Glial cell line neurotrophic factor (GDNF) is a potent survival factor for several types of neurons. GDNF binds with high affinity to the GDNF-family receptor a-1 (GFRa-1) which is expressed in different brain areas. In the present study, by using anatomical techniques, we document the phenotypic diversity among GFRa-1 expressing neurons in the central nervous system (CNS). We found expression of GFRa-1 in GABA (g-aminobutyric acid) -containing neurons distributed in the cortex, reticular thalamic nucleus and septum. While high expression of GFRa-1 was often observed in cholinergic motoneurons in the spinal cord, very few septal cholinergic neurons were found to express GFRa-1. GFRa-1 transcripts were also detected in catecholaminergic neurons in the periventricular hypothalamic nucleus, dorsal raphe nucleus and locus ceruleus. Within the raphe nucleus, GFRa-1 expression was prominent in many serotonergic neurons and in few neurons containing the enzyme nitric oxide synthase (NOS). As GFRa-1 is activated by GDNF and GDNF-related neurotrophic factors, the widespread distribution of GFRa-1 in neurons with different phenotypes indicates that the neuronal activity of these neurons is likely to be affected by GDNF and GDNF-related neurotrophic factors. This would result in the regulation of diverse neuronal pathways in the adult brain.

Agency
National Institute of Health (NIH)
Institute
National Institute on Drug Abuse (NIDA)
Type
Intramural Research (Z01)
Project #
1Z01DA000407-05
Application #
6680368
Study Section
(CNL)
Project Start
Project End
Budget Start
Budget End
Support Year
5
Fiscal Year
2002
Total Cost
Indirect Cost
Name
National Institute on Drug Abuse
Department
Type
DUNS #
City
State
Country
United States
Zip Code
Sarabi, A; Hoffer, B J; Olson, L et al. (2003) Glial cell line neurotrophic factor-family receptor alpha-1 is present in central neurons with distinct phenotypes. Neuroscience 116:261-73
Sarabi, A; Chang, C F; Wang, Y et al. (2001) Time course study of GFRalpha-1 expression in an animal model of stroke. Exp Neurol 170:283-9