Enhanced nitric oxide release/synthesis in the posterior hypothalamus during nitroglycerin tolerance in rats

Ma, Sheng-Xing; Ji, A.; Pandjaitan, Marintan; Ojije, Goodluck

doi:10.1016/s0014-2999(03)01937-x

Cited by 8 publications

(13 citation statements)

References 42 publications

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“…A heating pad was used to prevent heat loss and maintain body temperature at 37.5°C. A CMA 12 microdialysis siliconized guide (CMA/Microdialysis, North Chelmsford, MA, USA) was implanted into the GN using previously described methods [38, 39]. The guide cannula was secured in place with dental cement.…”

Section: Methodsmentioning

confidence: 99%

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Electroacupuncture Zusanli (ST36) on Release of Nitric Oxide in the Gracile Nucleus and Improvement of Sensory Neuropathies in Zucker Diabetic Fatty Rats

Rong

2011

Evidence-Based Complementary and Alternative Medicine

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The purpose of these studies was to examine the effects of electroacupuncture (EA) Zusanli (ST36) on release of nitric oxide (NO) in the gracile nucleus (GN) and determine if functional neuropathic changes were modified by EA ST36-induced NO in the nucleus in Zucker diabetic fatty (ZDF) rats. The foot withdrawal responses to mechanical, thermal and cold stimuli were measured before and after EA stimulation. A microdialysis probe was implanted in the GN and dialysate samples were collected 20 min before, during and after EA ST36. Total nitrate and nitrite (NOx −) concentrations in the samples were quantified by using chemiluminescence. The baseline dialysate NOx − concentrations in the GN were decreased in ZDF rats compared to lean control (LC) rats (P < .05). In ZDF rats, dialysate NOx − releases in the GN were markedly increased during EA ST36, whereas in LC rats, the releases were moderately enhanced at 20–40 min after EA ST36. The withdrawal latencies to mechanical, cold and thermal stimuli were significantly improved 20 min after EA ST36 both in LC and ZDF rats, but not altered by non-acupoint stimulation. The withdrawal latencies to EA ST36 were further potentiated by 3-morpholinyl-sydnoneimine and inhibited by NG-Propyl-l-arginine infused into the GN in ZDF rats (P < .05). These results show that EA ST36 increases NO release in the GN, and NO in the nucleus modifies withdrawal latencies to mechanical, cold, and thermal nociception stimuli. Data suggest that EA ST36 induces NO release in the GN, which contributes to improvement of sensory neuropathies in rats.

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Section: Methodsmentioning

confidence: 99%

“…The concentrations of NO x − (NO 2 − and NO 3 − ) in the dialysate samples were measured using an ozone phase chemiluminescence (NOA280i, GE Analytical Instruments, Boulder, CO, USA) as described [38, 41]. The measurement was conducted in a blinded manner.…”

Section: Methodsmentioning

confidence: 99%

Electroacupuncture Zusanli (ST36) on Release of Nitric Oxide in the Gracile Nucleus and Improvement of Sensory Neuropathies in Zucker Diabetic Fatty Rats

Rong

2011

Evidence-Based Complementary and Alternative Medicine

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“…Similar effects were observed using two other NOS inhibitors (Sammut et al 2007b). Other studies performed in intact animals have used NPA at doses ranging from 1–20 mg/kg (Ma et al 2003; Atalla and Kuschinsky 2006). Based on outcomes from these reports, the current studies with NPA were performed using a dose of 20 mg/kg.…”

Section: Methodsmentioning

confidence: 99%

Impact of dopamine–glutamate interactions on striatal neuronal nitric oxide synthase activity

et al. 2009

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Rationale-It is known that dopamine (DA) D1 receptor activation stimulates striatal nitric oxide (NO) synthesis, whereas D2 receptor activation produces the opposite effect. However, the mechanisms involved in the dopaminergic modulation of NO synthase (NOS) are unknown.Objectives-We hypothesized that the effects of DA on striatal NO signaling are dependent on ongoing glutamatergic activation of NOS. Therefore, the current study examined whether intact NMDA receptor activation is required for the dopaminergic modulation of NOS activity. Methods-We assessed the impact of pharmacological manipulations of D1, D2 and NMDA receptors on NOS activity in the dorsal striatum and motor cortex using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. Drugs were administered systemically to conscious animals and NADPH-d staining was quantified in these regions using ex vivo measurements of tissue optical density.Results-Administration of the neuronal NOS inhibitor N G -propyl-L-arginine (NPA), the D1 receptor antagonist SCH 23390, and the NMDA receptor antagonist 3-phosphonopropylpiperazine-2-carboxylic acid (CPP) all attenuated staining selectively in the striatum. Administration of the D2 receptor agonist quinpirole decreased NADPH-d staining in both the striatum and cortex. Striatal NADPH-d staining elicited by administration of the D1 receptor agonist SKF 81297 or the D2 receptor antagonist eticlopride was attenuated by NPA, SCH 23390, and CPP pretreatment. Quinpirole pretreatment also abolished the facilitatory effect of SKF 81297.Conclusions-These studies show for the first time that ongoing NMDA receptor activation is necessary for modulation of striatal NOS activity by both facilitatory (D1 receptor activation) and inhibitory (D2 receptor activation) dopaminergic signaling mechanisms. Keywords dopamine; nitric oxide; nitric oxide synthase; NMDA receptor; striatum; cortex Nitric oxide (NO) is a key modulator of neuronal activity in the dorsal striatum and is thought to play an important role in complex processes including control of motor function and motivated behavior (Prast and Philippu 2001;West et al. 2002;Del Bel et al. 2005). NO is synthesized within medium-sized aspiny interneurons by type-1/neuronal NO synthase (nNOS). Striatal nNOS expressing interneurons and their processes are readily labeled using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical staining techniques (Hope et al.

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“… Figure 2 traces out the mechanisms by which acupuncture stimulation of ST36 activates the neurotransmitter network in the brain. At the cellular level, needling ST36 induces the enzyme nitric oxide synthase in keratinocytes [79, 80]. In response, these skin cells produce the neurotransmitter nitric oxide [79] which sends signals via the spinal cord to the brain [34, 81, 82].…”

Section: Molecular Mechanisms Of Actionmentioning

confidence: 99%

Acupuncture May Stimulate Anticancer Immunity via Activation of Natural Killer Cells

Johnston¹,

Ortíz‐Sánchez

Vujanović

et al. 2011

Evidence-Based Complementary and Alternative Medicine

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This article presents the hypothesis that acupuncture enhances anticancer immune functions by stimulating natural killer (NK) cells. It provides background information on acupuncture, summarizes the current scientific understanding of the mechanisms through which NK cells act to eliminate cancer cells, and reviews evidence that acupuncture is associated with increases in NK cell quantity and function in both animals and humans. The key contribution of this article involves the use of cellular immunology and molecular biological theory to interpret and synthesize evidence from disparate animal and human studies in formulating the ‘acupuncture immuno-enhancement hypothesis': clinicians may use acupuncture to promote the induction and secretion of NK-cell activating cytokines that engage specific NK cell receptors that endogenously enhance anticancer immune function.

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Enhanced nitric oxide release/synthesis in the posterior hypothalamus during nitroglycerin tolerance in rats

Cited by 8 publications

References 42 publications

Electroacupuncture Zusanli (ST36) on Release of Nitric Oxide in the Gracile Nucleus and Improvement of Sensory Neuropathies in Zucker Diabetic Fatty Rats

Electroacupuncture Zusanli (ST36) on Release of Nitric Oxide in the Gracile Nucleus and Improvement of Sensory Neuropathies in Zucker Diabetic Fatty Rats

Impact of dopamine–glutamate interactions on striatal neuronal nitric oxide synthase activity

Acupuncture May Stimulate Anticancer Immunity via Activation of Natural Killer Cells

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