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The Journal of Neuroscience, January 1, 2001, 21(1):117-124

Expression of Brain-Derived Neurotrophic Factor in Cortical Neurons Is Regulated by Striatal Target Area

Josep M. Canals¹, Núria Checa¹, Sònia Marco¹, Peter Åkerud², Alice Michels¹, Esther Pérez-Navarro¹, Eduard Tolosa³, Ernest Arenas², and Jordi Alberch¹

¹ Departament de Biologia Cel·lular i Anatomia Patològica, Facultat de Medicina, Universitat de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Casanova 143, E-08036 Barcelona, Spain, ² Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm S-17177, Sweden, and ³ Servei de Neurologia, Hospital Clínic, Universitat de Barcelona, IDIBAPS, Villarroel 170, E-08036 Barcelona, Spain

Changes in BDNF expression after different types of brain insults are related to neuroprotection, stimulation of sprouting, and synaptic reorganization. In the cerebral cortex, an autocrine-paracrine mechanism for BDNF has been proposed because the distribution patterns of BDNF and TrkB expression are almost identical. Moreover, cortical BDNF is anterogradely transported to the striatum, suggesting a role of BDNF in the functional interaction between the two brain regions. Here we have examined the expression of this neurotrophin in the cerebral cortex after various striatal lesions. Intrastriatal injection of quinolinate, kainate, 3-nitropropionic acid, or colchicine increased BDNF mRNA levels in cerebral cortex. In contrast, stimulation of neuronal activity in the striatum did not change cortical BDNF expression. Both excitatory amino acids increased BDNF expression in neurons of cortical layers II/III, V, and VI that project to the striatum. Moreover, grafting a BDNF-secreting cell line prevented both the loss of striatal neurons and the cortical upregulation of BDNF induced by excitotoxins. Because retrograde transport in the corticostriatal pathway was intact after striatal lesions, our results suggest that striatal damage upregulates endogenous BDNF in corticostriatal neurons by a transneuronal mechanism, which may constitute a protective mechanism for striatal and/or cortical cells.

Key words: corticostriatal pathway; anterograde transport; excitatory amino acids; 3-nitropropionic acid; neurotrophins; synaptic activity; Huntington's disease

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Copyright © 2001 Society for Neuroscience  0270-6474/01/211117-08$05.00/0

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