Distribution of nitric oxide synthase and nitric oxide-receptive, cyclic GMP-producing structures in the rat brain

Vente, Jan de; Hopkins, David A.; Ittersum, Marjanne Markerink‐van; Emson, Piers C.; Schmidt, Harald; Steinbusch, Harry W.M.

doi:10.1016/s0306-4522(98)00171-7

Cited by 138 publications

(111 citation statements)

References 91 publications

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“…Alternative methodologies such as radioimmunoassay may have been more sensitive, however the ability to define specific neuronal populations is lost and in a study examining hippocampal slices, analysis of cGMP radioimmunoassay versus cGMP immunofluorescence intensity showed comparable sensitivities [46]. The lack of detectable cGMP expression in neurons of the RVLM is in accord with a detailed study by De Vente et al [22], who similarly observed cGMP in the NA and nucleus tractus solitarii (NTS) in the brain stem region, but do not comment on its expression in the RVLM, despite the use of invitro stimulation paradigms as applied in this study. In the work by De Vente et al, the importance of IBMX to reveal otherwise non-detectable cGMP populations was stressed [22,47] and this has also been noted by other authors [48].…”

Section: Discussionsupporting

confidence: 71%

“…To date, no studies have described the immunohistochemical localisation of neurons capable of expressing cGMP within the C1 region [22]. Given the strong evidence that NO signalling plays a functional role in the RVLM, we sought to identify the cellular targets for NO in the RVLM, visualising cGMP and its neuroanatomical relationship with the C1 cell group, as identified by the presence of tyrosine hydroxylase (TH) or phenylethanolamine N-methyltransferase (PNMT), and the more medially located nNOS expressing cell population [18,23].…”

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical assessment of cyclic guanosine monophosphate (cGMP) and soluble guanylate cyclase (sGC) within the rostral ventrolateral medulla

et al. 2008

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2008).Immunohistochemical assessment of cyclic guanosine monophosphate (cGMP) and soluble guanylate cyclase (sGC) within the rostral ventrolateral medulla. Journal of Biomedical Science, 15 (6), 801-812. Immunohistochemical assessment of cyclic guanosine monophosphate (cGMP) and soluble guanylate cyclase (sGC) within the rostral ventrolateral medulla AbstractFunctional evidence suggests that nitric oxide (NO) signalling in the rostral ventrolateral medulla (RVLM) is cGMP-dependent and that this pathway is impaired in hypertension. We examined cGMP expression as a marker of active NO signalling in the C1 region of the RVLM, comparing adult (>18 weeks) Wistar-Kyoto (WKY, n = 4) and spontaneously hypertensive rats (SHR, n = 4). Double label immunohistochemistry for cGMP-immunoreactivity (IR) and C1 neurons [as identified by phenylethanolamine N-methyltransferase (PNMT-IR) or tyrosine hydroxylase TH-IR)], or neuronal NO synthase (nNOS) neurones, failed to reveal cGMP-IR neurons in the RVLM of either strain, despite consistent detection of cGMP-IR in the nucleus ambiguus (NA). This was unchanged in the presence of isobutylmethylxanthine (IBMX; 0.5 mM, WKY, n = 4, SHR n = 2) and in young animals (WKY, 10-weeks, n = 3). Incubation of RVLM-slices (WKY, 10-weeks, n = 9) in DETA-NO (100 μm; 10 min) or NMDA (10 μM; 2 min) did not uncover cGMP-IR. In all studies, cGMP was prominent within the vasculature. Soluble guanylate cyclase (sGC)-IR was found throughout neurones of the RVLM, but did not co-localise with PNMT, TH or nNOS-IR neurons (WKY, 10-weeks, n = 6). Results indicate that within the RVLM, cGMP is not detectable using immunohistochemistry in the basal state and cannot be elicited by phosphodiesterase inhibition, NMDA receptor stimulation or NO donor application. Abstract Functional evidence suggests that nitric oxide (NO) signalling in the rostral ventrolateral medulla (RVLM) is cGMP-dependent and that this pathway is impaired in hypertension. We examined cGMP expression as a marker of active NO signalling in the C1 region of the RVLM, comparing adult ([18 weeks) Wistar-Kyoto (WKY, n = 4) and spontaneously hypertensive rats (SHR, n = 4). Double label immunohistochemistry for cGMPimmunoreactivity (IR) and C1 neurons [as identified by phenylethanolamine N-methyltransferase (PNMT-IR) or tyrosine hydroxylase TH-IR)], or neuronal NO synthase (nNOS) neurones, failed to reveal cGMP-IR neurons in the RVLM of either strain, despite consistent detection of cGMP-IR in the nucleus ambiguus (NA). This was unchanged in the presence of isobutylmethylxanthine (IBMX; 0.5 mM, WKY, n = 4, SHR n = 2) and in young animals (WKY, 10-weeks, n = 3). Incubation of RVLMslices (WKY, 10-weeks, n = 9) in DETA-NO (100 lm; 10 min) or NMDA (10 lM; 2 min) did not uncover cGMP-IR. In all studies, cGMP was prominent within the vasculature. Soluble guanylate cyclase (sGC)-IR was found throughout neurones of the RVLM, but did not co-localise with PNMT, TH or nNOS-IR neurons (WKY, 10-weeks, n = 6). Results indicate that within the RVLM, cGMP is not ...

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Immunohistochemical assessment of cyclic guanosine monophosphate (cGMP) and soluble guanylate cyclase (sGC) within the rostral ventrolateral medulla

et al. 2008

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“…Although this specific issue remains to be experimentally tested, our previous data obtained in both the STN and the striatum, as well as some considerations on the distribution of drug-induced effects among neurons, lead us to hypothesize a role for cGMP in some of the observed effects. Moreover, it must be noted that, with some sparse exception, no co-localization of nNOS and sGC has been observed in the same neurons (De Vente et al, 1998). From this point of view, taking into consideration the NO/cGMP pathway, a locally applied NO donor (e.g.…”

Section: Possible Mechanisms Involved In the No-dependent Modulation mentioning

confidence: 98%

“…Such gaseous messenger is a modulator of neurotransmission (Prast and Philippu, 2001) and the neuronal isoform of NO-synthase (nNOS), the NO-producing enzyme, is widely distributed in the rat brain (De Vente et al, 1998), including GP (Rodrigo et al, 1994). In a previous study we observed that the systemic administration of 7-nitro-indazole, a preferential inhibitor of nNOS, induced a decrease of the firing rate of responsive GP neurons; similarly, the microiontophoretic application of Nω-nitro-L-arginine methyl ester (L-NAME), a nonspecific inhibitor of nNOS, induced a decrease in the firing rate of most recorded neurons; furthermore, the local administration of 3-morpholinosydnonimin-hydrocloride (SIN-1), a NO donor, induced an increase of the firing activity of GP neurons (Sardo et al, 2002a).…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide-active compounds modulate the intensity of glutamate-evoked responses in the globus pallidus of the rat

et al. 2011

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Aim: The effects of local applied NO-active compounds on glutamate (GLU)-evoked responses were investigated in globus pallidus (GP) neurons. Main methods: Extracellularly recorded single units from anesthetized rats were treated with GLU before and during the microiontophoretic application of S-nitrosoglutathione (SNOG), a NO donor, and Nω-nitro-Larginine methyl ester (L-NAME), a NOS inhibitor. Key findings: Most GP cells were excited by SNOG whereas administration of L-NAME induced decrease of GP neurons activity. Nearly all neurons responding to SNOG and/or L-NAME showed significant modulation of their excitatory responses to the administration of iontophoretic GLU. In these cells, the changes induced by NO-active drugs in the magnitude of GLU-evoked responses were used as indicators of NO modulation. In fact, when a NO-active drug was co-iontophoresed with GLU, significant changes in GLU-induced responses were observed: generally, increased magnitudes of GLU-evoked responses were observed during SNOG ejection, whereas the administration of L-NAME decreased responses to GLU. Significance: The results suggest that the NO-active drugs modulate the response of GP neurons to glutamatergic transmission. Nitrergic modulation of glutamatergic transmission could play an important role in the control of GP bioelectric activity, considered a fundamental key in the BG function.

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“…After treatment, slices were fixed with 4% paraformaldehyde overnight at 4°C, washed in phosphate buffered saline with 0.3 % triton X-100 (PBS-TX), and then incubated for 48 hr at 4°C in an anti-cGMP primary antibody (De Vente and Steinbusch, 1992;De Vente et al, 1998). After washing over a period of an hour, slices were incubated in fluorescently labeled secondary antibody overnight (goat anti-sheep, Jackson Immunoresearch Labs, West Grove, PA) at 4°C.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Developmental appearance of cyclic guanosine monophosphate (cGMP) production and nitric oxide responsiveness in embryonic mouse cortex and striatum

2006

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The second messenger cyclic guanosine monophosphate (cGMP) regulates multiple aspects of both structural development and physiological function in the developing nervous system. Recent in vitro experiments have shown that cGMP also modulates the response of developing vertebrate neurons to guidance molecules. This has led to the proposal that in vivo cGMP plays a critical role in directing the outgrowth of the apical dendrites of developing neurons in the cerebral cortex. Despite this proposed role, the onset, localization, and dynamics of cGMP production in the embryonic cortex are unknown. To investigate the potential contribution of cGMP in the embryo, we have used a pharmacological and immunohistochemical approach to test whether the endogenous production of cGMP, and the capacity to produce cGMP in response to nitric oxide (NO), in the cerebral cortex is compatible with the proposed developmental roles for cGMP. We find that cortical cGMP production and NO sensitivity are regionally and developmentally regulated. Cortical cGMP production begins at E15, later than in the ganglionic eminences, becomes high in the cortical plate but not the ventricular zone, and is dependent on nitric oxide synthase activity. Furthermore, although radially migrating neurons were not NO responsive until they reached the cortical plate, NO exposure revealed an additional population of tangentially migrating presumptive interneurons from the ganglionic eminences with the capacity to produce cGMP. These results provide a new level of understanding of the stage and cell type specific regulation of the NO/cGMP pathway during embryonic development.

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Distribution of nitric oxide synthase and nitric oxide-receptive, cyclic GMP-producing structures in the rat brain

Cited by 138 publications

References 91 publications

Immunohistochemical assessment of cyclic guanosine monophosphate (cGMP) and soluble guanylate cyclase (sGC) within the rostral ventrolateral medulla

Immunohistochemical assessment of cyclic guanosine monophosphate (cGMP) and soluble guanylate cyclase (sGC) within the rostral ventrolateral medulla

Nitric oxide-active compounds modulate the intensity of glutamate-evoked responses in the globus pallidus of the rat

Developmental appearance of cyclic guanosine monophosphate (cGMP) production and nitric oxide responsiveness in embryonic mouse cortex and striatum

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