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Updated: May 23, 2026
Pentylenetetrazole-Induced Kindling Mouse Model
Published on: June 12, 2018
Decreased GABABR expression and increased neuronal cell death in developing rat brain after PTZ-induced seizure
Muhammad Imran Naseer1, Ikram Ullah, Mohammed H Al-Qahtani
1Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia. mimrannaseer@yahoo.com
Insights
Pentylenetetrazol (PTZ) seizures reduce GABAB receptor expression and cause brain cell death in developing rats. Baclofen treatment reversed these negative effects, highlighting GABAB receptor
Area of Science:
- Neuroscience
- Pharmacology
- Developmental Biology
Background:
- GABAB receptors play a crucial role in regulating neuronal excitability.
- Seizures can disrupt normal brain development and function.
- Understanding the impact of seizures on GABAB receptor expression is vital for developing therapeutic strategies.
Purpose of the Study:
- To investigate the effect of pentylenetetrazol (PTZ)-induced seizures on GABAB receptor expression in the developing rat brain.
- To assess the neurodegenerative consequences of PTZ-induced seizures, specifically focusing on apoptosis.
- To evaluate the potential neuroprotective role of baclofen, a GABAB receptor agonist, against PTZ-induced effects.
Main Methods:
- Developing rats (5 weeks old) were administered PTZ (40 mg/kg) for 4 days to induce seizures.
- Baclofen (GABAB agonist) and phaclofen (GABAB antagonist) were co-administered with PTZ.
- Western blot analysis was employed to quantify GABAB receptor protein levels.
- Confocal microscopy was used to detect apoptotic neurodegeneration via caspase-3 and propidium iodide staining.
- Electroencephalography (EEG) confirmed seizure activity.
Main Results:
- PTZ-induced seizures significantly decreased GABAB receptor expression in the cortex and hippocampus.
- PTZ administration led to increased neuronal apoptosis, evidenced by caspase-3 release and PI staining.
- Baclofen treatment counteracted the PTZ-induced decrease in GABAB receptor expression.
- Baclofen mitigated PTZ-induced neuronal apoptosis.
Conclusions:
- PTZ-induced seizures negatively impact GABAB receptor expression and promote neurodegeneration in the developing rat brain.
- GABAB receptor signaling is critical for protecting against seizure-induced neuronal damage during development.
- Baclofen demonstrates therapeutic potential in reversing the detrimental effects of PTZ-induced seizures on GABAB receptor expression and neuronal survival.
Abstract:
The objective of this study was to evaluate the PTZ-induced seizures effects on GABAB receptor (R) expression and to observe its neurodegenerative effect in hippocampal part of developing rat brain. In the present study, high dose of pentylenetetrazol (PTZ 40 mg/kg) was injected in developing rats of age 5 weeks having average weight of 60-65 g for 4 days. Further, baclofen (B 3 mg/kg i.p) agonist and phaclofen (P 30 μg/rat) antagonist of GABABR were injected along with PTZ. Western blot analysis was used to elucidate expression of GABABR protein upon PTZ, baclofen and phaclofen exposure in the developing rat brain. Furthermore, PTZ-induced apoptotic neurodegeneration was also observed through the release of caspase-3 antibody and propidium iodide (PI) staining using confocal microscopy. Seizure was confirmed using electroencephalography (EEG) data obtained from the Laxtha EEG-monitoring device in the EEG recording room and EEG was monitored 5-15 min after PTZ injection. The results of the present study showed that PTZ-induced seizure significantly decreased GABABR expression and induced neuronal apoptosis in cortical and hippocampal part of brain. While, baclofen reverse the effect of PTZ by increasing the expression of GABABR as compared to the PTZ- , PTZ plus B- and PTZ plus P-treated groups. Our findings indicated that PTZ-induced seizure showed not only decrease in GABABR expression but also cause neuronal apoptosis in the developing rat brain.
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