CART peptide induces neuroregeneration in stroke rats

J Cereb Blood Flow Metab. 2013 Feb;33(2):300-10. doi: 10.1038/jcbfm.2012.172. Epub 2012 Dec 5.

Abstract

Utilizing a classic stroke model in rodents, middle cerebral artery occlusion (MCAo), we describe a novel neuroregenerative approach using the repeated intranasal administration of cocaine- and amphetamine-regulated transcript (CART) peptide starting from day 3 poststroke for enhancing the functional recovery of injured brain. Adult rats were separated into two groups with similar infarction sizes, measured by magnetic resonance imaging on day 2 after MCAo, and were treated with CART or vehicle. The CART treatment increased CART level in the brain, improved behavioral recovery, and reduced neurological scores. In the subventricular zone (SVZ), CART enhanced immunolabeling of bromodeoxyuridine, a neural progenitor cell marker Musashi-1, and the proliferating cell nuclear antigen, as well as upregulated brain-derived neurotrophic factor (BDNF) mRNA. AAV-GFP was locally applied to the SVZ to examine migration of SVZ cells. The CART enhanced migration of GFP(+) cells from SVZ toward the ischemic cortex. In SVZ culture, CART increased the size of neurospheres. The CART-mediated cell migration from SVZ explants was reduced by anti-BDNF blocking antibody. Using (1)H-MRS (proton magnetic resonance spectroscopy), increases in N-acetylaspartate levels were found in the lesioned cortex after CART treatment in stroke brain. Cocaine- and amphetamine-regulated transcript increased the expression of GAP43 and fluoro-ruby fluorescence in the lesioned cortex. In conclusion, our data suggest that intranasal CART treatment facilitates neuroregeneration in stroke brain.

Publication types

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

MeSH terms

  • Administration, Intranasal
  • Animals
  • Behavior, Animal / drug effects
  • Brain-Derived Neurotrophic Factor / biosynthesis
  • Cell Movement / drug effects
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • Cerebral Cortex / physiopathology
  • Disease Models, Animal
  • GAP-43 Protein / biosynthesis
  • Male
  • Nerve Tissue Proteins / metabolism
  • Nerve Tissue Proteins / toxicity*
  • Neural Stem Cells / metabolism
  • Neural Stem Cells / pathology
  • Neurodegenerative Diseases / chemically induced
  • Neurodegenerative Diseases / metabolism*
  • Neurodegenerative Diseases / pathology
  • Neurodegenerative Diseases / physiopathology
  • RNA, Messenger / biosynthesis
  • RNA-Binding Proteins / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Stroke / complications
  • Stroke / metabolism*
  • Stroke / pathology
  • Stroke / physiopathology
  • Time Factors
  • Up-Regulation / drug effects

Substances

  • Brain-Derived Neurotrophic Factor
  • GAP-43 Protein
  • Msi1 protein, rat
  • Nerve Tissue Proteins
  • RNA, Messenger
  • RNA-Binding Proteins
  • cocaine- and amphetamine-regulated transcript protein