This study investigates the temporal dynamics of ictal electrical activity induced by injection of the GABA(A) receptor antagonist bicuculline, and the glutamate agonist kainic acid, into the CA3 area of hippocampus. Experiments were conducted in freely moving adult Wistar rats implanted with microelectrodes in multiple brain areas. Wide-band electrical activity (0.1-3000 Hz) was recorded, and the latency of seizure onset as well as the pattern of electrical activity were investigated for each drug. The latencies between injection and the occurrence of first epileptiform events were 3.93 +/- 2.76 (+/-STD) min for bicuculline and 6.37 +/- 7.66 min for kainic acid, suggesting the existence of powerful seizure-suppressive mechanisms in the brain. Bicuculline evoked high-amplitude rhythmic epileptiform events at the site of injection which resembled interictal EEG spikes and rapidly propagated to adjacent and remote brain areas. Kainic acid evoked a completely different pattern with a gradual increase in the amplitude of 30-80 Hz activity. Whereas there was strong temporal correlation between EEG events at the site of bicuculline injection and discharges in distant areas, much less correlation was seen with kainic acid injection. Both patterns were followed by generalized ictal EEG discharges and behavioral seizures. Our results illustrate that the same area of the brain can trigger seizures with different electrographic patterns. The knowledge of the network mechanisms underlying these two distinct electrographic patterns might be helpful in designing differential strategies for preventing seizure occurrence.
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http://dx.doi.org/10.1523/JNEUROSCI.5309-08.2009 | DOI Listing |
Front Pharmacol
January 2025
Department of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Background: For patients with epilepsy, antiseizure medication remains the primary treatment; however, it is ineffective in approximately 30% of cases. These patients experience progressive neuronal damage and poor outcomes. Therefore, there is an urgent need for disease-modifying therapy (DMT) that targets the pathogenesis of epilepsy.
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January 2025
Department of Mechanical Engineering, University of Rochester, Rochester, United States.
We hypothesized that active outer hair cells drive cochlear fluid circulation. The hypothesis was tested by delivering the neurotoxin, kainic acid, to the intact round window of young gerbil cochleae while monitoring auditory responses in the cochlear nucleus. Sounds presented at a modest level significantly expedited kainic acid delivery.
View Article and Find Full Text PDFF1000Res
January 2025
Faculty of Teaching and Education Sciences, Islamic University of Malang, Malang, East Java, Indonesia.
Background: Neurodegeneration due to neurotoxicity is one of the phenomena in temporal lobe epilepsy. Experimentally, hippocampal excitotoxicity process can occur due to kainic acid exposure, especially in the CA3 area. Neuronal death, astrocyte reactivity and increased calcium also occur in hippocampal excitotoxicity, but few studies have investigated immediate effect after kainic acid exposure.
View Article and Find Full Text PDFiScience
January 2025
School of Biosystems and Biomedical Sciences, College of Health Sciences, Korea University, Seoul 02841, Republic of Korea.
TWIK-1 belongs to the two-pore domain K (K2P) channel family, which plays an essential role in the background K conductance of cells. Despite the development of exon 2-deleted knockout (KO) mice, the physiological role of TWIK-1 has remained largely unknown. Here, we observed that the exon 2-deleted KO mice expressed an internally deleted TWIK-1 (TWIK-1 ΔEx2) protein, which unexpectedly acts as a functional K channel.
View Article and Find Full Text PDFActa Pharmacol Sin
January 2025
Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Medical Science, Tyrosine Peptide Multiuse Research Group, Anti-aging Bio Cell Factory Regional Leading Research Center, Gyeongsang National University, Jinju, Gyeongnam, Republic of Korea.
Glutamine synthetase (GS) plays a crucial role in the homeostasis of the glutamate-glutamine cycle in the brain. Hypoactive GS causes depressive behaviors. Under chronic stress, GS has no change in expression, but its activity is decreased due to nitration of tyrosine (Tyr).
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