GABAB receptors in the hypothalamic paraventricular nucleus mediate β-adrenoceptor-induced elevations of plasma noradrenaline in rats

Yamaguchi, Naoko; Mimura, Kazuya; Okada, Shoshiro

doi:10.1016/j.ejphar.2019.01.029

Cited by 7 publications

(7 citation statements)

References 45 publications

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“…Catecholamine levels in plasma samples were assessed as described in our previous reports (Yamaguchi et al, 2019a;Okada and Yamaguchi, 2017). In brief, plasma catecholamines and a standard mixture were extracted using alumina, and the extracted samples were assayed by high-performance liquid chromatography (HPLC) with electrochemical detection (HTEC-510, Eicom, Kyoto, Japan).…”

Section: Measurement Of Plasma Catecholaminesmentioning

confidence: 99%

Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Yamaguchi

Kakinuma

Yakura

et al. 2022

Autonomic Neuroscience

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Section: Measurement Of Plasma Catecholaminesmentioning

confidence: 99%

Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Yamaguchi

Kakinuma

Yakura

et al. 2022

Autonomic Neuroscience

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“…The present results showed that the NMDAR-independent LTP in PVN MNCs in acute stress rats was abolished by blockade of β-AR but not α-AR, indicating that the NMDAR-independent LTP in PVN MNCs in acute stress rats was mediated by β-AR. AR subtypes have been found abundantly expressed in the hypothalamic PVN, and activation of PVN β-ARs contributed to modulation of the PVN neuronal synaptic transmission [44], as well as modulation of some anxiety-like behaviors during stress challenge [61]. Activation of β-AR modulates long-term synaptic plasticity has been found in various regions of the brain.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, activation of α-and β-ARs modulated the strength of synaptic transmission and long-term plasticity via cAMP /PKA signaling pathway in the brain [37,[40][41][42][43]. Notably, both α-AR and β-AR subtypes are abundantly expressed in the hypothalamic PVN, and contributes to modulation the neuronal activity and synaptic transmission during various stress response [44,45], suggesting that ARs contributes to modulating the long-term synaptic plasticity of the excitatory glutamatergic inputs in the PVN MNCs in response to stressor. Therefore, we here investigated the effect of acute stress on the long-term glutamatergic synaptic plasticity in the PVN MNCs in vitro in rats.…”

Section: Introductionmentioning

confidence: 99%

Acute stress facilitates glutamatergic long-term potentiation in PVN magnocellular neurons through beta-adrenergic receptor/PKA cascade in vitro in rats

Jin,

Zhang,

Liu

et al. 2024

Preprint

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Acute stress alternates the hypothalamic paraventricular nucleus (PVN) magnocellular neuronal activity through modulation of excitatory and inhibitory synaptic inputs, leading to abnormal secretion of oxytocin (OT) and vasopressin (VP). However, mechanism of acute stress modulates the glutamatergic long-term potentiation (LTP) in PVN magnocellular neuroendocrine cells (MNCs) is unclear. We here investigated the effect of acute stress on the glutamatergic LTP of PVN MNCs, by whole-cell patch-clamp recording with biocytin staining and pharmacological methods. Delivery of high frequency stimulation (HFS) induced a glutamatergic LTP accompanied with a decrease in paired-pulse ratio in PVN MNCs, which was significantly enhanced in acute stress rats. Blockade of N-methyl-D-aspartate receptors (NMDAR) activity abolished the LTP of PVN MNCs in control group, but reveal a NMDAR-independent LTP in acute stress group. The NMDAR-independent LTP of PVN MNCs in stress rats was abolished by a β-AR inhibitor, propranolol, but not by an α-AR inhibitor, Phentolamine. The NMDAR-independent LTP of PVN MNCs in stress rats was abolished by bath application of a potent protein kinase A (PKA) inhibitor, KT5720 (200 nM), but not by a PKC inhibitor. Moreover, postsynaptic blockade of PKA completely prevented the HFS-induced glutamatergic LTP in PVN MNCs of stress rats. These results indicate that acute stress triggers an NMDAR-independent glutamatergic LTP of the PVN MNCs through a postsynaptic β-AR/PKA signaling pathway, resulting in an enhancement of an NMDAR-dependent presynaptic LTP in vitro in rats. The results suggest that acute stress upregulates OT and VP secretion by enhancing the excitatory glutamatergic LTP of PVN MNCs.

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“…Our results showed that RS exposure significantly increased 5-HT, GABA, and ACh, but not histamine, in the PVN, and that repeated administration of YKS suppressed the RS-induced increase in these neurotransmitters. It has been reported that the activities of 5-HT, 45 GABA (via GABA B , but not GABA A , receptors), 46,47 and ACh 48 in the PVN are involved in sympathetic activation. Therefore, it is possible that the YKS-induced decrease in these transmitter levels in the PVN shown in our study might be related to YKS-dependent suppression of sympathetic activation during stress exposure.…”

Section: Discussionmentioning

confidence: 99%

“…Neurotransmitters (5-HT, GABA, Ach, and histamine) in PVN microdialysates were analyzed according to our previously published methods 47,51 by LC-ITMS n analysis. To measure neurotransmitter concentrations in the dialysates, the peak area ratio relative to an internal standard was calculated and determined from the corresponding calibration curve.…”

Section: Measurement Of Neurotransmitters In Pvn Microdialysatesmentioning

confidence: 99%

Yokukansan, a Traditional Japanese Medicine, Suppresses Stress-Induced Sympathetic Activation via Central Responses in Rats

Yamaguchi,

Maruyama,

Okada

2023

Natural Product Communications

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Objectives: Yokukansan (YKS) is a traditional Japanese Kampo medicine approved by the Ministry of Health, Labour and Welfare of Japan. Recently, in addition to its indications as a drug treatment, YKS has been shown to have ameliorative effects on various psychological and behavioral responses such as anxiety, aggression, and stress responses. Stress exposure activates not only the hypothalamic–pituitary–adrenal axis but also the sympathetic nervous system. Sympathetic activation in brain regions such as the paraventricular hypothalamic nucleus (PVN) stimulates elevation of plasma catecholamine (noradrenaline and adrenaline) levels. We previously reported that various stress-related neuropeptides and several kinds of stressors, such as restraint stress (RS), increase plasma catecholamine and that brain prostanoids and their synthases mediate these responses in rats. In the present study, to determine if YKS treatment can affect stress-induced sympathetic activation, we examined the effects of YKS treatment on the RS-induced elevation of plasma catecholamine levels and related prostanoid production in the PVN of rats. Methods: YKS (1000 mg/10 mL/kg, p.o.) or vehicle was administered to rats daily for 14 days, and all rats were exposed to RS for 60 min on day 14. Before and during stress exposure on day 14, blood samples and PVN dialysates were collected and analyzed by high-performance liquid chromatography and liquid chromatography-ion trap tandem mass spectrometry, respectively. Results: Our results showed that repeated administration of YKS suppressed the RS-induced increase in plasma adrenaline but not noradrenaline. Furthermore, YKS administration also suppressed the RS-induced elevation of both prostaglandin E2 and thromboxane B2 levels in the PVN. In addition, we found that repeated administration of YKS suppressed the RS-induced increase in serotonin, gamma-aminobutyric acid, and acetylcholine in the PVN. Conclusion: Our results suggest that YKS can ameliorate stress-induced sympathetic activation via inhibition of stress responses in the brain.

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GABAB receptors in the hypothalamic paraventricular nucleus mediate β-adrenoceptor-induced elevations of plasma noradrenaline in rats

Cited by 7 publications

References 45 publications

Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Acute stress facilitates glutamatergic long-term potentiation in PVN magnocellular neurons through beta-adrenergic receptor/PKA cascade in vitro in rats

Yokukansan, a Traditional Japanese Medicine, Suppresses Stress-Induced Sympathetic Activation via Central Responses in Rats

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