Continuous exposure to glial cell line-derived neurotrophic factor to mature dopaminergic transplants impairs the graft's ability to improve spontaneous motor behavior in parkinsonian rats

Neuroscience. 2006 Aug 11;141(1):521-31. doi: 10.1016/j.neuroscience.2006.03.068. Epub 2006 May 11.

Abstract

Functional recovery following intrastriatal transplantation of fetal dopaminergic neurons in animal models of Parkinson's disease is, at least in part, dependent on the number of surviving dopaminergic neurons and the degree of graft-derived dopaminergic reinnervation of the host striatum. In the present study, we analyzed whether continuous exposure of glial cell line-derived neurotrophic factor (GDNF) to mature dopaminergic grafts could further boost the functional outcome of widespread intrastriatal dopaminergic grafts. Rats with dopamine-denervating lesions received multiple intrastriatal transplants of fetal dopaminergic cells and graft-induced behavioral effects were analyzed in drug-induced and spontaneous motor behaviors. At three months after grafting, animals received intrastriatal injections of recombinant lentiviral vectors encoding for either human GDNF or the green fluorescent protein. Continuous exposure of GDNF to the grafts did not boost the functional recovery beyond what was observed in the control animals. Rather, in some of the spontaneous motor behaviors, animals in the GDNF-group showed deterioration as compared with control animals, and this negative effect of GDNF was associated with a down-regulation of the tyrosine hydroxylase enzyme. Based on these and our earlier results, we propose that intrastriatal administration of GDNF at the time of or shortly after grafting is highly effective in initially promoting the cell survival and fiber outgrowth from the grafts. However, once the grafts are mature, GDNF's ability to boost dopaminergic neurotransmission follows the same dynamics as for the native nigral dopaminergic neurons, which appears to be dependent on the concentration of GDNF. Since rather low doses of glial cell line-derived neurotrophic factor at nanogram levels appear to saturate these effects, it may be critical to adjust GDNF levels using tightly regulated gene expression systems.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Apomorphine / pharmacology
  • Behavior, Animal
  • Cell Count / methods
  • Cell Transplantation / methods*
  • Corpus Striatum / cytology
  • Corpus Striatum / metabolism
  • Corpus Striatum / transplantation
  • Disease Models, Animal
  • Dopamine / metabolism*
  • Drug Interactions
  • Female
  • Glial Cell Line-Derived Neurotrophic Factor / administration & dosage*
  • Green Fluorescent Proteins / metabolism
  • Motor Activity / drug effects*
  • Motor Activity / physiology
  • Neurons / drug effects
  • Neurons / metabolism
  • Parkinson Disease / drug therapy*
  • Parkinson Disease / surgery*
  • Psychomotor Performance / drug effects
  • Psychomotor Performance / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Recovery of Function / drug effects
  • Recovery of Function / physiology
  • Rotarod Performance Test / methods
  • Transplants
  • Tyrosine 3-Monooxygenase / metabolism
  • Vesicular Monoamine Transport Proteins / metabolism

Substances

  • Glial Cell Line-Derived Neurotrophic Factor
  • Slc18a2 protein, rat
  • Vesicular Monoamine Transport Proteins
  • Green Fluorescent Proteins
  • Tyrosine 3-Monooxygenase
  • Apomorphine
  • Dopamine