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Formalin pain increases the concentration of serotonin and its 5-hydroxyindoleacetic acid metabolite in the CA1 region of hippocampus

BACKGROUND AND THE PURPOSE OF THE STUDY: The hippocampal formation is involved in nociception. Prenatal serotonin depletion results in a significant decrease in the concentration of nociceptive sensitivity during the second phase of behavioral response in the formalin test. METHODS: A microdialysis...

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Detalles Bibliográficos
Autores principales: Soleimannejad, E., Naghdi, N., Khatami, Sh., Semnanian, S., Fathollahi, Y.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Tehran University of Medical Sciences 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232082/
https://www.ncbi.nlm.nih.gov/pubmed/22615590
Descripción
Sumario:BACKGROUND AND THE PURPOSE OF THE STUDY: The hippocampal formation is involved in nociception. Prenatal serotonin depletion results in a significant decrease in the concentration of nociceptive sensitivity during the second phase of behavioral response in the formalin test. METHODS: A microdialysis probe was inserted via a guide cannula into the right CA1 region of the hippocampus. Extracellular serotonin (5HT) and its 5- hydroxyindoleacetic acid (5HIAA) metabolite overflow were collected every 10 min during the formalin test and measured by HPLC with electrochemichal detector. RESULTS: Compared to the sham group, formalin injection in the hind paw of the rat significantly increased 5HT after 10, 30, 40, and 50 min and increased 5HIAA after 10, 30, 40, 50, and 60 min collection time periods in hippocampal dialysate. (n=6 for each group at each sampling time). In the formalin treated rats serotonin and 5HIAA concentrations increased in the biphasic pattern in concert with the first and second phases of formalin pain. CONCLUSION: The hippocampal formation might be involved in the processing of nociceptive information and serotonin-related mechanisms in the hippocampus may play a role in the biphasic behavioral responses to formalin noxious stimulation.