become clear that the central nucleus of the amygdala is one of the key structures involved in unconditioned responses to inescapable footshock. These responses include freezing behaviour, tachycardia and the release of adrenaline, noradrenaline, prolactin and corticosterone. However, this nucleus is involved only in the freezing behaviour and bradycardiac responses to conditioned emotional stress or to social defeat. 4. Both peptidergic (corticotropin releasing hormone and vasopressin/oxytocin) and aminergic (noradrenaline and dopamine) mechanisms in the central amygdala are involved in the regulation of integrated behavioural, physiological and neuroendocrine stress responses. This is indicated by studies with an infusion of an agonist and/or antagonist of the peptides or neurotransmitters into the central amygdala of freely moving rats. Sympathetic cardiac control is intensified by corticotropin releasing hormone and oxytocin, probably by inhibiting vagal output. In contrast, vagal activity is facilitated by vasopressin, noradrenaline and dopamine.
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PMID:Forebrain pathways and their behavioural interactions with neuroendocrine and cardiovascular function in the rat. 881 49

The amygdala plays a pivotal role in the generation of appropriate responses to emotional stimuli. In the case of emotional stressors, these responses include activation of the hypothalamic-pituitary-adrenal (HPA) axis. This effect is generally held to depend upon the central nucleus of the amygdala, but recent evidence suggests a role for the medial nucleus. In the present study, c-fos expression, amygdala lesion and retrograde tracing experiments were performed on adult rats in order to re-evaluate the role of the central as opposed to the medial amygdala in generating neuroendocrine responses to an emotional stressor. Brief restraint (15 min) was used as a representative emotional stressor and was found to elicit c-fos expression much more strongly in the medial than central nucleus of the amygdala; relatively few Fos-positive cells were seen in other amygdala nuclei. Subsequent experiments showed that ibotenic acid lesions of the medial amygdala, but not the central amygdala, greatly reduced restraint-induced activation of cells of the medial paraventricular nucleus, the site of the tuberoinfundibular corticotropin-releasing factor cells that constitute the apex of the HPA axis. Medial amygdala lesions also reduced the activation of supraoptic and paraventricular nucleus oxytocinergic neurosecretory cells that commonly accompanies stress-induced HPA axis activation in rodents. To assess whether the role of the medial amygdala in the control of neuroendocrine cell responses to emotional stress might involve a direct projection to such cells, retrograde tracing of amygdala projections to the paraventricular nucleus was performed in combination with Fos immunolabelling. This showed that although some medial amygdala cells activated by exposure to an emotional stressor project directly to the paraventricular nucleus, the number is very small. These findings provide the first direct evidence that it is the medial rather than the central amygdala that is critical to hypothalamic neuroendocrine cell responses during an emotional response, and also provide the first evidence that the amygdala governs oxytocin as well as HPA axis responses to an emotional stressor.
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PMID:Neuroendocrine responses to an emotional stressor: evidence for involvement of the medial but not the central amygdala. 1038 20

Previous experiments have shown that an exposure to defined stressors activates not only the 'classical' endocrine stress response but also the intrahypothalamic and peripheral release of oxytocin. In the present study we investigated the effects of an acute social defeat experience on the release of oxytocin within the hypothalamic supraoptic nucleus, just outside of the supraoptic nucleus toward the midline within the anterior ventro-lateral part of the hypothalamus, and into plasma of adult male rats. Our results demonstrate that emotional stress triggers the release of oxytocin into the extracellular fluid of both the supraoptic nucleus and the anterior ventro-lateral part of the hypothalamus (up to approximately 320% and 170%, respectively). Interestingly, oxytocin release within the latter brain area, which is likely to originate from axons forming the hypothalamo-neurohypophysial tract, was higher in absolute terms than that within the supraoptic nucleus itself, both under basal conditions and in response to social defeat. In contrast to intrahypothalamic release patterns, plasma oxytocin levels remained virtually unchanged upon stressor exposure. This demonstrates that the release of oxytocin within the hypothalamus is triggered by emotional stress. Furthermore, it indicates that under physiological conditions the release of oxytocin from the dendrites and somata upon axon terminals in the neurohypophysis is differentially regulated. Although not yet studied in detail, it may be hypothesized that the spatial and temporal release pattern of oxytocin is controlled by integrative neuronal networks at different brain levels (including hypothalamus and posterior pituitary) to ensure the appropriate involvement of this peptide in the stress response of the animal.
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PMID:Emotional stress triggers intrahypothalamic but not peripheral release of oxytocin in male rats. 1052 Jan 37


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