Imaging parallel fiber and climbing fiber responses and their short-term interactions in the mouse cerebellar cortex in vivo

Neuroscience ◽  
2004 ◽  
Vol 126 (1) ◽  
pp. 213-227 ◽  
Author(s):  
R.L Dunbar ◽  
G Chen ◽  
W Gao ◽  
K.C Reinert ◽  
R Feddersen ◽  
...  
2007 ◽  
Vol 98 (3) ◽  
pp. 1697-1705 ◽  
Author(s):  
Fredrik Bengtsson ◽  
Henrik Jörntell

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°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.


2019 ◽  
Vol 688 ◽  
pp. 26-36 ◽  
Author(s):  
M.M. ten Brinke ◽  
H.J. Boele ◽  
C.I. De Zeeuw

2005 ◽  
Vol 94 (2) ◽  
pp. 1287-1298 ◽  
Author(s):  
Gang Chen ◽  
Wangcai Gao ◽  
Kenneth C. Reinert ◽  
Laurentiu S. Popa ◽  
Claudia M. Hendrix ◽  
...  

Spreading acidification and depression (SAD) is a form of propagated activity in the cerebellar cortex characterized by acidification and a transient depression in excitability. This study investigated the role of Kv1 potassium channels in SAD using neutral red, flavoprotein autofluorescence, and voltage-sensitive dye optical imaging in the mouse cerebellar cortex, in vivo. The probability of evoking SAD was greatly increased by blocking Kv1.1 as well as Kv1.2 potassium channels by their specific blockers dendrotoxin K (DTX-K) and tityustoxin (TsTX), respectively. DTX-K not only greatly lowered the threshold for evoking SAD but also resulted in multiple cycles of spread and spontaneous SAD. The occurrence of spontaneous SAD originating from spontaneous parallel fiber-like beams of activity suggests that blocking Kv1 channels increased parallel fiber excitability. This was confirmed by the generation of parallel fiber-like beams with the microinjection of glutamate into the upper molecular layer in the presence of DTX-K. The dramatic effects of DTX-K suggest a possible connection between SAD and episodic ataxia type 1 (EA1), a Kv1.1 potassium channelopathy. The threshold for evoking SAD was significantly lowered in the Kv1.1 heterozygous knockout mouse compared with wild-type littermates. Carbamazepine and acetazolamide, both effective in the treatment of EA1, significantly decreased the likelihood of evoking SAD. Blocking GABAergic neurotransmission did not alter the effectiveness of DTX-K. The cyclin D2 null mouse, which lacks cerebellar stellate cells, also exhibited SAD. Therefore blocking Kv1 potassium channels establishes the conditions needed to generate SAD. Furthermore, the results are consistent with the hypothesis that SAD may underlie the transient attacks of ataxia characterizing EA1.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Michael A Gaffield ◽  
Matthew J M Rowan ◽  
Samantha B Amat ◽  
Hirokazu Hirai ◽  
Jason M Christie

Motor learning involves neural circuit modifications in the cerebellar cortex, likely through re-weighting of parallel fiber inputs onto Purkinje cells (PCs). Climbing fibers instruct these synaptic modifications when they excite PCs in conjunction with parallel fiber activity, a pairing that enhances climbing fiber-evoked Ca2+ signaling in PC dendrites. In vivo, climbing fibers spike continuously, including during movements when parallel fibers are simultaneously conveying sensorimotor information to PCs. Whether parallel fiber activity enhances climbing fiber Ca2+ signaling during motor behaviors is unknown. In mice, we found that inhibitory molecular layer interneurons (MLIs), activated by parallel fibers during practiced movements, suppressed parallel fiber enhancement of climbing fiber Ca2+ signaling in PCs. Similar results were obtained in acute slices for brief parallel fiber stimuli. Interestingly, more prolonged parallel fiber excitation revealed latent supralinear Ca2+ signaling. Therefore, the balance of parallel fiber and MLI input onto PCs regulates concomitant climbing fiber Ca2+ signaling.


2019 ◽  
Vol 130 ◽  
pp. 32-43 ◽  
Author(s):  
Elias Begas ◽  
Maria Bounitsi ◽  
Thomas Kilindris ◽  
Evangelos Kouvaras ◽  
Konstantinos Makaritsis ◽  
...  

Author(s):  
Daniel L. Villeneuve ◽  
Brett R. Blackwell ◽  
Jenna E. Cavallin ◽  
Wan‐Yun Cheng ◽  
David J. Feifarek ◽  
...  

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