Stimulatory action of oxytocin on neurones of the dorsal motor nucleus of the vagus nerve

Charpak, Serge; Armstrong, William E.; Mühlethaler, Michel; Dreifuss, Jean-Jacques

doi:10.1016/0006-8993(84)91342-8

Cited by 103 publications

(54 citation statements)

References 18 publications

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“…However, involvement of interneurones within the DMV that have All receptors cannot be excluded. Charpak et al (1984) demonstrated that application of oxytocin in vitro produced excitation of the DMV neurones at a lower concentration than AVP, and that AVP showed minute agonistic action on the uterine oxytocin receptors. They suggested that the effects of the neurohypophyseal peptides in the DMV could result from the a.ctions on oxytocin receptors, although it was not determined whether the action of AVP was blocked by specific oxytocin antagonists in their study.…”

Section: Discussionmentioning

confidence: 99%

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Katafuchi

Muratani

et al. 1992

The Journal of Physiology

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SUMMARY1. Extracellular recordings were made from 297 spontaneously firing neurones in the dorsal motor nucleus of the vagus (DMV) in slice preparations of rat medulla oblongata. Some of the neurones recorded were identified to be vagal motoneurones by antidromic stimulation. The cells fired with a slow irregular pattern at an average rate of 1 1 + 041 spikes/s (mean + S.E.M.).2. Arginine vasopressin (AVP) was applied by perfusion in 196 of the 297 cells. Most of the neurones (190/196, 97 %) were excited by 10-6 M AVP with an increase in firing rate from the basal level of 11 + 0-1 to a maximum of 2-5 + 0-2 spikes/s. There was a dose-dependent relation between the concentration of AVP and the increased firing rate in all DMV neurones tested (n = 38). The threshold concentration of the peptide to produce changes in firing rate was assumed to be about 10-10 M. The remaining six neurones were not affected by application of AVP.3. Application of oxytocin (OXT, 10-6 M) increased the firing rate of all thirtyeight neurones tested. The effects of AVP and OXT on all neurones examined (n = 20 and 4, respectively) still persisted after blocking the synaptic transmission in a low-Ca2+ or Ca2+-free-high-Mg2+ solution, indicating the direct action of both AVP and OXT on the postsynaptic membranes.4. The AVP-induced excitatory responses were completely but reversibly blocked by the Vl-type receptor antagonists, [1-(,f-mercapto-/,,i-cyclopentamethylene-(n = 5) and Phaa-D-Tyr(Et)Phe-Gln-Asn-Lys-Pro-Arg-NH2 (n = 6), whereas a selective and reversible OXT receptor antagonist, desGly-NH2d(CH2)jTyr-(Me)2Thr4]ornithine vasotocin, which suppressed the OXT-induced excitation, did not block the responses to AVP (n = 11). 5. Application of angiotensin II (AII, 10-6 M) to 153 neurones increased the firing rates of 60 (39%) neurones. The firing rate was increased from the basal level of 1-0+041 to a maximum of 1-8+0-2 spikes/s (n = 60). The effect of All was completely abolished by an All receptor antagonist, [Sarl,lle8]angiotensin II (n = 6). There was a dose dependence of the excitatory response on All concentration in all of eleven neurones tested. The threshold concentration was assumed to be about MS 9206 Z -L. MO AND OTHERS 10-9 M. The activity of 5 (3 %) of 153 neurones was decreased, and the remaining 88 (58%) neurones were not affected by AII.6. After blocking synaptic transmission with low-Ca2+-high-Mg2+ medium, ten of sixteen neurones that had been excited by application of All in normal medium still responded to All, and the effects were abolished in the remaining six cells.7.Of fifty-nine cells tested with both AVP and AII applied at 10-6 M, responses of fifty-four (92 %) to AVP were excitation. Of these fifty-four, fifteen were also excited by application of All, one was inhibited, and All had no effect on the remaining thirty-eight (70 %).8. The excitatory responses induced by AVP were completely or partially blocked by simultaneous perfusion of All in normal medium, which were restored by [Sarl,lle8]AII, whereas the appli...

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Section: Discussionmentioning

confidence: 99%

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Katafuchi

Muratani

et al. 1992

The Journal of Physiology

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“…On the other hand, training partially compensated for the hypertension-associated deficit in OT modulation, most likely by increasing central peptide content. Considering that activation of the central OT system both changes neuronal activity in brainstem areas 18,19 and facilitates vagal outflow and slowing of the heart, 14 -16,20 it is reasonable to speculate that training-induced effects are beneficial to hypertensive individuals, who have high sympathetic activity and high HR levels. The effectiveness of training on OT modulatory effects, however, seems to be larger in normotensive than hypertensive individuals.…”

Section: Discussionmentioning

confidence: 99%

Hypertension and Exercise Training Differentially Affect Oxytocin and Oxytocin Receptor Expression in the Brain

et al. 2005

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Abstract-We have previously shown that exercise training activates nucleus tractus solitarii (NTS) oxytocinergic projections, resulting in blunted exercise tachycardia. The objective of this study was to determine the effects of hypertension and training on oxytocin (OT) and OT receptor expression in the hypothalamic paraventricular nucleus (PVN) and projection areas (dorsal brain stem [DBS]). Male, normotensive, Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were trained (55% maximal exercise capacity, 3 months) or kept sedentary, and pressure was measured weekly. DBS sections were processed for immunohistochemistry (polyclonal guinea pig anti-OT) or in situ hybridization for OT and OT receptor ( 35 S-oligonucleotide probes). Other groups of rats had brains removed and frozen to isolate the DBS and PVN; samples were processed for OT and OT receptor cDNA reverse transcription-polymerase chain reaction amplification with ␤-actin as the housekeeping gene. Training was equally effective in improving running distance in both groups, with pressure reduction only in SHR (Ϫ10%, PϽ0.05). In trained WKY, baseline bradycardia (PϽ0.05) occurred simultaneously with increased NTS OT immunostaining and mRNA expression (ϩ3.5-fold), without any change in OT receptor mRNA expression. PVN OT mRNA and DBS OT receptor mRNA expressions were significantly lower in SHR versus WKY (Ϫ39% and Ϫ56%, respectively). Training did not alter DBS OT receptor density in the SHR group but increased OT mRNA in both PVN and DBS areas (ϩ78% and ϩ45%, respectively). Our results show a marked hypertension-induced reduction in OT receptor mRNA expression, not altered by training. In contrast, training increased OT mRNA expression in sedentary and hypertensive rats, which may facilitate traininginduced cardiac performance. Key Words: hypothalamus Ⅲ exercise Ⅲ rats, spontaneously hypertensive Ⅲ neurotransmitter Ⅲ genetics Ⅲ autonomic nervous system Ⅲ immunohistochemistry H ypertension is a highly prevalent disease and a common risk factor for different cardiovascular diseases, with a major impact on morbidity and mortality. 1 Hypertensive individuals present with a series of functional and anatomic deficits, such as increased vascular resistance, vessel rarefaction, increased heart energy expenditure, increased stroke work, impaired baroreceptor reflex control, hormonal imbalance with overactivation of the renin-angiotensin system, and increased insulin resistance. Most of these effects contribute to increased sympathetic activity and depressed cardiovascular control. 1 On the other hand, exercise training has been associated with a variety of beneficial cardiovascular adjustments in hypertensive individuals, such as eutrophic remodeling of arterioles causing wall-lumen ratio normalization, 2,3 capillary angiogenesis and venule neoformation in exercised muscles resulting in increased vascular capacity and O 2 extraction, 3-7 and remodeling of the heart with simultaneous stroke volume increase and heart rate decrease. 8,9 Although there are ...

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“…Oxytocin can also modulate parasympathetic activity by stimulating the dorsal motor nucleus of the vagus nerve (Charpak et al, 1984). Peripherally, the neurobiological basis of oxytocin release in both labour and breastfeeding is stimulation of sensory nerves within the cervix and nipple respectively.…”

Section: Introductionmentioning

confidence: 99%

C-tactile afferents: Cutaneous mediators of oxytocin release during affiliative tactile interactions?

et al. 2017

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Low intensity, non-noxious, stimulation of cutaneous somatosensory nerves has been shown to trigger oxytocin release and is associated with increased social motivation, plus reduced physiological and behavioural reactivity to stressors. However, to date, little attention has been paid to the specific nature of the mechanosensory nerves which mediate these effects. In recent years, the neuroscientific study of human skin nerves (microneurography studies on single peripheral nerve fibres) has led to the identification and characterisation of a class of touch sensitive nerve fibres named C-Tactile afferents. Neither itch nor pain receptive, these unmyelinated, low threshold mechanoreceptors, found only in hairy skin, respond optimally to low force/velocity stroking touch. Notably, the speed of stroking which c-tactile afferents fire most strongly to is also that which people perceive to be most pleasant. The social touch hypothesis posits that this system of nerves has evolved in mammals to signal the rewarding value of physical contact in nurturing and social interactions. In support of this hypothesis, in this paper we review the evidence that cutaneous stimulation directly targeted to optimally activate c-tactile afferents reduces physiological arousal, carries a positive affective value and, under healthy conditions, inhibits responses to painful stimuli. These effects mirror those, we also review, which have been reported following endogenous release and exogenous administration of oxytocin. Taken together this evidence suggests c-tactile afferent stimulation may mediate oxytocin release during affiliative tactile interactions.

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Stimulatory action of oxytocin on neurones of the dorsal motor nucleus of the vagus nerve

Cited by 103 publications

References 18 publications

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Hypertension and Exercise Training Differentially Affect Oxytocin and Oxytocin Receptor Expression in the Brain

C-tactile afferents: Cutaneous mediators of oxytocin release during affiliative tactile interactions?

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