Involvement of <scp>NMDA</scp> Receptors, Nitric Oxide, and <scp>GABA</scp> in Rostral Ventrolateral Medulla in Acute Ethanol‐Induced Cardiovascular Responses in Rats

Lo, Hsuan; Lin, Hsun-Hsun; Chen, Jun-Kai; Situmorang, Jiro Hasegawa; Lai, Chih-Chia

doi:10.1111/acer.13800

Cited by 9 publications

(9 citation statements)

References 53 publications

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“…However, facial stimulation induced MLI-PC LTD, in EtOH consumption mice in the absence of NOS activity. These results indicate that chronic EtOH consumption impairs MLI-PC LTD, may relate to the enhancement of NOS activity in vivo in mice Moreover, the application of the NO donor prevented the facial stimulation induced MLI-PC LTD in control mice, suggesting that an increase of NO levels inhibits the induction of MLI-PC LTD. Our results are supported by several previous studies (Yu et al, 2013; Finnerty et al, 2015; Lo et al, 2018), suggesting that EtOH consumption increases the NO level under in vivo conditions. First, systemic administration of EtOH resulted in a dose-dependent increase in NO levels, which was attenuated by administration of the NOS inhibitor (Finnerty et al, 2015).…”

Section: Discussionsupporting

confidence: 92%

“…Furthermore, acute treatment with EtOH increased the NOS activity and NO production in the brain regions associated with memory, including the prefrontal cortex, amygdala and the hippocampus of adult mice (Yu et al, 2013). Moreover, EtOH consumption causes an increase in the level of glutamate, NO, and GABA in the rostral ventrolateral medulla during the hypotensive responses, suggesting that EtOH enhances the glutamatergic NMDA receptor/NO/GABA pathways in the rostral ventrolateral medulla and may participate in the hypotensive effects induced by acute administration of EtOH (Lo et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

“…Acute treatment with EtOH increased NOS activity and NO production in brain memory related regions, such as the prefrontal cortex, amygdala and the hippocampus in adult mice (Yu et al, 2013). Recently, it has been demonstrated that EtOH caused an increase in the level of glutamate, NO, and GABA in the rostral ventrolateral medulla during the hypotensive responses, suggesting that EtOH enhanced glutamatergic NMDA receptors /NO/GABA pathways in the rostral ventrolateral medulla and may participate in the hypotensive effects induced by acute administration of EtOH (Lo et al, 2018). NO also has been involved in cerebellar cortical PF-PC presynaptic LTP under in vitro (Qiu and Knöpfel, 2007) and in vivo conditions (Chu et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell Synapses in vivo in Mice

Bing

Chu

et al. 2019

Front. Cell. Neurosci.

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The cerebellum is sensitive to ethanol (EtOH) consumption. Chronic EtOH consumption impairs motor learning by modulating the cerebellar circuitry synaptic transmission and long-term plasticity. Under in vitro conditions, acute EtOH inhibits both parallel fiber (PF) and climbing fiber (CF) long-term depression (LTD). However, thus far it has not been investigated how chronic EtOH consumption affects sensory stimulation-evoked LTD at the molecular layer interneurons (MLIs) to the Purkinje cell (PC) synapses (MLI-PC LTD) in the cerebellar cortex of living animals. In this study, we investigated the effect of chronic EtOH consumption on facial stimulation-evoked MLI-PC LTD, using an electrophysiological technique as well as pharmacological methods, in urethane-anesthetized mice. Our results showed that facial stimulation induced MLI–PC LTD in the control mice, but it could not be induced in mice with chronic EtOH consumption (0.8 g/kg; 28 days). Blocking the cannabinoid type 1 (CB1) receptor activity with AM-251, prevented MLI-PC LTD in the control mice, but revealed a nitric oxide (NO)-dependent long-term potentiation (LTP) of MLI–PC synaptic transmission (MLI-PC LTP) in the EtOH consumption mice. Notably, with the application of a NO donor, S-nitroso-N-Acetyl-D, L-penicillamine (SNAP) alone prevented the induction of MLI–PC LTD, but a mixture of SNAP and AM-251 revealed an MLI-PC LTP in control mice. In contrast, inhibiting NO synthase (NOS) revealed the facial stimulation-induced MLI-PC LTD in EtOH consumption mice. These results indicate that long-term EtOH consumption can impair the sensory stimulation-induced MLI–PC LTD via the activation of a NO signaling pathway in the cerebellar cortex in vivo in mice. Our results suggest that the chronic EtOH exposure causes a deficit in the cerebellar motor learning function and may be involved in the impaired MLI–PC GABAergic synaptic plasticity.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell Synapses in vivo in Mice

Bing

Chu

et al. 2019

Front. Cell. Neurosci.

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“…Nitric oxide is well characterized for its vasodilatory role in cardiovascular regulation; and a number of studies have linked NO to cardiovascular activity in the RVLM (Machado et al, 2016;Lo et al, 2018). However, the complicated responses and potential mechanisms are not well established yet.…”

Section: Discussionmentioning

confidence: 99%

The Release of Nitric Oxide Is Involved in the β-Arrestin1-Induced Antihypertensive Effect in the Rostral Ventrolateral Medulla

Sun

Tan

et al. 2021

Front. Physiol.

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β-Arrestin1 is a multifunctional scaffold protein with the ability to interact with diverse signaling molecules independent of G protein-coupled receptors. We previously reported that overexpression of β-arrestin1 in the rostral ventrolateral medulla (RVLM) decreased blood pressure (BP) and renal sympathetic nerve activity (RSNA) in spontaneously hypertensive rats (SHRs). Nitric oxide (NO) is widely reported to be involved in central cardiovascular regulation. The goal of this study was to investigate whether NO signaling contributes to the β-arrestin1-mediated antihypertensive effect in the RVLM. It was found that bilateral injection of adeno-associated virus containing Arrb1 gene (AAV-Arrb1) into the RVLM of SHRs significantly increased NO production and NO synthase (NOS) activity. Microinjection of the non-selective NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME; 10 nmol) into the RVLM prevented the β-arrestin1-induced cardiovascular inhibitory effect. Furthermore, β-arrestin1 overexpression in the RVLM significantly upregulated the expression of phosphorylated neuronal NOS (nNOS) by 3.8-fold and extracellular regulated kinase 1/2 (ERK1/2) by 5.6-fold in SHRs. The β-arrestin1-induced decrease in BP and RSNA was significantly abolished by treatment with ERK1/2 small interfering RNA (ERK1/2 siRNA). Moreover, ERK1/2 siRNA attenuated the β-arrestin1-induced NO production, NOS activity, and nNOS phosphorylation in the RVLM. Taken together, these data demonstrate that the antihypertensive effect of β-arrestin1 in the RVLM is mediated by nNOS-derived NO release, which is associated with ERK1/2 activation.

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“…The procedures for the RVLM microinjections and microdialysis were similar to our previous study [18]. Five days after i.c.v.…”

Section: Microinjection Into the Rvlmmentioning

confidence: 92%

Activation of mGluR5 and NMDA Receptor Pathways in the Rostral Ventrolateral Medulla as a Central Mechanism for Methamphetamine-Induced Pressor Effect in Rats

et al. 2020

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Acute hypertension produced by methamphetamine (MA) is well known, mainly by the enhancement of catecholamine release from sympathetic terminals. However, the central pressor mechanism of the blood-brain-barrier-penetrating molecule remains unclear. We used radio-telemetry and femoral artery cannulation to monitor the mean arterial pressure (MAP) in conscious free-moving and urethane-anesthetized rats, respectively. Expression of Fos protein (Fos) and phosphorylation of N-methyl-D-aspartate receptor subunit GluN1 in the rostral ventrolateral medulla (RVLM) were detected using Western blot analysis. ELISA was carried out for detection of protein kinase C (PKC) activity in the RVLM. MA-induced glutamate release in the RVLM was assayed using in vivo microdialysis and HPLC. Systemic or intracerebroventricular (i.c.v.) administration of MA augments the MAP and increases Fos expression, PKC activity, and phosphorylated GluN1-ser 896 (pGluN1-ser 896) in the RVLM. However, direct microinjection of MA into the RVLM did not change the MAP. Unilateral microinjection of a PKC inhibitor or a metabotropic glutamate receptor 5 (mGluR5) antagonist into the RVLM dose-dependently attenuated the i.c.v. MA-induced increase in MAP and pGluN1-ser 896. Our data suggested that MA may give rise to glutamate release in the RVLM further to the activation of mGluR5-PKC pathways, which would serve as a central mechanism for the MA-induced pressor effect.

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Involvement of NMDA Receptors, Nitric Oxide, and GABA in Rostral Ventrolateral Medulla in Acute Ethanol‐Induced Cardiovascular Responses in Rats

Abstract: Our results indicate that EtOH augmentation of glutamatergic NMDA receptors/NO/GABA pathways in the RVLM may participate in the hypotensive effects induced by acute administration of EtOH.

Cited by 9 publications

References 53 publications

Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell Synapses in vivo in Mice

Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell Synapses in vivo in Mice

The Release of Nitric Oxide Is Involved in the β-Arrestin1-Induced Antihypertensive Effect in the Rostral Ventrolateral Medulla

Activation of mGluR5 and NMDA Receptor Pathways in the Rostral Ventrolateral Medulla as a Central Mechanism for Methamphetamine-Induced Pressor Effect in Rats

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