Purkinje Cell

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Related to Purkinje cells: GABA, Purkinje cell layer, Pyramidal cells, Granule cells

Purkinje cell

[pər′kin·jē ‚sel]
(histology)
Any of the cells of the cerebral cortex with large, flask-shaped bodies forming a single cell layer between the molecular and granular layers.

Purkinje Cell

 

any one of numerous large neurons of the cerebellar cortex whose axons extend beyond the cortex; first described in 1837 by J. E. Purkinje.

Purkinje cells transmit the commands of the cerebellar cortex to its subordinate motor centers, the cerebellar and vestibular nuclei. In mammals and birds, the bodies of Purkinje cells are arranged in the cerebellar cortex in a single layer, called the gangliar, or Purkinje, layer. The Purkinje layer is located between the molecular layer, into which each Purkinje cell extends a dendrite, and the granular layer, through which the axon of a Purkinje cell passes into the white matter of the cerebellum. The flattened dendrite of a Purkinje cell has smooth branches of the first, second, and third orders and short branches (not more than 20 μ long) that are covered with spines. These branches come in contact with the axon endings of the granular cells of the cerebellar cortex; in a cat, for example, there are about 0.2 million synapses per dendrite. The smooth branches of a dendrite and the body of the Purkinje cell come in contact with a convoluted liana-like fiber (one per Purkinje cell) that enters the cerebellum from the inferior olivas and some other nuclei of the medulla oblongata. Both types of synapses are excitatory.

The inhibitory endings of Purkinje cells are formed by intercellular cortical neurons (basket, stellate, and Golgi cells); gamma-aminobutyric acid seems to be the mediator. The same mediator is probably secreted by the axon endings of Purkinje cells onto the neurons of the cerebellar and vestibular nuclei.

The dendrites of Purkinje cells have become progressively more complex and flattened in the course of vertebrate evolution; the total number of Purkinje cells has also increased, totaling 15–20 million in man.

D. A. SAKHAROV

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In most cases of PCA, the neurological symptom has stabilized by the time treatment is started, meaning that Purkinje cell damage and neuronal loss have most probably already occurred (5).
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