Abstract
Temporal lobe epilepsy (TLE), the most common type of focal epilepsy, affects learning and memory; these effects are thought to emerge from changes in synaptic plasticity. Levetiracetam (LEV) is a widely used antiepileptic drug that is also associated with the reversal of cognitive dysfunction. The long-lasting effect of LEV treatment and its participation in synaptic plasticity have not been explored in early chronic epilepsy. Therefore, through the measurement of evoked field potentials, this study aimed to comprehensively identify the alterations in the excitability and the short-term (depression/facilitation) and long-term synaptic plasticity (long-term potentiation, LTP) of the dentate gyrus of the hippocampus in a lithium–pilocarpine rat model of TLE, as well as their possible restoration by LEV (1 week; 300 mg/kg/day). TLE increased the population spike (PS) amplitude (input/output curve); interestingly, LEV treatment partially reduced this hyperexcitability. Furthermore, TLE augmented synaptic depression, suppressed paired-pulse facilitation, and reduced PS-LTP; however, LEV did not alleviate such alterations. Conversely, the excitatory postsynaptic potential (EPSP)-LTP of TLE rats was comparable to that of control rats and was decreased by LEV. LEV caused a long-lasting attenuation of basal hyperexcitability but did not restore impaired synaptic plasticity in the early chronic phase of TLE.
Highlights
Epilepsy is one of the most common and widespread neurological disorders, affecting more than 65 million people around the world [1]
Our results showed that in the dentate gyrus (DG) of the hippocampus of early chronic EPI rats, the excitatory postsynaptic potential (EPSP)-long-term potentiation (LTP) slopes were comparable to nonepileptic animals; there was a decrease in population spike (PS)-LTP amplitude
Our results showed that Temporal lobe epilepsy (TLE) provoked profound changes in the basal excitability and synaptic plasticity of the DG and provide evidence that LEV has a long-lasting effect, reducing the basal excitability of granule cells in TLE rats
Summary
Epilepsy is one of the most common and widespread neurological disorders, affecting more than 65 million people around the world [1]. Brain Sci. 2020, 10, 634 structures in the temporal lobe, is the most common form of focal epilepsy [3,4] and accounts for approximately 60% of all epilepsy cases in adults [5]. TLE is the most common drug-resistant focal epilepsy disorder [6,7], and seizures are not controlled by medical treatment in up to 30% of these patients [8]. Studies are needed to investigate new drug targets for the treatment of epilepsy and its comorbidities. Another concerning aspect of TLE is its cognitive sequelae due to specific deficits in temporal lobe-related functions [9]. The underlying mechanisms of such impairments are not yet well understood
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