Intravenous Anesthetic, Propofol Affects Synaptic Responses in Cerebellar Purkinje Cells

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Abstract

Objective

Propofol is an intravenously administered anesthetic that enhances γ-aminobutyric acid-mediated inhibition in the central nerve system. Other mechanisms may also be involved in general anesthesia. Propofol has been implicated in movement disorders. The cerebellum is important for motor coordination and motor learning. The aim of the present study was to investigate the propofol effect on excitatory synaptic transmissions in cerebellar cortex.

Methods

Excitatory postsynaptic currents by parallel fiber stimulation and complex spikes by climbing fiber stimulation were monitored in Purkinje cells of Wister rat cerebellar slice using whole-cell patch-clamp techniques.

Results

Decay time, rise time and amplitude of excitatory postsynaptic currents at parallel fiber Purkinje cell synapses and area of complex spikes at climbing fiber Purkinje cell synapses were significantly increased by propofol administration.

Conclusion

The detected changes of glutamatergic synaptic transmission in cerebellar Purkinje cell, which determine cerebellar motor output, could explain cerebellar mechanism of motor deficits induced by propofol.

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Most cited references 33

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Short-term synaptic plasticity.

Robert S. Zucker, Wade Regehr (2002)

Synaptic transmission is a dynamic process. Postsynaptic responses wax and wane as presynaptic activity evolves. This prominent characteristic of chemical synaptic transmission is a crucial determinant of the response properties of synapses and, in turn, of the stimulus properties selected by neural networks and of the patterns of activity generated by those networks. This review focuses on synaptic changes that result from prior activity in the synapse under study, and is restricted to short-term effects that last for at most a few minutes. Forms of synaptic enhancement, such as facilitation, augmentation, and post-tetanic potentiation, are usually attributed to effects of a residual elevation in presynaptic [Ca(2+)]i, acting on one or more molecular targets that appear to be distinct from the secretory trigger responsible for fast exocytosis and phasic release of transmitter to single action potentials. We discuss the evidence for this hypothesis, and the origins of the different kinetic phases of synaptic enhancement, as well as the interpretation of statistical changes in transmitter release and roles played by other factors such as alterations in presynaptic Ca(2+) influx or postsynaptic levels of [Ca(2+)]i. Synaptic depression dominates enhancement at many synapses. Depression is usually attributed to depletion of some pool of readily releasable vesicles, and various forms of the depletion model are discussed. Depression can also arise from feedback activation of presynaptic receptors and from postsynaptic processes such as receptor desensitization. In addition, glial-neuronal interactions can contribute to short-term synaptic plasticity. Finally, we summarize the recent literature on putative molecular players in synaptic plasticity and the effects of genetic manipulations and other modulatory influences.

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General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal.

Nicholas Franks (2008)

The mechanisms through which general anaesthetics, an extremely diverse group of drugs, cause reversible loss of consciousness have been a long-standing mystery. Gradually, a relatively small number of important molecular targets have emerged, and how these drugs act at the molecular level is becoming clearer. Finding the link between these molecular studies and anaesthetic-induced loss of consciousness presents an enormous challenge, but comparisons with the features of natural sleep are helping us to understand how these drugs work and the neuronal pathways that they affect. Recent work suggests that the thalamus and the neuronal networks that regulate its activity are the key to understanding how anaesthetics cause loss of consciousness.

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Cerebellar circuitry as a neuronal machine.

Masao ITO (2006)

Shortly after John Eccles completed his studies of synaptic inhibition in the spinal cord, for which he was awarded the 1963 Nobel Prize in physiology/medicine, he opened another chapter of neuroscience with his work on the cerebellum. From 1963 to 1967, Eccles and his colleagues in Canberra successfully dissected the complex neuronal circuitry in the cerebellar cortex. In the 1967 monograph, "The Cerebellum as a Neuronal Machine", he, in collaboration with Masao Ito and Janos Szentágothai, presented blue-print-like wiring diagrams of the cerebellar neuronal circuitry. These stimulated worldwide discussions and experimentation on the potential operational mechanisms of the circuitry and spurred theoreticians to develop relevant network models of the machinelike function of the cerebellum. In following decades, the neuronal machine concept of the cerebellum was strengthened by additional knowledge of the modular organization of its structure and memory mechanism, the latter in the form of synaptic plasticity, in particular, long-term depression. Moreover, several types of motor control were established as model systems representing learning mechanisms of the cerebellum. More recently, both the quantitative preciseness of cerebellar analyses and overall knowledge about the cerebellum have advanced considerably at the cellular and molecular levels of analysis. Cerebellar circuitry now includes Lugaro cells and unipolar brush cells as additional unique elements. Other new revelations include the operation of the complex glomerulus structure, intricate signal transduction for synaptic plasticity, silent synapses, irregularity of spike discharges, temporal fidelity of synaptic activation, rhythm generators, a Golgi cell clock circuit, and sensory or motor representation by mossy fibers and climbing fibers. Furthermore, it has become evident that the cerebellum has cognitive functions, and probably also emotion, as well as better-known motor and autonomic functions. Further cerebellar research is required for full understanding of the cerebellum as a broad learning machine for neural control of these functions.

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Author and article information

Journal

Journal ID (nlm-ta): Clin Psychopharmacol Neurosci

Journal ID (iso-abbrev): Clin Psychopharmacol Neurosci

Title: Clinical Psychopharmacology and Neuroscience

Publisher: Korean College of Neuropsychopharmacology

ISSN (Print): 1738-1088

ISSN (Electronic): 2093-4327

Publication date (Print): May 2018

Publication date (Electronic): 31 May 2018

Volume: 16

Issue: 2

Pages: 176-183

Affiliations

[1 ]Department of Molecular and Integrative Physiology, School of Molecular and Cellular Biology, University of Illinois at Urbana-Champaign, Urbana, IL, USA

[2 ]Department of Physiology, Konyang University College of Medicine, Daejeon, Korea

[5 ]Department of Anatomy, Konyang University College of Medicine, Daejeon, Korea

[3 ]Department of Anesthesiology, Yeosu Chonnam Hospital, Yeosu, Korea

[4 ]Department of Physiology, Jeju National University School of Medicine, Jeju, Korea

[6 ]Myunggok Medical Research Institute, Konyang University, Daejeon, Korea

Author notes

Address for correspondence: Dong Kwan Kim, MD, PhD, Department of Physiology, Konyang University College of Medicine, 158 Gwanjeodong-ro, Seo-gu, Daejeon 35365, Korea., Tel: +82-42-600-6475, Fax: +82-42-600-6314, E-mail: 92dodong@ 123456gmail.com , ORCID: https://orcid.org/0000-0001-9890-1752

[*]

These authors contributed equally to this work.

Article

Publisher ID: cpn-16-176

DOI: 10.9758/cpn.2018.16.2.176

PMC ID: 5953017

PubMed ID: 29739131

SO-VID: 63ab5739-bcbe-4e88-b815-56d3115764a7

License:

This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 02 February 2017

Date revision received : 30 March 2017

Date accepted : 07 April 2017

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Intravenous Anesthetic, Propofol Affects Synaptic Responses in Cerebellar Purkinje Cells

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Abstract

Objective

Methods

Results

Conclusion

Related collections

Gamma Delta T cells

Most cited references 33

Short-term synaptic plasticity.

General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal.

Cerebellar circuitry as a neuronal machine.

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Journal

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Article

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