Localization of Nitric Oxide Neurons in the Central Nervous System

Vincent, Steven R.

doi:10.1016/b978-012721985-1/50007-1

Cited by 44 publications

(34 citation statements)

References 199 publications

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“…However, NADPH specificity for NOS can be unreliable (cf. Vincent, 1995). The appearance of nNOS immunofluorescence in excised skin patches confirmed the presence of NOS in skin cells of Xenopus embryos at stage 37/38, with the pattern of staining being similar to the punctate distribution of NADPH-d staining.…”

Section: Discussionmentioning

confidence: 60%

Nitric oxide modulation of the electrically excitable skin ofXenopus laevisfrog tadpoles

Alpert

Zhang²,

Molinari

et al. 2007

Journal of Experimental Biology

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The skin is the main interface between the external environment and internal body structures of an organism and as such represents a strategic point of defense. Typically, the skin is a passive structure that acts as a protective barrier, and lacks a means of direct communication between constituent cells. However, the skin of many amphibian tadpoles functions as a sensory system in its own right. For a brief period from midembryonic until early larval development, cells of the tadpole skin exhibit properties of nervous tissue when presented with a noxious stimulus anywhere on their surface (reviewed in Roberts, 1998). This excitability takes the form of an action potential or 'skin impulse,' which resembles a cardiac action potential in duration and waveform, and propagates from the point of initiation throughout the skin via electrical connections between neighbouring cells. A range of anurans, including the South African clawed frog Xenopus laevis (Daudin), the common frog Rana temporaria, the common toad Bufo bufo, and salamanders such as Amystoma, have been shown to display such excitability (Roberts, 1998). One known function of the skin impulse is to trigger escape behaviour and thereby allow the tadpole to evade predation.In Xenopus, the skin impulse pathway is one of two sensory systems in the skin that operate in parallel (Roberts and Smyth, 1974), the second one involving a more conventional innervation by mechanosensory Rohon-Beard (R-B) cells, a subset of extra-ganglionic sensory neurones (Hughes, 1957). In early embryos, at stage 27 [about 24·h post-fertilization (Nieuwkoop and Faber, 1956)], the skin is already excitable, including in areas yet to be innervated by R-B cells. Both the skin impulse and the R-B cells can activate neural circuitry of the spinal cord to initiate trunk flexion in young embryos and rhythmic swimming movements in older embryos and larvae, but through different routes. R-B cells directly activate spinal neurons (Clarke et al., 1984;Sillar and Roberts, 1988), while the skin impulse appears to gain access to the central nervous system (CNS) via a branch of the trigeminal nerve, bypassing primary sensory R-B neurons in the skin (Roberts, 1996). Thus the electrically excitable epithelium functions as a bona fide sensory system, which initially precedes and then operates in parallel with more conventional mechanosensory innervation, before its excitable properties disappear during later larval life.Most cutaneous sensory systems are subject to modification under different circumstances (Sillar, 1989). The presence of a range of neuromodulatory substances in the skin of Xenopus raises the possibility that the skin impulse and its propagation through the epithelium may be subject to regulation, as is the case for other, more conventional sensory systems. One such modulator, which is produced by the skin of many vertebrates, including humans (Weller, 1997), is the free radical, nitric oxide (NO). NADPH-diaphorase labeling, a marker for the presence of the NO synthetic enzyme NOS, ...

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Section: Discussionmentioning

confidence: 60%

Nitric oxide modulation of the electrically excitable skin ofXenopus laevisfrog tadpoles

Alpert

Zhang²,

Molinari

et al. 2007

Journal of Experimental Biology

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“…Consistent with the location of NO in brain regions important for motor control (Vincent, 1995), studies impairing the normal production of neuronal NO in mammals have demonstrated dramatic locomotor deficits (Nelson et al, 1995;Dzoljic et al, 1997). However, unlocking the cellular and synaptic mechanisms for such deficits in higher vertebrates is by no means trivial.…”

Section: Nitric Oxide and Motor Controlmentioning

confidence: 84%

Metamodulation of a Spinal Locomotor Network by Nitric Oxide

McLean

Sillar

2004

J. Neurosci.

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Flexibility in the output of spinal networks can be accomplished by the actions of neuromodulators; however, little is known about how the process of neuromodulation itself may be modulated. Here we investigate the potential "meta"-modulatory hierarchy between nitric oxide (NO) and noradrenaline (NA) in Xenopus laevis tadpoles. NO and NA have similar effects on fictive swimming; both potentiate glycinergic inhibition to slow swimming frequency and GABAergic inhibition to reduce episode durations. In addition, both modulators have direct effects on the membrane properties of motor neurons. Here we report that antagonism of noradrenergic pathways with phentolamine dramatically influences the effect of the NO donor S-nitroso-N-acetylpenicillamine (SNAP) on swimming frequency, but not its effect on episode durations. In contrast, scavenging extracellular NO with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) does not influence any of the effects of NA on fictive swimming. These data place NO above NA in the metamodulatory hierarchy, strongly suggesting that NO works via a noradrenergic pathway to control glycine release but directly promotes GABA release. We confirmed this possibility using intracellular recordings from motor neurons. In support of a natural role for NO in the Xenopus locomotor network, PTIO not only antagonized all of the effects of SNAP on swimming but also, when applied on its own, modulated both swimming frequency and episode durations in addition to the underlying glycinergic and GABAergic pathways. Collectively, our results illustrate that NO and NA have parallel effects on motor neuron membrane properties and GABAergic inhibition, but that NO serially metamodulates glycinergic inhibition via NA.

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“…If, on the other hand, intracerebroventricular SIN-1 activated the PVN by acting on its afferents, potential candidates should be those that can respond to NO and therefore express cGMP, which is considered a functional NO receptor (Snyder and Dawson, 1995). However, the wide distribution of this enzyme (Vincent, 1995) does not provide useful guidance in this regard. Although NO that is formed in response to SIN-1 does not depend on the presence of NOS, we used this compound to study the endocrine responses that are induced by increased NO levels.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Stimulates ACTH Secretion and the Transcription of the Genes Encoding for NGFI-B, Corticotropin-Releasing Factor, Corticotropin-Releasing Factor Receptor Type 1, and Vasopressin in the Hypothalamus of the Intact Rat

1999

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We investigated the effect of the intracerebroventricular injection of the nitric oxide (NO) donor 3-morpholino-sydnonimine (SIN-1) on the release of adrenocorticotropin hormone (ACTH) and the neuronal response of hypothalamic neurons responsible for this release. Rats that were administered SIN-1 showed significant elevations in plasma ACTH levels, a response that was virtually abolished by antibodies against corticotropinreleasing factor (CRF) and significantly blunted by vasopressin (VP) antiserum. SIN-1 also upregulated heteronuclear (hn) transcripts for CRF and VP and messenger RNA (mRNA) levels for the immediate early gene NGFI-B and for CRF receptor type 1 (CRF-R 1 ) in the parvocellular portion of the paraventricular nucleus (PVN) of the hypothalamus. Blockade of prostaglandin synthesis with ibuprofen did not alter the ACTH or the PVN response to SIN-1. The central nucleus of the amygdala and the supraoptic nucleus, regions that are involved in autonomic adjustments to altered cardiovascular activity, also responded to SIN-1 with elevated NGFI-B mRNA levels. However, the only change in mean arterial blood pressure caused by this NO donor was a transient and modest increase. To our knowledge, this is the first demonstration that in the intact rat NO stimulates the activity of PVN neurons that control the hypothalamicpituitary-adrenal axis. It must be noted, however, that our results do not allow us to determine whether this effect was direct or mediated through PVN afferents. This study should help resolve the controversy generated by the use of isolated brain tissues to investigate the net effect of NO on hypothalamic peptide production.

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Localization of Nitric Oxide Neurons in the Central Nervous System

Cited by 44 publications

References 199 publications

Nitric oxide modulation of the electrically excitable skin ofXenopus laevisfrog tadpoles

Nitric oxide modulation of the electrically excitable skin ofXenopus laevisfrog tadpoles

Metamodulation of a Spinal Locomotor Network by Nitric Oxide

Nitric Oxide Stimulates ACTH Secretion and the Transcription of the Genes Encoding for NGFI-B, Corticotropin-Releasing Factor, Corticotropin-Releasing Factor Receptor Type 1, and Vasopressin in the Hypothalamus of the Intact Rat

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