scholarly journals Cerebellar Globular Cells Receive Monoaminergic Excitation and Monosynaptic Inhibition from Purkinje Cells

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e29663 ◽  
Author(s):  
Moritoshi Hirono ◽  
Fumihito Saitow ◽  
Moeko Kudo ◽  
Hidenori Suzuki ◽  
Yuchio Yanagawa ◽  
...  
2011 ◽  
Vol 71 ◽  
pp. e322-e323
Author(s):  
Moritoshi Hirono ◽  
Fumihito Saitow ◽  
Moeko Kudo ◽  
Hidenori Suzuki ◽  
Yuchio Yanagawa ◽  
...  

1998 ◽  
Vol 119 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Stephen G. Lisberger

The vestibulo-ocular reflex has been used extensively for study of the neural mechanisms of learning that is dependent on an intact cerebellum. Anatomic, physiologic, behavioral, and computational approaches have revealed the neural circuits that are used to generate the vestibulo-ocular reflex and have identified two likely sites of plasticity within those circuits. One site of plasticity is in the vestibular inputs to floccular target neurons, which are located in the vestibular nuclei and receive monosynaptic inhibition from Purkinje cells in the floccular complex of the cerebellar cortex. The other site of plasticity is in the vestibular inputs to Purkinje cells in the floccular complex, possibly in the cerebellar cortex. After reviewing the evidence that supports these conclusions, I consider a number of observations showing that the dynamics of neural circuits or cellular mechanisms play important roles in learning in the vestibulo-ocular reflex. (Otolaryngol Head Neck Surg 1998;119:43–8.)


Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros

In severe cerebral ischemia, Purkinje cells of the cerebellum are one of the cell types most vulnerable to anoxic damage. In the partial (forebrain) global ischemic (PGI) model of the rat, Paljärvi noted at the light microscopic level that cerebellar damage is inconsistant and when present, milder than in the telencephalon, diencephalon and rostral brain stem. Cerebellar injury was observed in 3 of 4 PGI rats following 5 minutes of reperfusion but in none of the rats after 90 min of reperfusion. To evaluate a time between these two extremes (5 and 90 min), the present investigation used the PGI model to study the effects of ischemia on the ultrastructure of cerebellar Purkinje cells in rats that were sacrificed after 30 min of reperfusion. This time also was chosen because lactic acid that is thought to contribute to ischemic cell changes in PGI is at a maximum after 30 min of reperfusion.


Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros

Although a previous study in this laboratory determined that Purkinje cells of the rat cerebellum did not appear to be damaged following 30 min of forebrain ischemia followed by 30 min of reperfusion, it was suggested that an increase in rough endoplasmic reticulum (RER) and/or polysomes had occurred in these cells. The primary objective of the present study was to morphometrically determine whether or not this increase had occurred. In addition, since there is substantial evidence that glial cells may be affected by ischemia earlier than other cell types, glial cells also were examined. To ascertain possible effects on other cerebellar components, granule cells and neuropil near Purkinje cells as well as neuropil in the molecular layer also were evaluated in this investigation.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Juan Alejandro Oliva Trejo ◽  
Isei Tanida ◽  
Chigure Suzuki ◽  
Soichiro Kakuta ◽  
Norihiro Tada ◽  
...  

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