Nitroglycerin enhances cGMP expression in specific neuronal and cerebrovascular structures of the rat brain

Tassorelli, Cristina; Blandini, Fabio; Greco, Rosaria; Nappi, Giuseppe

doi:10.1016/j.jchemneu.2003.08.006

Cited by 32 publications

(18 citation statements)

References 44 publications

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“…Since GTN easily passes the BBB, it has also been suggested that GTN-induced headache could be due to liberation of NO in the CNS, e.g. in the second-order neurons in the trigeminal nucleus caudalis (14,23). Given that SNP cannot pass the BBB but liberates NO in the bloodstream, the present results suggest that headache was induced at the level of extra-or intracerebral blood vessels.…”

Section: Discussionsupporting

confidence: 48%

The effect of sodium nitroprusside on cerebral hemodynamics and headache in healthy subjects

et al. 2013

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Investigation: Sodium nitroprusside (SNP) is a powerful vasodilatory agent that, similarly to glyceryl trinitrate (GTN), releases nitric oxide (NO) but in contrast does not pass the blood-brain barrier. Nevertheless, it has already been used in animal models without any knowledge of its headache-inducing potential. We hypothesized that SNP would induce headache and vasodilation of cephalic and radial but not cerebral arteries. Methods: Five healthy volunteers received intravenous infusions of SNP in a non-randomized dose-titration (1-5 mg/kg/min) study. We recorded headache intensity (verbal rating scale from 0 to 10), velocity in the middle cerebral artery (V MCA ), and diameters of the superficial temporal artery (STA) and radial artery (RA). Results: All participants reported a dose-related headache (median peak ¼ 2.5, range 0-3). SNP dilated the STA and RA, caused a marked increase of heart rate and a decrease of mean arterial pressure (MAP) and partial pressure of end-tidal carbon dioxide (P et CO 2 ). We found that SNP decreased the velocity of the V MCA , but this was canceled by a decrease of cerebral blood flow (CBF) due to hypocapnia.Conclusion: The present study shows that SNP is a headache-inducing agent with close similarities to headaches induced by GTN and probably without effect on intracerebral arteries.

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Section: Discussionsupporting

confidence: 48%

The effect of sodium nitroprusside on cerebral hemodynamics and headache in healthy subjects

et al. 2013

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“…However, these drugs do not usually cause ataxia or amnesia by disturbing synapses. This may appear to contradict our model, but it can be explained by the fact that systemic administration of an NO donor does not increase [NO] in neurons sufficiently to activate their intracellular signaling cascades, even at a dose that considerably affects hemodynamics [181] .…”

Section: B Various States Of Memory In the Model And Corresponding Econtrasting

confidence: 60%

Systems Biology Perspectives on Cerebellar Long-Term Depression

Ogasawara

Doi

Kawato³

2008

Neurosignals

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Long-term depression (LTD) at parallel fiber-Purkinje cell (PF-PC) synapses is thought to be the cellular correlate of cerebellar associative learning. The molecular processes are, in brief, phosphorylation of AMPA-type glutamate receptors (AMPARs) and their subsequent removal from the surface of the PF-PC synapse. In order to elucidate the fundamental mechanisms for cerebellar LTD and further the understanding of its computational role, we have investigated its systems biology and proposed the following hypotheses, some of which have already been experimentally verified: (1) due to the mitogen-activated protein kinase (MAPK)-protein kinase C (PKC) positive feedback loop, phosphorylation of AMPARs is an all-or-none event; (2) the inositol 1,4,5-triphosphate receptor detects concurrent PF and climbing fiber inputs, forming the cellular basis for associative learning, and (3) the local concentration of nitric oxide in the PC dendrite reflects the relevance of a given context, enabling context-dependent selection of learning modules within the cerebellum. In this review, we first introduce theoretical studies on cerebellar LTD, mainly focusing on our own published work, followed by a discussion of the effects of stochasticity, localization, diffusion, and scaffolding. Neurons embody two features that are apparently contradictory, yet necessary for synaptic memory: stability and plasticity. We will also present models for explaining how neurons solve this dilemma. In the final section, we propose a conceptual model in which a cascade of excitable dynamics with different time scales, i.e., Ca²⁺-induced Ca²⁺ release, the MAPK-PKC positive feedback loop, and protein kinase Mζ (PKMζ)-induced PKMζ synthesis, provides a mechanism for stable memory that is still amenable to modifications.

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“…Additionally, the increase of blood flow in the cortex may be also a consequence of neuronal activity. Cerebral circulation indeed may be influenced by neuronal activity via pathways extrinsic and intrinsic to the central nervous system (40,41). NO is a likely mediator of the coupling between neuronal activation and CBF (40)(41)(42)(43)(44).…”

Section: Discussionmentioning

confidence: 99%

Temporal profile of vascular changes induced by systemic nitroglycerin in the meningeal and cortical districts

et al. 2010

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Nitroglycerin enhances cGMP expression in specific neuronal and cerebrovascular structures of the rat brain

Cited by 32 publications

References 44 publications

The effect of sodium nitroprusside on cerebral hemodynamics and headache in healthy subjects

The effect of sodium nitroprusside on cerebral hemodynamics and headache in healthy subjects

Systems Biology Perspectives on Cerebellar Long-Term Depression

Temporal profile of vascular changes induced by systemic nitroglycerin in the meningeal and cortical districts

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