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Special Features |

Cystic Fibrosis and the Nervous System

Leah R. Reznikov
Author and Funding Information

Conflict of Interest: The author claims no financial or intellectual conflicts of interest.

Funding Information: None.

Prior Abstract Publication or Presentation: None.

Department of Physiological Sciences, University of Florida, Gainesville, FL 32610

Contact Information: Leah Reznikov PhD, University of Florida, College of Veterinary Medicine 1333 Center Drive PO Box 100144, Gainesville FL 32610.


Copyright 2016, . All Rights Reserved.


Chest. 2016. doi:10.1016/j.chest.2016.11.009
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Abstract

Cystic Fibrosis (CF) is a life-shortening autosomal recessive disorder caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR is an anion channel that conducts bicarbonate and chloride across cell membranes. While defective anion transport across epithelial cells is accepted as the basic defect in CF, many of the features observed in people with CF and organs affected in CF are modulated by the nervous system. This is of interest because CFTR expression has been reported in both the peripheral and central nervous systems, and it is well known that the transport of anions, such as chloride, greatly modulates neuronal excitability. Thus, it is predicted that in CF, lack of CFTR in the nervous system affects neuronal function. Consistent with this prediction, several nervous system abnormalities and nervous system disorders have been described in people with CF and animal models of CF. The goal of this special feature article is to highlight the expression and function of CFTR in the nervous system. Special emphasis is placed on nervous system abnormalities described in people with and animal models of CF. Lastly, features of CF that may be modulated by or attributed to faulty nervous system function are discussed.


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Cystic Fibrosis and the Nervous System. Chest Published online Nov 19, 2016;
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    Print ISSN: 0012-3692
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