Etomidate reduces initiation of backpropagating dendritic action potentials: implications for sensory processing and synaptic plasticity during anesthesia

van den Burg EH, Engelmann J, Bacelo J, Gómez L, Grant K (2007)
Journal of neurophysiology 97(3): 2373-2384.

Zeitschriftenaufsatz | Veröffentlicht | Englisch
 
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Abstract / Bemerkung
Anesthetics may induce specific changes that alter the balance of activity within neural networks. Here we describe the effects of the GABA(A) receptor potentiating anesthetic etomidate on sensory processing, studied in a cerebellum-like structure, the electrosensory lateral line lobe (ELL) of mormyrid fish, in vitro. Previous studies have shown that the ELL integrates sensory input and removes predictable features by comparing reafferent sensory signals with a descending electromotor command-driven corollary signal that arrives in part through parallel fiber synapses with the apical dendrites of GABAergic interneurons. These synapses show spike timing-dependent depression when presynaptic activation is associated with postsynaptic backpropagating dendritic action potentials. Under etomidate, almost all neurons become tonically hyperpolarized. The threshold for action potential initiation increased for both synaptic activation and direct intracellular depolarization. Synaptically evoked inhibitory postsynaptic potentials (IPSPs) were also strongly potentiated and prolonged. Current source density analysis showed that backpropagation of action potentials through the apical dendritic arborization in the molecular layer was reduced but could be restored by increasing stimulus strength. These effects of etomidate were blocked by bicuculline or picrotoxin. It is concluded that etomidate affects both tonic and phasic inhibitory conductances at GABA(A) receptors and that increased shunting inhibition at the level of the proximal dendrites also contributes to increasing the threshold for action potential backpropagation. When stimulus strength is sufficient to evoke backpropagation, repetitive association of synaptic excitation with postsynaptic action potential initiation still results in synaptic depression, showing that etomidate does not interfere with the molecular mechanism underlying plastic modulation.
Stichworte
Neuronal Plasticity/physiology; Neurons; Neuronal Plasticity/drug effects; Membrane Potentials/physiology; Membrane Potentials/radiation effects; Inhibitory Postsynaptic Potentials; Membrane Potentials/drug effects; Afferent Pathways/cytology; Action Potentials/drug effects; Afferent Pathways/drug effects; Afferent Pathways/physiology; Anesthesia; Animals; Bicuculline/pharmacology; Dendrites/drug effects; Dose-Response Relationship; Radiation; Electric Fish/anatomy & histology; Drug Interactions; Electric Fish/physiology; Electric Organ/cytology; Electric Stimulation/methods; Etomidate/pharmacology; Excitatory Amino Acid Antagonists/pharmacology; Hypnotics and Sedatives/pharmacology; GABA Antagonists/pharmacology; Afferent/cytology; Neurons; Afferent/drug effects
Erscheinungsjahr
2007
Zeitschriftentitel
Journal of neurophysiology
Band
97
Ausgabe
3
Seite(n)
2373-2384
ISSN
0022-3077
eISSN
1522-1598
Page URI
https://pub.uni-bielefeld.de/record/2488867

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van den Burg EH, Engelmann J, Bacelo J, Gómez L, Grant K. Etomidate reduces initiation of backpropagating dendritic action potentials: implications for sensory processing and synaptic plasticity during anesthesia. Journal of neurophysiology. 2007;97(3):2373-2384.
van den Burg, E. H., Engelmann, J., Bacelo, J., Gómez, L., & Grant, K. (2007). Etomidate reduces initiation of backpropagating dendritic action potentials: implications for sensory processing and synaptic plasticity during anesthesia. Journal of neurophysiology, 97(3), 2373-2384. doi:10.1152/jn.00395.2006
van den Burg, E. H., Engelmann, J., Bacelo, J., Gómez, L., and Grant, K. (2007). Etomidate reduces initiation of backpropagating dendritic action potentials: implications for sensory processing and synaptic plasticity during anesthesia. Journal of neurophysiology 97, 2373-2384.
van den Burg, E.H., et al., 2007. Etomidate reduces initiation of backpropagating dendritic action potentials: implications for sensory processing and synaptic plasticity during anesthesia. Journal of neurophysiology, 97(3), p 2373-2384.
E.H. van den Burg, et al., “Etomidate reduces initiation of backpropagating dendritic action potentials: implications for sensory processing and synaptic plasticity during anesthesia”, Journal of neurophysiology, vol. 97, 2007, pp. 2373-2384.
van den Burg, E.H., Engelmann, J., Bacelo, J., Gómez, L., Grant, K.: Etomidate reduces initiation of backpropagating dendritic action potentials: implications for sensory processing and synaptic plasticity during anesthesia. Journal of neurophysiology. 97, 2373-2384 (2007).
van den Burg, Erwin H, Engelmann, Jacob, Bacelo, João, Gómez, Leonel, and Grant, Kirsty. “Etomidate reduces initiation of backpropagating dendritic action potentials: implications for sensory processing and synaptic plasticity during anesthesia”. Journal of neurophysiology 97.3 (2007): 2373-2384.

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