GDNF and protection of adult central catecholaminergic neurons

  1. José López-Barneo1,2
  1. 1Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Avenida Manuel Siurot s/n, 41013 Sevilla, Spain
    2Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Sevilla, Spain
  1. (Correspondence should be addressed to A Pascual at Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Avenida Manuel Siurot s/n, 41013 Sevilla, Spain; Email: apascual-ibis{at}us.es; J Lopez-Barneo at Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Avenida Manuel Siurot s/n, 41013 Sevilla, Spain; Email: lbarneo{at}us.es)
  1. Figure 1

    Schematic representation of regions with high GDNF expression levels in adult brains. Light blue represents the areas where GDNF mRNA or activity of the GDNF promoter is detected. CPu, caudate putamen (striatum); Acb, accumbens nucleus; Ms, medial septal nucleus; AVVL, anteroventral thalamic nucleus, ventrolateral part; AM, anteromedial thalamic nucleus. Ventricles are shown in gray.

  2. Figure 2

    Schematic representation of GDNF signaling pathways. Arrows indicate interactions and boxes contain receptor protein domains (top) and cytoplasmic proteins (bottom). Protein domains are not represented scaled.

  3. Figure 3

    Catecholaminergic phenotype after genetic GDNF downregulation in the adult conditional GDNF mice (cGDNF). (A) Histological analysis of cGDNF animals 7 months after GDNF depletion. A marked cell death was observed in substantia nigra (SN), ventral tegmental area (VTA), and, particularly, in locus coeruleus (LC). Scale bars, 100 μm. (B) Behavioral analysis of adult GDNF-depleted mice. Spontaneous activity in open field (distance traveled) is recorded.

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