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  Effects of the volatile anesthetic enflurane on spontaneous discharge rate and GABA(A)-mediated inhibition of Purkinje cells in rat cerebellar slices

Antkowiak, B., & Heck, D. (1997). Effects of the volatile anesthetic enflurane on spontaneous discharge rate and GABA(A)-mediated inhibition of Purkinje cells in rat cerebellar slices. Journal of Neurophysiology, 77(5), 2525-2538. doi:10.1152/jn.1997.77.5.2525.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0013-EA8C-A Version Permalink: http://hdl.handle.net/21.11116/0000-0005-E396-1
Genre: Journal Article

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Antkowiak, B1, 2, Author              
Heck, D2, 3, Author              
Affiliations:
1Former Department Comparative Neurobiology, Max Planck Institute for Biological Cybernetics, Max Planck Society, ou_1497800              
2Max Planck Institute for Biological Cybernetics, Max Planck Society, ou_1497794              
3Former Department Structure and Function of Natural Nerve-Net , Max Planck Institute for Biological Cybernetics, Max Planck Society, ou_1497803              

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 Abstract: Effects of the volatileanesthetic enflurane on spontaneous discharge rate and GABAA-mediated inhibition of Purkinje cells in rat cerebellar slices.J. Neurophysiol. 77: 2525–2538, 1997. The effects of the volatile anesthetic enflurane on the spontaneous action potential firing and on γ-aminobutyric acid-A (GABAA)-mediated synaptic inhibition of Purkinje cells were investigated in sagittal cerebellar slices. The anesthetic shifted the discharge patterns from continuous spiking toward burst firing and decreased the frequency of extracellularly recorded spontaneous action potentials in a concentration-dependent manner. Half-maximal reduction was observed at a concentration corresponding to 2 MAC (1 MAC induces general anesthesia in 50% of patients and rats). When the GABAA antagonist bicuculline was present, 2 MAC enflurane reduced action potential firing only by 13 ± 8% (mean ± SE). In further experiments, inhibitory postsynaptic currents (IPSCs) were monitored in the whole cell patch-clamp configuration from cells voltage clamped close to −80 mV. At 1 MAC, enflurane attenuated the mean amplitude of IPSCs by 54 ± 3% while simultaneously prolonging the time courses of monoexponential current decays by 413 ± 69%. These effects were similar when presynaptic action potentials were suppressed by 1 μM tetrodotoxin. At 1–2 MAC, enflurane increased GABAA-mediated inhibition of Purkinje cells by 97 ± 20% to 159 ± 38%. During current-clamp recordings, the anesthetic (2 MAC) hyperpolarized the membrane potential by 5.2 ± 1.1 mV in the absence, but only by 1.6 ± 1.2 mV in the presence, of bicuculline. These results suggest that enflurane-induced membrane hyperpolarizations, as well as the reduction of spike rates, were partly caused by an increase in synaptic inhibition. Induction of burst firing was related to other actions of the anesthetic, probably an accelerated activation of an inwardly directed cationic current and a depression of spike after hyperpolarizations.

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 Dates: 1997-05
 Publication Status: Published in print
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 Rev. Type: -
 Identifiers: BibTex Citekey: 489
DOI: 10.1152/jn.1997.77.5.2525
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Title: Journal of Neurophysiology
  Other : J. Neurophysiol.
Source Genre: Journal
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Publ. Info: Bethesda, MD : The Society
Pages: - Volume / Issue: 77 (5) Sequence Number: - Start / End Page: 2525 - 2538 Identifier: ISSN: 0022-3077
CoNE: https://pure.mpg.de/cone/journals/resource/954925416959