Research reportChronic and single administration of pentylenetetrazol modifies benzodiazepine receptor-binding: an autoradiographic study
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The threshold of pentylenetetrazole-induced convulsive seizures, but not that of nonconvulsive seizures, is controlled by the nitric oxide levels in murine brains
2013, Experimental NeurologyCitation Excerpt :This animal model is well known for studying primary generalized epilepsy (Löscher et al., 1991); however, the pathophysiological mechanisms of PTZ remain unknown. Generally, PTZ-induced convulsive seizures are caused by the enhancement of glutamatergic neuronal activity by antagonism of γ-aminobutyric acidA receptors (GABAAR) in the brain (Psarropoulou et al., 1994; Rocha et al., 1996). Neuron-derived nitric oxide (NO) synthesized from l-arginine by neuronal NO synthase (nNOS) in the brain is considered to be both a neurotransmitter and a neuromodulator, and the involvement of NO in epileptic disorders has been demonstrated in experiments using systemic injections of NOS inhibitors (Banach et al., 2011; Snyder and Bredt., 1991).
Effects of neuropeptide S on seizures and oxidative damage induced by pentylenetetrazole in mice
2012, Pharmacology Biochemistry and BehaviorCitation Excerpt :In fact, NPS facilitated the effects of PTZ by increasing the duration of seizures and DNA damage in the hippocampus, and, in contrast, NPS attenuated the effects of PTZ-induced oxidative damage to proteins and lipids in the hippocampus and cerebral cortex. Studies have suggested that the GABAergic (Rocha et al., 1996), but also there is an involvement of glutamatergic (Jensen et al., 1997), and adenosinergic systems (Pagonopoulou and Angelatou, 1998) are involved in PTZ-induced seizures. Additionally, alterations in NMDA, kainite, A1 receptors and benzodiazepine binding site densities were detected in the brain of mice repeatedly treated with PTZ (Cremer et al., 2009).
Convulsant agent pentylenetetrazol does not alter the structural and dynamical properties of dipalmitoylphosphatidylcholine model membranes
2011, Journal of Pharmaceutical and Biomedical AnalysisCitation Excerpt :The widely accepted mechanism is that PTZ displays its activity by binding to the picrotoxin binding site at GABAA receptor complex [12]. Accordingly, some binding studies revealed that PTZ also affects the function of benzodiazepine receptor [13], GABAA receptor [14], both ionotropic and metabotropic glutamate receptors [15]. Moreover, it was also shown that PTZ is not effective when injected into the neuron [7].
Diphenyl diselenide and 2,3-dimercaptopropanol increase the PTZ-induced chemical seizure and mortality in mice
2006, Brain Research BulletinInfluence of adenosine receptor agonists on benzodiazepine withdrawal signs in mice
2005, European Journal of Pharmacology