Pentylenetetrazole: A review.

Autor: Monteiro ÁB; Laboratory of Psychopharmacology, Institute of Drugs and Medicines Research, Federal University of Paraíba, Brazil., Alves AF; Laboratory of Psychopharmacology, Institute of Drugs and Medicines Research, Federal University of Paraíba, Brazil., Ribeiro Portela AC; Laboratory of Psychopharmacology, Institute of Drugs and Medicines Research, Federal University of Paraíba, Brazil., Oliveira Pires HF; Laboratory of Psychopharmacology, Institute of Drugs and Medicines Research, Federal University of Paraíba, Brazil., Pessoa de Melo M; Laboratory of Psychopharmacology, Institute of Drugs and Medicines Research, Federal University of Paraíba, Brazil., Medeiros Vilar Barbosa NM; Laboratory of Psychopharmacology, Institute of Drugs and Medicines Research, Federal University of Paraíba, Brazil., Bezerra Felipe CF; Laboratory of Psychopharmacology, Institute of Drugs and Medicines Research, Federal University of Paraíba, Brazil. Electronic address: cicero@dbm.ufpb.br.
Jazyk: angličtina
Zdroj: Neurochemistry international [Neurochem Int] 2024 Nov; Vol. 180, pp. 105841. Date of Electronic Publication: 2024 Aug 28.
DOI: 10.1016/j.neuint.2024.105841
Abstrakt: Pentylenetetrazole (PTZ), a tetrazole derivative, is commonly used as a chemical agent to induce neurological disorders and replicate the characteristics of human epileptic seizures in animal models. This review offers a comprehensive analysis of the behavioral, neurophysiological, and neurochemical changes induced by PTZ. The epileptogenic and neurotoxic mechanisms of PTZ are associated with an imbalance between the GABAergic and glutamatergic systems. At doses exceeding 60 mg/kg, PTZ exerts its epileptic effects by non-competitively antagonizing GABA A receptors and activating NMDA receptors, resulting in an increased influx of cations such as Na + and Ca 2+ . Additionally, PTZ promotes oxidative stress, microglial activation, and the synthesis of pro-inflammatory mediators, all of which are features characteristic of glutamatergic excitotoxicity. These mechanisms ultimately lead to epileptic seizures and neuronal cell death, which depend on the dosage and method of administration. The behavioral, electroencephalographic, and histological changes associated with PTZ further establish it as a valuable preclinical model for the study of epileptic seizures, owing to its simplicity, cost-effectiveness, and reproducibility.
Competing Interests: Declaration of competing interest The authors confirm that they have no conflicts of interest with respect to the work described in this manuscript.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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