The role of GABAergic receptors in acute, subacute, and withdrawal syndrome on pain and seizure thresholds in mice: A connection to mitochondrial function and oxidative stress in the brain
Roghayeh Jahani, Paria Pourbahram, Mohammad Seyedabadi, Fatemeh Nasiri, Hamidreza Mohammadi

TL;DR
This study shows that baclofen, a GABA receptor agonist, increases seizure thresholds and reduces oxidative damage in mice brains, especially with long-term use.
Contribution
The study reveals the dose- and time-dependent effects of baclofen on seizure thresholds and mitochondrial oxidative stress in mice.
Findings
Baclofen increased seizure thresholds in both short- and long-term exposure.
Long-term baclofen improved mitochondrial oxidative damage by reducing ROS and MDA levels.
Baclofen increased pain thresholds through a muscle relaxant effect.
Abstract
One of the most serious neurological disorders is epilepsy. This study aimed to investigate the effects of baclofen, a GABA receptor agonist, on pain and seizure thresholds, as well as on oxidative damage in brain mitochondrial membranes of mice. Sixty male mice were divided into 10 groups. Control, baclofen (1, 5, and 10 mg/kg) with short-term exposure (1 day), long-term exposure (7 days), and withdrawal syndrome (eight days). The withdrawal syndrome was evaluated one day after the last dose of the drug. Hotplate and tail-flick tests were performed to assess pain threshold, and the rotarod was used to assess motor coordination. The seizure threshold and oxidative stress markers, including reactive oxygen species (ROS), malondialdehyde (MDA), protein carbonyl (PC), glutathione (GSH), and the MTT assay, were investigated. The results showed that baclofen (10 mg/kg) in short-term and all…
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Taxonomy
TopicsNeuroscience and Neuropharmacology Research · Pain Mechanisms and Treatments · Botulinum Toxin and Related Neurological Disorders
