Evidence for independent hypertensive effects of oxytocin and vasopressin in the rat dorsal vagal complex

Tian, Puxuan; Ingram, C.D.

doi:10.1016/s0168-0102(97)01161-9

Cited by 7 publications

(4 citation statements)

References 20 publications

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“…3, C and E). To determine whether the OXT response was due to activation of the OXTR or to activation of AVP receptors for which OXT has a low affinity, we used the highly selective OXTR agonist, TGOT, which has a 16,000-fold greater affinity for the OXTR than for AVP receptors (11,27,35,50). In the presence of TTX (1 M), TGOT (1 M) evoked a depolarization of 4.2 Ϯ 2.0 mV (P Ͻ 0.05; n ϭ 6; t-test, Fig.…”

Section: Resultsmentioning

confidence: 99%

Vasopressin and oxytocin excite MCH neurons, but not other lateral hypothalamic GABA neurons

Yao

Zhang

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Neurons that synthesize melanin-concentrating hormone (MCH) colocalize GABA, regulate energy homeostasis, modulate water intake, and influence anxiety, stress, and social interaction. Similarly, vasopressin and oxytocin can influence the same behaviors and states, suggesting that these neuropeptides may exert part of their effect by modulating MCH neurons. Using whole cell recording in MCH-green fluorescent protein (GFP) transgenic mouse hypothalamic brain slices, we found that both vasopressin and oxytocin evoked a substantial excitatory effect. Both peptides reversibly increased spike frequency and depolarized the membrane potential in a concentration-dependent and tetrodotoxin-resistant manner, indicating a direct effect. Substitution of lithium for extracellular sodium, Na(+)/Ca(2+) exchanger blockers KB-R7943 and SN-6, and intracellular calcium chelator BAPTA, all substantially reduced the vasopressin-mediated depolarization, suggesting activation of the Na(+)/Ca(2+) exchanger. Vasopressin reduced input resistance, and the vasopressin-mediated depolarization was attenuated by SKF-96265, suggesting a second mechanism based on opening nonselective cation channels. Neither vasopressin nor oxytocin showed substantial excitatory actions on lateral hypothalamic inhibitory neurons identified in a glutamate decarboxylase 67 (GAD67)-GFP mouse. The primary vasopressin receptor was vasopressin receptor 1a (V1aR), as suggested by the excitation by V1aR agonist [Arg(8)]vasotocin, the selective V1aR agonist [Phe(2)]OVT and by the presence of V1aR mRNA in MCH cells, but not in other nearby GABA cells, as detected with single-cell RT-PCR. Oxytocin receptor mRNA was also detected in MCH neurons. Together, these data suggest that vasopressin or oxytocin exert a minimal effect on most GABA neurons in the lateral hypothalamus but exert a robust excitatory effect on presumptive GABA cells that contain MCH. Thus, some of the central actions of vasopressin and oxytocin may be mediated through MCH cells.

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Section: Resultsmentioning

confidence: 99%

Vasopressin and oxytocin excite MCH neurons, but not other lateral hypothalamic GABA neurons

Yao

Zhang

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Whilst these latter findings may reflect a mixed population of receptors within the testis, they may be due to another subtype of receptor. More recently a novel subtype of OT receptor has also been postulated in the rat dorsal vagal complex (Tian & Ingram 1997). This receptor modulates the hypertensive effects of OT and is reported to be neither a classical V 1a nor OT 1a receptor.…”

Section: Discussionmentioning

confidence: 99%

Characterisation of the biological effects of neurohypophysial peptides on seminiferous tubules

Harris

Nicholson²

1998

Journal of Endocrinology

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Oxytocin (OT) is present in the mammalian testis and has been postulated to play a role in modulation of seminiferous tubule contractility. However, recent evidence suggests that the myoid cells responsible for such contractile activity do not express OT receptors. In this study computer-assisted analysis and time-lapse videomicrography were used to investigate the biological effects of neurohypophysial peptides and their analogues on seminiferous tubule contractility. Adult rat testes were placed in fresh oxygenated Dulbecco's modified Eagle's medium (DMEM) F12 medium, decapsulated and the tubules gently teased apart. A small section of tubule was placed in a microslide chamber and perifused with medium. Seminiferous tubules were treated with OT (2 nM), [Arg8]-vasopressin (AVP, 0.2 nM) or [Thr4,Gly7]-OT (TGOT, 2 nM, 8 nM and 0.2 microM). Specific antagonists were also given simultaneously with OT and AVP treatments. Data were analysed to give arbitrary units of contractility. Both OT and AVP increased tubule contractility, with AVP being at least 10 times more potent than OT. Treatment with the selective OT antagonist, desGly-NH2,d(CH2)5[d-Tyr2,Thr4]-ornithine vasotocin (OTA, 0.2 microM and 2 microM) significantly reduced OT-induced increases in seminiferous tubule contractility but had no effect on AVP-induced responses. In contrast, the AVP antagonist, Phaa-d-Tyr(Me)-Phe-Gln-Asn-Arg-Pro-Arg-Tyr-NH2 (AVPA) was more potent at reducing AVP-induced increases than OT-induced responses. The selective non-peptide AVPA SR 49059 blocked the response to both peptides in a similar manner, whilst the non-peptide OTA L367,773 did not block OT-induced increases in seminiferous tubule contractility at doses that were slightly inhibitory to AVP-induced responses. The specific OT agonist TGOT did not induce a contractile response. The data in this study demonstrate that in the testis AVP acts via V1a receptors to stimulate contractile activity and suggest that OT may act via a receptor which differs from the classical V1a and uterine-type OT receptor. These findings support a role for OT in the regulation of seminiferous tubule contractility and raise the possibility that AVP may also be important in this process.

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“…Neurons containing many neurotransmitters such as bombesin (Costello et al 1991), oxytocin (Olson et al 1992, vasopressin, somatostatin, L-enkephalin, and M-enkephalin (Sawchenko and Swanson 1982) have been shown projecting to the DVC. The possible roles of these neurotransmitters have been investigated extensively (Dubois-Dauphin et al 1992;Mo et al 1992;Tian and Ingram 1997). However, as mentioned by Sawchenko and Swanson, less than one-fourth of the PVN neurons projecting to the DVC contain recognized neurotransmitters.…”

Section: Introductionmentioning

confidence: 99%

Glutamate Mediates an Excitatory Influence of the Paraventricular Hypothalamic Nucleus on the Dorsal Motor Nucleus of the Vagus

Zhang

Fogel

2002

Journal of Neurophysiology

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Data have shown that the paraventricular nucleus of the hypothalamus (PVN) and the dorsal motor nucleus of the vagus (DMNV) play important roles in the regulation of gastrointestinal function and eating behavior. Anatomical studies have demonstrated direct projections from the PVN to the DMNV and physiological studies showed that the DMNV mediates many of the effects of PVN stimulation and electrical current stimulation of the PVN excites a subset of DMNV neurons. The aim of this study was to characterize the role of glutamate receptors in the excitatory influence of the PVN on gut-related DMNV neurons. Using single-cell recording techniques, we determined the effects of kynurenic acid, 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX), and DL-2-amino-5-phosphonopentanoic acid (DL-AP5) on the increase in firing rate due to electrical current stimulation of the PVN. In initial experiments, we studied 24 DMNV neurons excited by electrical current stimulation of the PVN. Kynurenic acid, a broad-spectrum glutamate receptor antagonist, prevented the PVN effect in 22 neurons and significantly attenuated the effect in the other cells. Nine of these neurons demonstrated an inhibition in firing rate with PVN stimulation after pretreatment with kynurenic acid. In a separate group of 12 neurons, we determined the effects of CNQX (1.2 nmol) injected into the DMNV. This AMPA receptor antagonist completely blocked the excitatory response to PVN stimulation of six DMNV neurons and significantly attenuated the response of the other six DMNV neurons. The addition of 1.2 nmol DL-AP5, a N-methyl-D-aspartate (NMDA) receptor antagonist, further attenuated the response to PVN stimulation in four of the five DMNV neurons that were still excited after CNQX treatment. The fifth neuron demonstrated PVN- induced inhibition of firing rate after treatment with CNQX and DL-AP5. In a separate group of 11 DMNV neurons excited by electrical stimulation of the PVN, DL-AP5 partially attenuated the excitatory responses of only four DMNV neurons and did not block the excitation of any cells. The mean latency (14 neurons tested) from the PVN to the DMNV was 37.71 +/- 2.40 (SE) ms. Monosynaptic action potentials and excitatory postsynaptic potentials were demonstrated in three DMNV neurons by intracellular recording. Our results indicate that glutamate released from PVN neurons projecting to the DMNV excite the gut-related vagal motor neurons by acting predominantly on the AMPA receptor. The NMDA receptor plays only a minor role in the excitatory effect.

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Evidence for independent hypertensive effects of oxytocin and vasopressin in the rat dorsal vagal complex

Cited by 7 publications

References 20 publications

Vasopressin and oxytocin excite MCH neurons, but not other lateral hypothalamic GABA neurons

Vasopressin and oxytocin excite MCH neurons, but not other lateral hypothalamic GABA neurons

Characterisation of the biological effects of neurohypophysial peptides on seminiferous tubules

Glutamate Mediates an Excitatory Influence of the Paraventricular Hypothalamic Nucleus on the Dorsal Motor Nucleus of the Vagus

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