Abstract
Clinically, temporal lobe epilepsy (TLE) is the most prevalent type of partial epilepsy and often accompanied by various comorbidities. The present study aimed to evaluate the effects of chronic treatment with the antiepileptic drug (AED) lacosamide (LCM) on spontaneous motor seizures (SMS), behavioral comorbidities, oxidative stress, neuroinflammation, and neuronal damage in a model of TLE. Vehicle/LCM treatment (30 mg/kg, p.o.) was administered 3 h after the pilocarpine-induced status epilepticus (SE) and continued for up to 12 weeks in Wistar rats. Our study showed that LCM attenuated the number of SMS and corrected comorbid to epilepsy impaired motor activity, anxiety, memory, and alleviated depressive-like responses measured in the elevated plus maze, object recognition test, radial arm maze test, and sucrose preference test, respectively. This AED suppressed oxidative stress through increased superoxide dismutase activity and glutathione levels, and alleviated catalase activity and lipid peroxidation in the hippocampus. Lacosamide treatment after SE mitigated the increased levels of IL-1β and TNF-α in the hippocampus and exerted strong neuroprotection both in the dorsal and ventral hippocampus, basolateral amygdala, and partially in the piriform cortex. Our results suggest that the antioxidant, anti-inflammatory, and neuroprotective activity of LCM is an important prerequisite for its anticonvulsant and beneficial effects on SE-induced behavioral comorbidities.
Highlights
Epilepsy is one of the most common neurological disorders, widespread all over the world, and affecting more than 50 million people of different ages, sex, race, and social class [1]
The hippocampus has a pivotal role in learning, memory, and mood control, and since it is highly susceptible to injury, these functions can be impaired in patients with Temporal lobe epilepsy (TLE) [10]
We propose that the antiepileptic drug (AED) LCM exerts anticonvulsant and beneficial effects on behavioral comorbidities in epilepsy via ameliorating activity against oxidative stress and neuronal loss in the brain
Summary
Epilepsy is one of the most common neurological disorders, widespread all over the world, and affecting more than 50 million people of different ages, sex, race, and social class [1]. Stroke, intracranial infections, brain tumors, or preceding status epilepticus (SE) are factors that can induce functional and chemical changes in the brain and development of epilepsy [2,3,4,5]. Due to alterations occurring during epileptogenesis, patients tend to develop various comorbidities such as cognitive and psychiatric disorders, which have a detrimental impact on their quality of life [6]. The pathological changes that are triggered in the first hours after SE can cause initial damage and severe widespread neuronal loss in different brain areas, including the hippocampus, endopiriform nucleus, and piriform cortex [9]. The hippocampus has a pivotal role in learning, memory, and mood control, and since it is highly susceptible to injury, these functions can be impaired in patients with TLE [10]
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