Anatomical structure alone cannot predict function

1997 ◽  
Vol 20 (2) ◽  
pp. 252-253 ◽  
Author(s):  
Dieter Jaeger ◽  
Erik De Schutter

The central hypothesis of Braitenberg et al.'s target article – that tidal waves of parallel fiber excitation precisely activate Purkinje cell spiking – is hard to reconcile with recent neurophysiological and modeling data. The assumed pattern of mossy fiber input seems unrealistic, inhibition is likely to interfere with the proposed excitatory responses, and moreover, computer simulations show that the Purkinje cell is a poor coincidence detector.

1997 ◽  
Vol 20 (2) ◽  
pp. 263-264 ◽  
Author(s):  
Patrick D. Roberts

Random-excitation granule cells are likely to overwhelm spatiotemporal sequences described as “tidal waves” in Braitenberg et al.'s target article. A mechanism is proposed involving the Golgi cells to reinforce tidal waves against noise. The recurrent inhibition by the Golgi calls can recruit random excitations of granule cells in phase with sequences of mossy fiber input.


2021 ◽  
Author(s):  
Jan Voogd

AbstractGerbrandus Jelgersma published extensively on the (pathological) anatomy of the cerebellum between 1886 and 1934. Based on his observations on the double innervation of the Purkinje cells, he formulated a hypothesis on the function of the cerebellum. Both afferent systems of the cerebellum, the mossy fiber-parallel fiber system and the climbing fibers terminate on the Purkinje cell dendrites. According to Jelgersma, the mossy fiber-parallel fiber system is derived from the pontine nuclei and the inferior olive, and would transmit the movement images derived from the cerebral cortex. Spinocerebellar climbing fibers would transmit information about the execution of the movement. When the Purkinje cell compares these inputs and notices a difference between instruction and execution, it sends a correction through the descending limb of the superior cerebellar peduncle to the anterior horn cells. Jelgersma postulates that this cerebro-cerebellar coordination system shares plasticity with other nervous connections because nerve cell dendritic protrusions possess what he called amoeboid mobility: dendritic protrusions can be extended or retracted and are so able to create new connections or to abolish them. Jelgersma’s theories are discussed against the background of more recent theories of cerebellar function that, similarly, are based on the double innervation of the Purkinje cells. The amoeboid hypothesis is traced to its roots in the late nineteenth century.


2016 ◽  
Vol 36 (17) ◽  
pp. 4846-4858 ◽  
Author(s):  
R. Ichikawa ◽  
K. Sakimura ◽  
M. Watanabe

2007 ◽  
Vol 97 (1) ◽  
pp. 824-836 ◽  
Author(s):  
Francis Crepel

At parallel fiber (PF) to Purkinje cell (PC) synapses, depolarization-induced suppression of excitation (DSE) and suppression of PF-excitatory postsynaptic currents (EPSCs) by activation of postsynaptic mGluR1 glutamate (Glu) receptors involve retrograde release of endocannabinoids. However, Levenes et al. suggested instead that Glu was the retrograde messenger in this latter case. Because the study by Levenes et al. was performed in nearly mature rats, whereas most others were performed in juvenile animals, DSE was re-investigated in juvenile versus nearly mature rats and mice. Indeed, DSE was preferred here to agonist-induced suppression of PF-EPSCs, to avoid possible indirect effects in this latter case. In 10- to 12-day-old rats, DSE of PF-EPSCs was entirely mediated through retrograde release of endocannabinoids. In 18- to 22-day-old-rats, DSE was partly resistant to CB1 cannabinoid receptor antagonists. The remaining component was potentiated by the Glu uptake inhibitor d-threo-beta-benzyloxyaspartate (d-TBOA) and blocked by the desensitizing kainate (KA) receptor agonist (2S,4R)-4-methylglutamic acid (SYM 2081). This SYM-2081-sensitive component of DSE was accompanied by a paired-pulse facilitation increase that was also potentiated by d-TBOA and blocked by SYM 2081. In nearly mature wild-type and GluR6 −/− mice, results fully confirmed the presence of an endocannabinoid-independent component of DSE that involves retrograde release of Glu and activation of presynaptic KA receptors including GluR6 receptor subunits. Therefore retrograde release of Glu by PCs participates to DSE at PF-PC synapses in nearly mature rodents but not in juvenile ones, and Glu probably operates through activation of presynaptic KA receptors that include GluR6 receptor subunits.


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