Role of electrical interactions in synchronization of epileptiform bursts.
Four general mechanisms can hypothetically contribute to or mediate localized synchronization of neuronal activity: (a) recurrent excitatory chemical synapses, (b) electrotonic coupling via gap junctions, (c) electrical field effects (ephaptic interactions), and (d) changes in the concentration of extracellular ions (e.g., K+). It has generally been believed that synchronization of epileptiform bursts derives primarily, if not exclusively, from recurrent excitatory chemical synapses. Dual intracellular recordings from the CA3 area of the hippocampus have been used to demonstrate the existence of recurrent synaptic excitation, and computer simulations have provided a theoretical framework for the idea that relatively sparse interactions through recurrent excitatory chemical synapses can generate synchronized bursting after inhibitory pathways are blocked with convulsant agents. Additional experimental studies have supported the hypothesis that a model for seizure discharge, the penicillin-induced paroxysmal depolarization shift (PDS), is associated with a large increase in excitatory synaptic conductance. However, recent studies have suggested that electrical interactions are also likely to play an important role in spike synchronization during epileptic discharges. Several research groups have used in vitro preparations to show that afterdischarges and spontaneous bursts of population spikes (which represent synchronized action potentials) can occur after chemical synaptic transmission has been blocked in solutions containing low [Ca2+]. Although this result was first observed in the CA1 area, it has recently been confirmed in other regions of the hippocampus. These experiments indicate that mechanisms other than chemical synaptic transmission are capable of synchronizing action potentials in the hippocampus. In this chapter, two forms of electrical interaction that could mediate synchronization will be considered: (a) electrotonic coupling through gap junctions and (b) electrical field effects through extracellular space. Changes in the concentration of extracellular ions are another mechanism not involving chemical synapses. However, it seems unlikely that ionic changes act on the rapid time scale of electrical interactions, and their contribution is discussed elsewhere in this volume. We review evidence for the existence of electrotonic coupling and electrical field effects in the hippocampus and neocortex, and discuss their possible involvement in the synchronization of epileptiform events.(ABSTRACT TRUNCATED AT 400 WORDS)
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D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology; D004594:Electrophysiology / Q000379:methods; D004827:Epilepsy / Q000503:physiopathology*; D005110:Extracellular Space / Q000378:metabolism; D006624:Hippocampus / Q000503:physiopathology / Q000648:ultrastructure; D007365:Intercellular Junctions / Q000648:ultrastructure; D007477:Ions; D007546:Isoquinolines; D008959:Models, Neurological; D009433:Neural Inhibition; D009462:Neurology / Q000639:trends; D009994:Osmolar Concentration; D051381:Rats; D013569:Synapses / Q000502:physiology; D013997:Time Factors
D007477:Ions; D007546:Isoquinolines; C017475:lucifer yellow