Temporal lobe epilepsy and changes in the M current

Hugo Solís, Anatomy, Laboratory of Neurophysiology, Facultad de Medicina, Universidad Autónoma de México, Mexico City, Mexico
Estela López-Hernández, Anatomy, Laboratory of Neurophysiology, Facultad de Medicina, Universidad Autónoma de México, Mexico City, Mexico

Objective: Acquired alterations of ion channel function occur after status epilepticus (SE). Kv7 channels mediate a sustained outward current (IM) that exerts pivotal control over neuronal excitability. Here, we investigate if pilocarpine-induced SE alters M-channel activity by quantifying the IM. Methods: Hippocampal slices were prepared from adult rats after pilocarpine-induced SE, when the animal was showing 3–5 spontaneous recurrent seizures (SRS) a day. A group of untreated, age-matchedrats was used as the control group. Recordings were made using the whole-cell configuration of the patch clamp techniqueand current clamp mode to measure the membrane time constant. Results: The IM measured amplitude in CA1 neuronsfrom pilocarpine-SE rats was significantly reduced compared to the control group (control, 208.72 ± 25.49 pA, n = 15; pilocarpine-SE, 49.28 ± 6.17 pA, n = 11; p < 0.05, Student’s t). The time constant was 27.7 ± 17.7 msec in the control group and48.9 ± 5.5 msec in the pilocarpine-SE group, and was significantly different (p < 0.05). Conclusions: In this study, wedemonstrated that the M-current amplitude is significantly reduced in CA1 pyramidal neurons after pilocarpine-SE. Considering the acute damage that SE induces, the silent interval between injury and the onset of spontaneous seizures, and thechronic epileptic state in which the M-current was measured, we can speculate about the lack of homeostatic regulation ofthe intrinsic properties of neuronal excitability.

Keywords: Hippocampus. M-current. Pilocarpine. Status epilepticus. Epileptogenesis.