Potassium diffusive coupling in neural networks

Abstract

Conventional neural networks are characterized by many neurons coupled together through synapses. The activity, synchronization, plasticity and excitability of the network are then controlled by its synaptic connectivity. Neurons are surrounded by an extracellular space whereby fluctuations in specific ionic concentration can modulate neuronal excitability. Extracellular concentrations of potassium ([K þ ] o ) can generate neuronal hyperexcitability. Yet, after many years of research, it is still unknown whether an elevation of potassium is the cause or the result of the generation, propagation and synchronization of epileptiform activity. An elevation of potassium in neural tissue can be characterized by dispersion (global elevation of potassium) and lateral diffusion (local spatial gradients). Both experimental and computational studies have shown that lateral diffusion is involved in the generation and the propagation of neural activity in diffusively coupled networks. Therefore, diffusion-based coupling by potassium can play an important role in neural networks and it is reviewed in four sections. Section 2 shows that potassium diffusion is responsible for the synchronization of activity across a mechanical cut in the tissue. A computer model of diffusive coupling shows that potassium diffusion can mediate communication between cells and generate abnormal and/or periodic activity in small ( §3) and in large networks of cells ( §4). Finally, in §5, a study of the role of extracellular potassium in the propagation of axonal signals shows that elevated potassium concentration can block the propagation of neural activity in axonal pathways. Taken together, these results indicate that potassium accumulation and diffusion can interfere with normal activity and generate abnormal activity in neural networks.

The influence of potassium concentration on epileptic seizures in a coupled neuronal model in the hippocampus

“…concentration in the ECS-NA could induce epileptic seizures? A number of results from biological experiments have answered this question (Ohno et al 2015;Cornog et al 1967; Traynelis and Dingledine 1988;Durand and Jensen 2010;Park and Durand 2006). In 2015, Ohno found that down-regulation or dysfunction of K ?…”

“…Previous studies have found that the K ? lateral diffusion between two neurons is a significant factor for non-synaptic epileptogenesis in a low-calcium in vitro model (Yaari et al 1986;Park and Durand 2006;Durand and Jensen 2010). Chemical synapses are abundant in the central nervous system.…”

“…lateral diffusion could lead to the generation of non-synaptic epilepsy in zero-Ca 2? in excitatory neuronal networks in the CA1 area (Durand and Jensen 2010;Park and Durand 2006). Therefore, studying the relations between these factors that affect the K ?…”

“…in the ECS-NA, and the K ? lateral diffusion between neurons and cotransporters (Kager et al 2000(Kager et al , 2007Larsen et al 2014;Øyehaug et al 2012;Yina et al 2014b;Østby 2009;Durand and Jensen 2010). Which of these factors that influences the K ?…”

The complexity of roles of P-glycoprotein in refractory epilepsy: Pharmacoresistance, epileptogenesis, SUDEP and relapsing marker after surgical treatment

“…Its overexpression leads to decreased plasma membrane electrical potential by increasing Cl -permeability and thus decreasing the dominance of membrane potential by K + conductance, and leads to altered pHi regulation [47,48]. So, brain P-gp overexpression could contribute to crucial factors detected in several types of epilepsy such as the intracellular acidosis associated with altered Na + /H + exchange [55], enhanced extracellular concentration of potassium [56], and particularly in the increased membrane depolarization [57].…”