Nitric oxide stimulates γ‐aminobutyric acid release and inhibits glycine release in retina

Yu, Di; Eldred, William D.

doi:10.1002/cne.20416

Cited by 56 publications

(57 citation statements)

References 58 publications

(43 reference statements)

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“…Differential responses to NO in GABAergic and glycinergic neurotransmission were reported in turtle retina slices where NO facilitated GABA and inhibited glycine release. 40 …”

Section: Discussionmentioning

confidence: 99%

NO Differentially Regulates Neurotransmission to Premotor Cardiac Vagal Neurons in the Nucleus Ambiguus

et al. 2006

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Abstract-NO is involved in the neural control of heart rate, and NO synthase expressing neurons and terminals have been localized in the nucleus ambiguus where parasympathetic cardiac vagal preganglionic neurons are located; however, little is known about the mechanisms by which NO alters the activity of premotor cardiac vagal neurons. This study examines whether the NO donor sodium nitroprusside ([SNP] 100 mol/L) and precursor, L-arginine (10 mmol/L), modulate excitatory and inhibitory synaptic neurotransmission to cardiac vagal preganglionic neurons. Glutamatergic, GABAergic, and glycinergic activity to cardiac vagal neurons was examined using whole-cell patch-clamp recordings in an in vitro brain slice preparation in rats. Both SNP, as well as L-arginine, increased the frequency of GABAergic neurotransmission to cardiac vagal preganglionic neurons but decreased the amplitude of GABAergic inhibitory postsynaptic currents. In contrast, both L-arginine and SNP inhibited the frequency of glutamatergic and glycinergic synaptic events in cardiac vagal preganglionic neurons. SNP and L-arginine also decreased glycinergic inhibitory postsynaptic current amplitude, and this response persisted in the presence of tetrodotoxin. Inclusion of the NO synthase inhibitor 7-nitroindazole (100 mol/L) prevented the L-arginine-evoked responses. These results demonstrate that NO differentially regulates excitatory and inhibitory neurotransmission, facilitating GABAergic and diminishing glutamatergic and glycinergic neurotransmission to cardiac vagal neurons. Key Words: nitric oxide Ⅲ parasympathetic Ⅲ vagal Ⅲ ambiguus Ⅲ cardiac Ⅲ brain stem N O, a gaseous neuromodulator, plays an important role in the central nervous system control of blood pressure and heart rate. In the brain stem, NO is localized to several medullary nuclei involved in cardiorespiratory and gastrointestinal function. 1,2 Neurons that contain the NO synthesizing enzyme, NO synthase (NOS), have been observed in many critical sites of central cardiovascular regulation, including the dorsal motor nucleus of the vagus, rostral ventrolateral medulla, caudal ventrolateral medulla, nucleus of the tractus solitarius (NTS), and the nucleus ambiguus (NA). 3 In the NA, NO is present in many of the terminal fields that surround cardiac vagal preganglionic neurons (CVPNs), including synaptic terminals from neurons that originate in the NTS. 4 CVPNs are primarily located within the external formation of the NA. 5-9 The CVPNs provide parasympathetic innervation to the heart and dominate control of the heart rate. CVPNs are intrinsically silent, and their activity is dominated by synaptic activation from other neurons that use neurotransmitters, such as acetylcholine, glutamate, GABA, and glycine, among others. 5,8 -12 NOS immunoreactivity is not directly colocalized with cholinergic neurons in the brain stem but rather is in small neurons, suggesting that NO is present in interneurons. 13,14 This indicates that NO may exert its actions by modulating synaptic inputs to CVPNs. ...

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“…Differential responses to NO in GABAergic and glycinergic neurotransmission were reported in turtle retina slices where NO facilitated GABA and inhibited glycine release. 40 …”

Section: Discussionmentioning

confidence: 99%

NO Differentially Regulates Neurotransmission to Premotor Cardiac Vagal Neurons in the Nucleus Ambiguus

et al. 2006

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“…In line with this, it was later shown that NO could also stimulate GABA release in a different experimental model, the adult turtle retina [93]. The authors observed that the NO effect was cGMP-dependent.…”

Section: Gaba and Glutamatementioning

confidence: 64%

“…donor DETA NONOate could stimulate GABA release. It was demonstrated that DETA NONOate-induced GABA release was mediated by the reversal of GABA transporters (GAT) in horizontal cells, which depended on Ca 2+ ions in the inner plexiform layer [93].…”

Section: Gaba and Glutamatementioning

confidence: 99%

“…NO is also capable of regulating the transport of glycine, another inhibitory retinal neuromodulator [93,94]. It was first observed, in rabbit retinas, that NO donors (SNP and SNAP) inhibited high potassium-mediated glycine release [94].…”

Section: Glycinementioning

confidence: 99%

“…Additionally, it was observed in the adult turtle retina that DETA NONOate could enhance glycine uptake and inhibit its release. To better evaluate this NO effect, Yu and Eldred used 8-Br-cGMP and SIN-1, a ONOO -donor, and observed that SIN-1, but not 8-Br-cGMP, mimicked DETA NONOate effect, suggesting therefore that NO may work through ONOO -to stimulate glycine uptake and inhibit its release [93]. In summary, different groups showed that NO is capable of modulating the release of inhibitory neurotransmitters in many retinal cell types and at different developmental stages of the vertebrate retina.…”

Section: Glycinementioning

confidence: 99%

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Studying Nitric Oxide in the Developing Retina: Neuromodulatory Functions and Signaling Mechanisms

Socodato

Portugal²,

Encarnação³

et al. 2013

TONOJ

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Abstract:The retina is a highly organized structure responsible for transducing light stimulation into electrical responses. Retinal organization is conserved in all vertebrate species and the generation of retinal cell types is chronologically determined and fairly documented from amphibians to humans. Furthermore, the chick retina is a well-established experimental paradigm for neurochemical and developmental studies regarding the nervous system. Among many signaling molecules regulating retinal physiology, nitric oxide (NO) is likely to play a prominent role within the retina. NO is a gaseous signaling transmitter, which regulates a plethora of physiological functions within an organism, including high-order signaling events both in the developing and mature nervous system. In this review we focus on different aspects of NO signaling in regulating retinal cell neurochemistry, focusing mainly on developing chick retina as a prevalent experimental model. Based on literature and data gathered from our group we conclude that NO is a major atypical neurotransmitter in the retina, regulating signaling events associated with the development of embryonic retinal neurons and glial cells.

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Availability of pediatric rheumatology training in United States pediatric residencies

Mayer

Brogan

Sandborg

2006

Arthritis & Rheumatism

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Objective. To characterize the availability of pediatric rheumatology training in general pediatric residencies. Methods. We surveyed 195 pediatric residency program directors in the US using a combined Web-based and paperbased survey format. The survey asked directors about the availability of an on-site pediatric rheumatologist in their institution, the availability of formal pediatric rheumatology rotations, and the types of physicians involved in teaching curriculum components related to pediatric rheumatology. Survey responses were analyzed using descriptive and bivariate statistics. Results. Of the 195 program directors surveyed, 127 (65%) responded. More than 40% of responding programs did not have a pediatric rheumatologist on site. Programs with on-site pediatric rheumatologists were significantly more likely than those without on-site pediatric rheumatologists to have an on-site pediatric rheumatology rotation available (94% versus 9%; P < 0.001). Although pediatric rheumatologists' involvement in 4 curriculum areas relevant to pediatric rheumatology is nearly universal in programs with on-site pediatric rheumatologists, nearly two-thirds of programs without on-site pediatric rheumatologists rely on internist rheumatologists, general pediatricians, or other physicians to cover these areas. Conclusion. Programs without pediatric rheumatologists on site are less likely to have pediatric rheumatology rotations and are more likely to rely on internist rheumatologists and nonrheumatologists to address rheumatology-related curriculum components. Lack of exposure to pediatric rheumatology during residency may impede general pediatricians' ability to identify and treat children with rheumatic diseases, undermine resident interest in this field, and perpetuate low levels of supply.

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Nitric oxide stimulates γ‐aminobutyric acid release and inhibits glycine release in retina

Cited by 56 publications

References 58 publications

NO Differentially Regulates Neurotransmission to Premotor Cardiac Vagal Neurons in the Nucleus Ambiguus

NO Differentially Regulates Neurotransmission to Premotor Cardiac Vagal Neurons in the Nucleus Ambiguus

Studying Nitric Oxide in the Developing Retina: Neuromodulatory Functions and Signaling Mechanisms

Availability of pediatric rheumatology training in United States pediatric residencies

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