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Título

Serotonin 5-HT1A receptor expression is selectively enhanced in the striosomal compartment of chronic Parkinsonian monkeys

AutorFrechilla, D.; Cobreros, A.; Saldise, L.; Moratalla, Rosario ; Insausti, R.; Luquin, M.R.; Del Ro, J.
Palabras claveMPTP Dopamine Neurodegeneration Parkinson Diseas
Fecha de publicación2001
EditorJohn Wiley & Sons
CitaciónSynapse 39: 288- 296 (2001)
ResumenCynomolgus monkeys (Macaca fascicularis) were chronically treated with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) until stable parkinsonism was reached. Two months later, monkeys were sacrificed and monoamine content was measured in different brain regions of the lesioned monkeys and of age-matched controls. 5-HT1A serotonin receptor density was measured in coronal sections labeled with [3H]8-OH-DPAT. As expected, dopamine was virtually nonexistent in the caudate nucleus and putamen of MPTP-treated monkeys. Serotonin levels were significantly reduced in different brain regions, particularly in the raphe nuclei. 5-HT1A receptor density of control animals was high in the hippocampus, notably in the CA1 field and also in the raphe nuclei, and much lower in the striatum, where 5-HT1A receptors showed a patchy distribution which corresponded to striosomes with poor calbindin immunostaining. 5-HT1A receptor density was reduced in hippocampal fields and in the raphe nuclei of parkinsonian monkeys. Conversely, in the severely lesioned striatal nuclei 5-HT1A receptor density was increased at caudal levels of the striatum, particularly in the putamen. The results tend to support the possibility of an increased synthesis of 5-HT1A receptors in brain regions with higher neuronal cell death. Upregulation of this 5-HT receptor subtype in the limbic compartment of the striatum may represent a compensatory event for the serotonergic dysfunction and associated mental disorders in neurodegenerative diseases such as Parkinson disease. © 2001 Wiley-Liss, Inc.
URIhttp://hdl.handle.net/10261/152145
DOI10.1002/1098-2396(20010315)39:4<288::AID-SYN1011>3.0.CO;2-V
Identificadoresdoi: 10.1002/1098-2396(20010315)39:4<288::AID-SYN1011>3.0.CO;2-V
issn: 0887-4476
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