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Ketamine and xylazine depress sensory-evoked parallel fiber and climbing fiber responses.

Författare

Summary, in English

Abstract

The last few years have seen an increase in the variety of in vivo experiments used for studying cerebellar physiological mechanisms. A combination of ketamine and xylazine has become a particularly popular form of anesthesia. However, because nonanesthetized control conditions are lacking in these experiments, so far there has been no evaluation of the effects of these drugs on the physiological activity in the cerebellar neuronal network. In the present study, we used the mossy fiber, parallel fiber, and climbing fiber field potentials evoked in the nonanesthetized, decerebrated rat to serve as a control condition against which the effects of intravenous drug injections could be compared. All anesthetics were applied at doses required for normal maintenance of anesthesia. We found that ketamine substantially depressed the evoked N3 field potential, which is an indicator of the activity in the parallel fiber synapses (-40%), and nearly completely abolished evoked climbing fiber field potentials (-90%). Xylazine severely depressed the N3 field (-75%) and completely abolished the climbing fiber field (-100%). In a combination commonly used for general anesthesia (20:1), ketamine-xylazine injections also severely depressed the N3 field (-75%) and nearly completely abolished the climbing fiber field (-90%). We also observed that lowered body and surface temperatures (<34 degrees C) resulted in a substantial depression of the N3 field (-50%). These results urge for some caution in the interpretations of studies on cerebellar network physiology performed in animals anesthetized with these drugs

Publiceringsår

2007

Språk

Engelska

Sidor

705-1697

Publikation/Tidskrift/Serie

Journal of Neurophysiology

Volym

98

Issue

3

Dokumenttyp

Artikel i tidskrift

Förlag

American Physiological Society

Ämne

  • Basic Medicine
  • Neurosciences

Status

Published

Forskningsgrupp

  • Neural Basis of Sensorimotor Control

ISBN/ISSN/Övrigt

  • ISSN: 0022-3077