Artigo Revisado por pares

Effects of Short-Term Random Noise Electrical Stimulation on Dissociated Pyramidal Neurons from the Cerebral Cortex

2019; Elsevier BV; Volume: 404; Linguagem: Inglês

10.1016/j.neuroscience.2019.01.035

ISSN

1873-7544

Autores

Leonardo Remedios, Pedro Mabil, Jorge Flores‐Hernández, Oswaldo Torres‐Ramírez, Nayeli Huidobro, Gerardo Castro, L. Cervantes, Jesus A. Tapia, Braniff de la Torre Valdovinos, Elı́as Manjarrez,

Tópico(s)

Advanced Memory and Neural Computing

Resumo

Transcranial random noise electrical stimulation (tRNS) of the human brain is a non-invasive technique that can be employed to increase the excitability of the cerebral cortex; however, the physiological mechanisms remain unclear. Here we report for the first time the effects of short-term (250 ms) random noise electrical stimulation (RNS) on in-vitro acutely-isolated brain pyramidal neurons from the somatosensory and auditory cerebral cortex. We analyzed the correlation between the peak amplitude of the Na+ current and its latency for different levels of RNS. We found three groups of neurons. The first group exhibited a positive correlation, the second, a negative correlation, and the third group of neurons did not exhibit correlation. In the first group, both the peak amplitude of a TTX-sensitive Na+ current and its inverse of latency followed similar inverted U-like functions relative to the electrical RNS level. In this group, the RNS levels in which the maximal values of the inverted U-like functions occurred were the same. In the second group, the maximal values of the inverted U-like functions occurred at different levels. In the third group, only the peak amplitude of the Na+ current exhibited a clear inverted U-like function, but the inverse of the latency versus the electrical RNS, did not exhibit a clear inverted U-like function. A Hodgkin-Huxley neuron model reproduces our experimental results and shows that the observed behavior in the Na+ current could be due to the impact of RNS on the kinetics of activation and inactivation of the Na+ channels.

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