Seizure-like afterdischarges simulated in a model neuron
To explore non-synaptic mechanisms in paroxysmal discharges, we used a computer model of a simplified hippocampal pyramidal cell, surrounded by interstitial space and a "glial-endothelial" buffer system. Ion channels for Na+, K+, Ca2+ and Cl- ion antiport 3Na/Ca, and "active" ion...
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| Veröffentlicht in: | Journal of computational neuroscience 2007-04, Vol.22 (2), p.105-128 |
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| description | To explore non-synaptic mechanisms in paroxysmal discharges, we used a computer model of a simplified hippocampal pyramidal cell, surrounded by interstitial space and a "glial-endothelial" buffer system. Ion channels for Na+, K+, Ca2+ and Cl- ion antiport 3Na/Ca, and "active" ion pumps were represented in the neuron membrane. The glia had "leak" conductances and an ion pump. Fluxes, concentration changes and cell swelling were computed. The neuron was stimulated by injecting current. Afterdischarge (AD) followed stimulation if depolarization due to rising interstitial K+ concentration ([K+]o) activated persistent Na+ current (INa.P). AD was either simple or self-regenerating; either regular (tonic) or burst-type (clonic); and always self-limiting. Self-regenerating AD required sufficient INa.P to ensure re-excitation. Burst firing depended on activation of dendritic Ca2+ currents and Ca-dependent K+ current. Varying glial buffer function influenced [K+]o accumulation and afterdischarge duration. Variations in Na+ and K+ currents influenced the threshold and the duration of AD. The data show that high [K+]o and intrinsic membrane currents can produce the feedback of self-regenerating afterdischarges without synaptic input. The simulated discharge resembles neuron behavior during paroxysmal firing in living brain tissue. |
| doi_str_mv | 10.1007/s10827-006-0001-y |
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Ion channels for Na+, K+, Ca2+ and Cl- ion antiport 3Na/Ca, and "active" ion pumps were represented in the neuron membrane. The glia had "leak" conductances and an ion pump. Fluxes, concentration changes and cell swelling were computed. The neuron was stimulated by injecting current. Afterdischarge (AD) followed stimulation if depolarization due to rising interstitial K+ concentration ([K+]o) activated persistent Na+ current (INa.P). AD was either simple or self-regenerating; either regular (tonic) or burst-type (clonic); and always self-limiting. Self-regenerating AD required sufficient INa.P to ensure re-excitation. Burst firing depended on activation of dendritic Ca2+ currents and Ca-dependent K+ current. Varying glial buffer function influenced [K+]o accumulation and afterdischarge duration. Variations in Na+ and K+ currents influenced the threshold and the duration of AD. The data show that high [K+]o and intrinsic membrane currents can produce the feedback of self-regenerating afterdischarges without synaptic input. The simulated discharge resembles neuron behavior during paroxysmal firing in living brain tissue.</description><identifier>ISSN: 0929-5313</identifier><identifier>EISSN: 1573-6873</identifier><identifier>DOI: 10.1007/s10827-006-0001-y</identifier><identifier>PMID: 17053996</identifier><identifier>CODEN: JCNEFR</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Animals ; Calcium - metabolism ; Computer Simulation ; Dendrites - drug effects ; Dendrites - physiology ; Electric Stimulation - methods ; Hippocampus - pathology ; Ion Channels - drug effects ; Ion Channels - physiology ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Membrane Potentials - radiation effects ; Models, Neurological ; Potassium - metabolism ; Potassium - pharmacology ; Pyramidal Cells - cytology ; Pyramidal Cells - drug effects ; Pyramidal Cells - physiopathology ; Receptors, N-Methyl-D-Aspartate - physiology ; Seizures - pathology ; Seizures - physiopathology ; Sodium - metabolism ; Sodium - pharmacology</subject><ispartof>Journal of computational neuroscience, 2007-04, Vol.22 (2), p.105-128</ispartof><rights>Springer Science+Business Media, LLC 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c326t-eed53c9dfaba25382821149134ce063a02efeafc28d5944dd73406068c24e2583</citedby><cites>FETCH-LOGICAL-c326t-eed53c9dfaba25382821149134ce063a02efeafc28d5944dd73406068c24e2583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17053996$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kager, H</creatorcontrib><creatorcontrib>Wadman, W J</creatorcontrib><creatorcontrib>Somjen, G G</creatorcontrib><title>Seizure-like afterdischarges simulated in a model neuron</title><title>Journal of computational neuroscience</title><addtitle>J Comput Neurosci</addtitle><description>To explore non-synaptic mechanisms in paroxysmal discharges, we used a computer model of a simplified hippocampal pyramidal cell, surrounded by interstitial space and a "glial-endothelial" buffer system. Ion channels for Na+, K+, Ca2+ and Cl- ion antiport 3Na/Ca, and "active" ion pumps were represented in the neuron membrane. The glia had "leak" conductances and an ion pump. Fluxes, concentration changes and cell swelling were computed. The neuron was stimulated by injecting current. Afterdischarge (AD) followed stimulation if depolarization due to rising interstitial K+ concentration ([K+]o) activated persistent Na+ current (INa.P). AD was either simple or self-regenerating; either regular (tonic) or burst-type (clonic); and always self-limiting. Self-regenerating AD required sufficient INa.P to ensure re-excitation. Burst firing depended on activation of dendritic Ca2+ currents and Ca-dependent K+ current. Varying glial buffer function influenced [K+]o accumulation and afterdischarge duration. Variations in Na+ and K+ currents influenced the threshold and the duration of AD. The data show that high [K+]o and intrinsic membrane currents can produce the feedback of self-regenerating afterdischarges without synaptic input. The simulated discharge resembles neuron behavior during paroxysmal firing in living brain tissue.</description><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Computer Simulation</subject><subject>Dendrites - drug effects</subject><subject>Dendrites - physiology</subject><subject>Electric Stimulation - methods</subject><subject>Hippocampus - pathology</subject><subject>Ion Channels - drug effects</subject><subject>Ion Channels - physiology</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Membrane Potentials - radiation effects</subject><subject>Models, Neurological</subject><subject>Potassium - metabolism</subject><subject>Potassium - pharmacology</subject><subject>Pyramidal Cells - cytology</subject><subject>Pyramidal Cells - drug effects</subject><subject>Pyramidal Cells - physiopathology</subject><subject>Receptors, N-Methyl-D-Aspartate - physiology</subject><subject>Seizures - pathology</subject><subject>Seizures - 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Ion channels for Na+, K+, Ca2+ and Cl- ion antiport 3Na/Ca, and "active" ion pumps were represented in the neuron membrane. The glia had "leak" conductances and an ion pump. Fluxes, concentration changes and cell swelling were computed. The neuron was stimulated by injecting current. Afterdischarge (AD) followed stimulation if depolarization due to rising interstitial K+ concentration ([K+]o) activated persistent Na+ current (INa.P). AD was either simple or self-regenerating; either regular (tonic) or burst-type (clonic); and always self-limiting. Self-regenerating AD required sufficient INa.P to ensure re-excitation. Burst firing depended on activation of dendritic Ca2+ currents and Ca-dependent K+ current. Varying glial buffer function influenced [K+]o accumulation and afterdischarge duration. Variations in Na+ and K+ currents influenced the threshold and the duration of AD. 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| subjects | Animals Calcium - metabolism Computer Simulation Dendrites - drug effects Dendrites - physiology Electric Stimulation - methods Hippocampus - pathology Ion Channels - drug effects Ion Channels - physiology Membrane Potentials - drug effects Membrane Potentials - physiology Membrane Potentials - radiation effects Models, Neurological Potassium - metabolism Potassium - pharmacology Pyramidal Cells - cytology Pyramidal Cells - drug effects Pyramidal Cells - physiopathology Receptors, N-Methyl-D-Aspartate - physiology Seizures - pathology Seizures - physiopathology Sodium - metabolism Sodium - pharmacology |
| title | Seizure-like afterdischarges simulated in a model neuron |
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