Vitamin E is essential for Purkinje neuron integrity

Neuroscience. 2014 Feb 28:260:120-9. doi: 10.1016/j.neuroscience.2013.12.001. Epub 2013 Dec 14.

Abstract

α-Tocopherol (vitamin E) is an essential dietary antioxidant with important neuroprotective functions. α-Tocopherol deficiency manifests primarily in neurological pathologies, notably cerebellar dysfunctions such as spinocerebellar ataxia. To study the roles of α-tocopherol in the cerebellum, we used the α-tocopherol transfer protein for the murine version (Ttpa(-/)(-)) mice which lack the α-tocopherol transfer protein (TTP) and are a faithful model of vitamin E deficiency and oxidative stress. When fed vitamin E-deficient diet, Ttpa(-/)(-) mice had un-detectable levels of α-tocopherol in plasma and several brain regions. Dietary supplementation with α-tocopherol normalized plasma levels of the vitamin, but only modestly increased its levels in the cerebellum and prefrontal cortex, indicating a critical function of brain TTP. Vitamin E deficiency caused an increase in cerebellar oxidative stress evidenced by increased protein nitrosylation, which was prevented by dietary supplementation with the vitamin. Concomitantly, vitamin E deficiency precipitated cellular atrophy and diminished dendritic branching of Purkinje neurons, the predominant output regulator of the cerebellar cortex. The anatomic decline induced by vitamin E deficiency was paralleled by behavioral deficits in motor coordination and cognitive functions that were normalized upon vitamin E supplementation. These observations underscore the essential role of vitamin E and TTP in maintaining CNS function, and support the notion that α-tocopherol supplementation may comprise an effective intervention in oxidative stress-related neurological disorders.

Keywords: 3-NT; 3-nitrotyrosine; AD; ANOVA; AVED; Alzheimer’s disease; CS; NPC; Niemann Pick disease type C; Purkinje neuron; SCA; TBARS; TTP; TTPA; Ttpa; US; analysis of variance; ataxia; ataxia with vitamin E deficiency; cerebellum; conditioned stimulus; oxidative stress; spinocerebellar ataxia; t-HODE; thiobarbituric acid reactive substances; tocopherol; total hydroxyoctadecadienoic acid; unconditioned stimulus; vitamin E; α-tocopherol transfer protein; α-tocopherol transfer protein gene for the human version; α-tocopherol transfer protein gene for the murine version.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Carrier Proteins / genetics
  • Cerebellum / drug effects
  • Cerebellum / metabolism
  • Cerebellum / pathology
  • Mice
  • Mice, Knockout
  • Motor Activity / drug effects
  • Motor Activity / physiology
  • Oxidative Stress / drug effects
  • Prefrontal Cortex / drug effects
  • Prefrontal Cortex / metabolism
  • Purkinje Cells / drug effects*
  • Purkinje Cells / metabolism*
  • Purkinje Cells / pathology
  • Tyrosine / analogs & derivatives
  • Tyrosine / metabolism
  • Vitamin E Deficiency / pathology
  • Vitamin E Deficiency / physiopathology
  • alpha-Tocopherol / blood
  • alpha-Tocopherol / pharmacology*

Substances

  • Carrier Proteins
  • alpha-tocopherol transfer protein
  • 3-nitrotyrosine
  • Tyrosine
  • alpha-Tocopherol