Synaptic impairment induced by paroxysmal ionic conditions in neocortex.
Summary of "Synaptic impairment induced by paroxysmal ionic conditions in neocortex."
Purpose:â€‚ Seizures are associated with a reduction in extracellular Ca(2+) concentration ([Ca(2+) ](o) ) and an increase in extracellular K(+) concentration ([K(+) ](o) ). The long-range synchrony observed between distant electrodes during seizures is weak. We hypothesized that changes in extracellular ionic conditions during seizures are sufficient to alter synaptic neuronal responses and synchrony in the neocortex. Methods:â€‚ We obtained in vivo and in vitro electrophysiologic recordings combined with microstimulation from cat/rat neocortical neurons during seizures and seizure-like ionic conditions. In vitro the [K(+) ](o) was 2.8, 6.25, 8.0, and 12â€ƒmm and the [Ca(2+) ](o) was 1.2 and 0.6â€ƒmm. Key Findings:â€‚ During seizures recorded in vivo, we observed abolition of evoked synaptic responses. In vitro, the membrane potential of both regular-spiking and fast-spiking neurons was depolarized in high [K(+) ](o) conditions and hyperpolarized in high [Ca(2+) ](o) conditions. During high [K(+) ](o) conditions, changes in [Ca(2+) ](o) did not affect membrane potential. The synaptic responsiveness of both regular-spiking and fast-spiking neurons was reduced during seizure-like ionic conditions. A reduction in [Ca(2+) ](o) to 0.6â€ƒmm increased failure rates but did not abolish responses. However, an increase in [K(+) ](o) to 12â€ƒmm abolished postsynaptic responses, which depended on a blockade in axonal spike propagation. Significance:â€‚ We conclude that concomitant changes in [K(+) ](o) and [Ca(2+) ](o) observed during seizures contribute largely to the alterations of synaptic neuronal responses and to the decrease in long-range synchrony during neocortical seizures.
Robert-Giffard Research Center, Laval University, QuÃ©bec, Canada Department of Psychiatry and Neuroscience, Laval University, QuÃ©bec, Canada.
This article was published in the following journal.
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21126243
- DOI: http://dx.doi.org/10.1111/j.1528-1167.2010.02784.x
Medical and Biotech [MESH] Definitions
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
Long-term Synaptic Depression
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The voltages across pre- or post-SYNAPTIC MEMBRANES.
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