ArticleNeuroscience bulletin2013
BDNF-TrkB signaling pathway is involved in pentylenetetrazole-evoked progression of epileptiform activity in hippocampal neurons in anesthetized rats.
Article in Neuroscience bulletin, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- From gastric to neuroprotection: pantoprazole mitigates epilepsy via TrkB/BDNF and KCC2 modulation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- BDNF-TrkB/proBDNF-p75Scientific reports · 2023Article
- Double-Edged Mossy Cells in Temporal Lobe Epilepsy: Evil in the Early Stage Through a BDNF-Dependent Strengthening Dentate Gyrus Circuit.Neuroscience bulletin · 2023Article
- Prevention of brain damage after traumatic brain injury by pharmacological enhancement of KCNQ (Kv7, "M-type") KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- A Mouse Model of Repetitive Blast Traumatic Brain Injury Reveals Post-Trauma Seizures and Increased Neuronal Excitability.Journal of neurotrauma · 2020Article
- Myricetin attenuates the severity of seizures and neuroapoptosis in pentylenetetrazole kindled mice by regulating the of BDNF-TrkB signaling pathway and modulating matrix metalloproteinase-9 and GABAExperimental and therapeutic medicine · 2019Article
- Effect of Nobiletin on Experimental Model of Epilepsy.Translational neuroscience · 2018Article
- M-Calpain Activation Facilitates Seizure Induced KCC2 Down Regulation.Frontiers in molecular neuroscience · 2018Article
- Garcinol Upregulates GABAA and GAD65 Expression, Modulates BDNF-TrkB Pathway to Reduce Seizures in Pentylenetetrazole (PTZ)-Induced Epilepsy.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Methionine increases BDNF DNA methylation and improves memory in epilepsy.Annals of clinical and translational neurology · 2015Article
- Activation of extrasynaptic GABA(A) receptors inhibits cyclothiazide-induced epileptiform activity in hippocampal CA1 neurons.Neuroscience bulletin · 2014Article
- Antiseizure effects of TrkB kinase inhibition.Epilepsia · 2014Article
- Downregulated GABA and BDNF-TrkB pathway in chronic cyclothiazide seizure model.Neural plasticity · 2014Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pentylenetetrazole (PTZ) is a widely-used convulsant used in studies of epilepsy; its subcutaneous injection generates an animal model with stable seizures. Here, we compared the ability of PTZ via the intravenous and subcutaneous routes to evoke progressive epileptiform activity in the hippocampal CA1 neurons of anesthetized rats. The involvement of the BDNF-TrkB pathway was then investigated. When PTZ was given intravenously, it induced epileptiform bursting activity at a short latency in a dose-dependent manner. However, when PTZ was given subcutaneously, it induced a slowly-developing pattern of epileptogenesis; first, generating multiple population-spike peaks, then spontaneous interictal discharge-like spike, leading to the final ictal discharge-like, highly synchronized bursting fi ring in the CA1 pyramidal layer of the hippocampus. K252a, a TrkB receptor antagonist, when given by intracerebroventricular injection, significantly reduced the probability of multiple population spike peaks induced by subcutaneous injection of PTZ, delayed the latency of spontaneous spikes, and reduced the burst frequency. Our results indicate that PTZ induces a progressive change of neuronal epileptiform activity in the hippocampus, and the BDNF-TrkB signaling pathway is mainly involved in the early phases of epileptogenesis, but not the synchronized neuronal burst activity associated with epileptic seizure in the PTZ animal model. These results provide basic insights into the changing pattern of hippocampal neuronal activity during the development of the PTZ seizure model, and establish an in vivo seizure model useful for future electrophysiological studies of epilepsy.
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