Opposing modifications in intrinsic currents and synaptic inputs in post-traumatic mossy cells
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Opposing modifications in intrinsic currents and synaptic inputs in post-traumatic mossy cells : evidence for single-cell homeostasis in a hyperexcitable network. / Howard, Allyson L; Neu, Axel; Morgan, Robert J; Echegoyen, Julio C; Soltesz, Ivan.
in: J NEUROPHYSIOL, Jahrgang 97, Nr. 3, 01.03.2007, S. 2394-409.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Opposing modifications in intrinsic currents and synaptic inputs in post-traumatic mossy cells
T2 - evidence for single-cell homeostasis in a hyperexcitable network
AU - Howard, Allyson L
AU - Neu, Axel
AU - Morgan, Robert J
AU - Echegoyen, Julio C
AU - Soltesz, Ivan
PY - 2007/3/1
Y1 - 2007/3/1
N2 - Recent experimental and modeling results demonstrated that surviving mossy cells in the dentate gyrus play key roles in the generation of network hyperexcitability. Here we examined if mossy cells exhibit long-term plasticity in the posttraumatic, hyperexcitable dentate gyrus. Mossy cells 1 wk after fluid percussion head injury did not show alterations in their current-firing frequency (I-F) and current-membrane voltage (I-V) relationships. In spite of the unchanged I-F and I-V curves, mossy cells showed extensive modifications in Na(+), K(+) and h-currents, indicating the coordinated nature of these opposing modifications. Computational experiments in a realistic large-scale model of the dentate gyrus demonstrated that individually, these perturbations could significantly affect network activity. Synaptic inputs also displayed systematic, opposing modifications. Miniature excitatory postsynaptic current (EPSC) amplitudes were decreased, whereas miniature inhibitory postsynaptic current (IPSC) amplitudes were increased as expected from a homeostatic response to network hyperexcitability. In addition, opposing alterations in miniature and spontaneous synaptic event frequencies and amplitudes were observed for both EPSCs and IPSCs. Despite extensive changes in synaptic inputs, cannabinoid-mediated depolarization-induced suppression of inhibition was not altered in posttraumatic mossy cells. These data demonstrate that many intrinsic and synaptic properties of mossy cells undergo highly specific, long-term alterations after traumatic brain injury. The systematic nature of such extensive and opposing alterations suggests that single-cell properties are significantly influenced by homeostatic mechanisms in hyperexcitable circuits.
AB - Recent experimental and modeling results demonstrated that surviving mossy cells in the dentate gyrus play key roles in the generation of network hyperexcitability. Here we examined if mossy cells exhibit long-term plasticity in the posttraumatic, hyperexcitable dentate gyrus. Mossy cells 1 wk after fluid percussion head injury did not show alterations in their current-firing frequency (I-F) and current-membrane voltage (I-V) relationships. In spite of the unchanged I-F and I-V curves, mossy cells showed extensive modifications in Na(+), K(+) and h-currents, indicating the coordinated nature of these opposing modifications. Computational experiments in a realistic large-scale model of the dentate gyrus demonstrated that individually, these perturbations could significantly affect network activity. Synaptic inputs also displayed systematic, opposing modifications. Miniature excitatory postsynaptic current (EPSC) amplitudes were decreased, whereas miniature inhibitory postsynaptic current (IPSC) amplitudes were increased as expected from a homeostatic response to network hyperexcitability. In addition, opposing alterations in miniature and spontaneous synaptic event frequencies and amplitudes were observed for both EPSCs and IPSCs. Despite extensive changes in synaptic inputs, cannabinoid-mediated depolarization-induced suppression of inhibition was not altered in posttraumatic mossy cells. These data demonstrate that many intrinsic and synaptic properties of mossy cells undergo highly specific, long-term alterations after traumatic brain injury. The systematic nature of such extensive and opposing alterations suggests that single-cell properties are significantly influenced by homeostatic mechanisms in hyperexcitable circuits.
KW - Animals
KW - Animals, Newborn
KW - Computer Simulation
KW - Craniocerebral Trauma
KW - Disease Models, Animal
KW - Dose-Response Relationship, Radiation
KW - Drug Interactions
KW - Electric Stimulation
KW - Membrane Potentials
KW - Models, Neurological
KW - Mossy Fibers, Hippocampal
KW - Nerve Net
KW - Neurons
KW - Patch-Clamp Techniques
KW - Piperidines
KW - Potassium Channel Blockers
KW - Pyrazoles
KW - Pyrimidines
KW - Rats
KW - Sodium Channel Blockers
KW - Tetraethylammonium
KW - Tetrodotoxin
U2 - 10.1152/jn.00509.2006
DO - 10.1152/jn.00509.2006
M3 - SCORING: Journal article
C2 - 16943315
VL - 97
SP - 2394
EP - 2409
JO - J NEUROPHYSIOL
JF - J NEUROPHYSIOL
SN - 0022-3077
IS - 3
ER -