title: Cortical expression of brain derived neurotrophic factor and type-1 cannabinoid receptor after striatal excitotoxic lesions.
abstract: An involvement of one particular neurotrophin, namely, the brain-derived neurotrophic factor (BDNF), has been demonstrated in the pathophysiology Huntington's disease. Type-1 cannabinoid (CB1) receptor has been postulated to upregulate BDNF gene transcription. To better understand the relationship between CB1 and BDNF levels in a situation where the striatum is degenerating, we studied, by dual label immunofluorescence, the distribution of CB1 and BDNF in cortical neurons projecting to the striatum in our rat quinolinic acid model of striatal excitotoxicity. We completed our study with quantitative analyses of BDNF protein levels and CB1 binding activity in the cortex. We show that, 2 weeks post lesion, cortical neurons contain more BDNF compared with controls and to earlier time points. Such BDNF up-regulation coincides with a higher binding activity and an increased protein expression of CB1. We suggest that after excitotoxic lesions, CB1 might, at least transiently, upregulate BDNF in the attempt to rescue striatal neurons from degeneration.
authors.affiliation: Laboratory of Neuroanatomy, Santa Lucia Foundation IRCCS at the European Center for Brain research, Via del Fosso Fiorano 64, 00143 Rome, Italy.
authors.forename: Z
authors.initials: Z
authors.lastname: De March
authors.forename: C
authors.initials: C
authors.lastname: Zuccato
authors.forename: C
authors.initials: C
authors.lastname: Giampà
authors.forename: S
authors.initials: S
authors.lastname: Patassini
authors.forename: M
authors.initials: M
authors.lastname: Bari
authors.forename: V
authors.initials: V
authors.lastname: Gasperi
authors.forename: M L
authors.initials: ML
authors.lastname: De Ceballos
authors.forename: G
authors.initials: G
authors.lastname: Bernardi
authors.forename: M
authors.initials: M
authors.lastname: Maccarrone
authors.forename: E
authors.initials: E
authors.lastname: Cattaneo
authors.forename: F R
authors.initials: FR
authors.lastname: Fusco
mesh_terms: D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D002450:Cell Communication / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D002540:Cerebral Cortex / Q000378:metabolism* / Q000503:physiopathology; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D019610:Cytoprotection / Q000502:physiology; D004195:Disease Models, Animal; D005455:Fluorescent Antibody Technique; D006816:Huntington Disease / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D009410:Nerve Degeneration / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D009498:Neurotoxins; D011485:Protein Binding; D017378:Quinolinic Acid; D051381:Rats; D017208:Rats, Wistar; D043884:Receptor, Cannabinoid, CB1 / Q000378:metabolism*; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D009498:Neurotoxins; D043884:Receptor, Cannabinoid, CB1; D017378:Quinolinic Acid