Levetiracetam Reduced the Basal Excitability of the Dentate Gyrus without Restoring Impaired Synaptic Plasticity in Rats with Temporal Lobe Epilepsy

Brain Sciences

ClaudioM. T. Queiroz¹  SergioR. Zamudio²  Karla Sánchez-Huerta³  Guillermo González-H³  ItzelJatziri Contreras-García³  JulietaG. Mendoza-Torreblanca³  LuisRicardo Gallardo Gudiño⁴ 

[1] Brain Institute, Federal University of Rio Grande do Norte, Natal 59056-450, Brazil;Departamento de Fisiología, Instituto Politécnico Nacional, Escuela Nacional de Ciencias Biológicas, Ciudad de Mexico 04530, Mexico;Laboratorio de Neurociencias, Subdirección de Medicina Experimental, Instituto Nacional de Pediatría, Ciudad de Mexico 04530, Mexico;Servicio de Electromedicina, Instituto Nacional de Pediatría, Ciudad de Mexico 04530, Mexico;

关键词: inhibitory transmission;    synaptic plasticity;    temporal lobe epilepsy;    evoked field potentials;    levetiracetam;   

DOI  :  10.3390/brainsci10090634

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown