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  Intranasal guanosine administration presents a wide therapeutic time window to reduce brain damage induced by permanent ischemia in rats.

Ramos, D. B., Muller, G. C., Rocha, G. B. M., Dellavia, G. H., Almeida, R. F., Pettenuzzo, L. F., et al. (2016). Intranasal guanosine administration presents a wide therapeutic time window to reduce brain damage induced by permanent ischemia in rats. Purinergic Signalling, 12(1), 149-159. doi:10.1007/s11302-015-9489-9.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0029-D32B-B Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002D-0B9A-6
Genre: Journal Article

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 Creators:
Ramos, D. B., Author
Muller, G. C., Author
Rocha, G. B. M., Author
Dellavia, G. H., Author
Almeida, R. F., Author
Pettenuzzo, L. F., Author
Loureiro, S. O., Author
Hansel, G., Author
Horn, A. C. M., Author
Souza, D. O., Author
Ganzella, M.1, Author              
Affiliations:
1Department of Neurobiology, MPI for Biophysical Chemistry, Max Planck Society, ou_578595              

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Free keywords: Guanosine; Intranasal; Purines; Ischemia; Neuroprotection
 Abstract: In addition to its intracellular roles, the nucleoside guanosine (GUO) also has extracellular effects that identify it as a putative neuromodulator signaling molecule in the central nervous system. Indeed, GUO can modulate glutamatergic neurotransmission, and it can promote neuroprotective effects in animal models involving glutamate neurotoxicity, which is the case in brain ischemia. In the present study, we aimed to investigate a new in vivo GUO administration route (intranasal, IN) to determine putative improvement of GUO neuroprotective effects against an experimental model of permanent focal cerebral ischemia. Initially, we demonstrated that IN [H-3] GUO administration reached the brain in a dose-dependent and saturable pattern in as few as 5 min, presenting a higher cerebrospinal GUO level compared with systemic administration. IN GUO treatment started immediately or even 3 h after ischemia onset prevented behavior impairment. The behavior recovery was not correlated to decreased brain infarct volume, but it was correlated to reduced mitochondrial dysfunction in the penumbra area. Therefore, we showed that the IN route is an efficient way to promptly deliver GUO to the CNS and that IN GUO treatment prevented behavioral and brain impairment caused by ischemia in a therapeutically wide time window.

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Language(s): eng - English
 Dates: 2015-12-232016-03
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
 Identifiers: DOI: 10.1007/s11302-015-9489-9
 Degree: -

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Title: Purinergic Signalling
Source Genre: Journal
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Pages: - Volume / Issue: 12 (1) Sequence Number: - Start / End Page: 149 - 159 Identifier: -