PreprintArticleVersion 1This version is not peer-reviewed
Seizures Triggered by Systemic Administration of 4-Aminopyridine Lead to Acute Brain Glucose Hypometabolism in Rats, as Assessed by PET Molecular Imaging
Version 1
: Received: 24 October 2024 / Approved: 25 October 2024 / Online: 25 October 2024 (11:51:20 CEST)
How to cite:
Gómez-Oliver, F.; Fernández de la Rosa, R.; Brackhan, M.; Bascuñana, P.; Pozo, M. A.; García-García, L. Seizures Triggered by Systemic Administration of 4-Aminopyridine Lead to Acute Brain Glucose Hypometabolism in Rats, as Assessed by PET Molecular Imaging. Preprints2024, 2024102027. https://doi.org/10.20944/preprints202410.2027.v1
Gómez-Oliver, F.; Fernández de la Rosa, R.; Brackhan, M.; Bascuñana, P.; Pozo, M. A.; García-García, L. Seizures Triggered by Systemic Administration of 4-Aminopyridine Lead to Acute Brain Glucose Hypometabolism in Rats, as Assessed by PET Molecular Imaging. Preprints 2024, 2024102027. https://doi.org/10.20944/preprints202410.2027.v1
Gómez-Oliver, F.; Fernández de la Rosa, R.; Brackhan, M.; Bascuñana, P.; Pozo, M. A.; García-García, L. Seizures Triggered by Systemic Administration of 4-Aminopyridine Lead to Acute Brain Glucose Hypometabolism in Rats, as Assessed by PET Molecular Imaging. Preprints2024, 2024102027. https://doi.org/10.20944/preprints202410.2027.v1
APA Style
Gómez-Oliver, F., Fernández de la Rosa, R., Brackhan, M., Bascuñana, P., Pozo, M. A., & García-García, L. (2024). Seizures Triggered by Systemic Administration of 4-Aminopyridine Lead to Acute Brain Glucose Hypometabolism in Rats, as Assessed by PET Molecular Imaging. Preprints. https://doi.org/10.20944/preprints202410.2027.v1
Chicago/Turabian Style
Gómez-Oliver, F., Miguel Angel Pozo and Luis García-García. 2024 "Seizures Triggered by Systemic Administration of 4-Aminopyridine Lead to Acute Brain Glucose Hypometabolism in Rats, as Assessed by PET Molecular Imaging" Preprints. https://doi.org/10.20944/preprints202410.2027.v1
Abstract
4-aminopyridine (4-AP) is a non-selective blocker of voltage-dependent K+ channels used to im-prove walking in multiple sclerosis patients, and it may be useful in the treatment of cerebellar diseases. In animal models, 4-AP is used as a convulsant agent. Intrahippocampal 4-AP induces acute local glucose hypermetabolism and significant brain damage, while i.p. administration causes less neuronal damage. This study aimed to investigate the effects of a single i.p. admin-istration of 4-AP on acute brain glucose metabolism and to assess the short-term effects on neu-ronal viability and signs of neuroinflammation. We evaluated 4-AP-induced acute changes in brain glucose metabolism by [18F]FDG PET neuroimaging evaluated by standard volumes of interest (VOIs) and voxel-based (SPM) analyses. We show that 4-AP induces acute generalized brain glucose hypometabolism, except in the cerebellum, area that was significantly more resilient to this effect. Accordingly, to the appropriate neurohistochemical assays, 4-AP induced hippocampal astrocyte reactivity 3 days after the insult, without changes in signs of neuronal integrity or micro-glia-mediated neuroinflammation. Thus, acute brain glucose metabolic and short-term neuroin-flammatory profiles in response to 4-AP i.p. clearly differ from that reported for intracerebral administration. Our results also suggest cerebellar metabolism as a potential marker of the effects of 4-AP.
Medicine and Pharmacology, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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