Activation of dopamine D2 receptors attenuates neuroinflammation and ameliorates the memory impairment induced by rapid eye movement sleep deprivation in a murine model
Por:
Ugalde-Muniz, Perla, Hernandez-Luna, Maria Guadalupe, Garcia-Velasco, Stephany, Lugo-Huitron, Rafael, Murcia-Ramirez, Jimena, Martinez-Tapia, Ricardo Jesus, Noriega-Navarro, Roxana, Navarro, Luz
Publicada:
5 oct 2022
Categoría:
Neuroscience (miscellaneous)
Resumen:
The proinflammatory state, which may be induced by sleep deprivation,
seems to be a determining factor in the development of neurodegenerative
processes. Investigations of mechanisms that help to mitigate the
inflammatory effects of sleep disorders are important. A new proposal
involves the neurotransmitter dopamine, which may modulate the
progression of the immune response by activating receptors expressed on
immune cells. This study aimed to determine whether dopamine D2 receptor
(D2DR) activation attenuates the proinflammatory response derived from
rapid eye movement (REM) sleep deprivation in mice. REM sleep
deprivation (RSD) was induced in 2-month-old male CD1 mice using the
multiple platform model for three consecutive days; during this period,
the D2DR receptor agonist quinpirole (QUIN) was administered (2
mg/kg/day i.p.). Proinflammatory cytokine levels were assessed in serum
and homogenates of the brain cortex, hippocampus, and striatum using
ELISAs. Long-term memory deficits were identified using the Morris water
maze (MWM) and novel object recognition (NOR) tests. Animals were
trained until learning criteria were achieved; then, they were subjected
to RSD and treated with QUIN for 3 days. Memory evocation was determined
afterward. Moreover, we found RSD induced anhedonia, as measured by the
sucrose consumption test, which is commonly related to the dopaminergic
system. Our data revealed increased levels of proinflammatory cytokines
(TNF alpha and IL-1 beta) in both the hippocampus and serum from RSD
mice. However, QUIN attenuated the increased levels of these cytokines.
Furthermore, RSD caused a long-term memory evocation deficit in both the
MWM and NOR tests. In contrast, QUIN coadministration during the RSD
period significantly improved the performance of the animals. On the
other hand, QUIN prevented the anhedonic condition induced by RSD. Based
on our results, D2DR receptor activation protects against memory
impairment induced by disturbed REM sleep by inhibiting
neuroinflammation.
Filiaciones:
Ugalde-Muniz, Perla:
Laboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico
Univ Nacl Autonoma Mexico, Lab Neuroendocrinol, Dept Fisiol, Fac Med, Mexico City, DF, Mexico
Hernandez-Luna, Maria Guadalupe:
Laboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico
Univ Nacl Autonoma Mexico, Lab Neuroendocrinol, Dept Fisiol, Fac Med, Mexico City, DF, Mexico
Garcia-Velasco, Stephany:
Laboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico
Univ Nacl Autonoma Mexico, Lab Neuroendocrinol, Dept Fisiol, Fac Med, Mexico City, DF, Mexico
Lugo-Huitron, Rafael:
Laboratory of Behavioral Neurobiology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico
Univ Nacl Autonoma Mexico, Fac Med, Dept Fisiol, Lab Behav Neurobiol, Mexico City, DF, Mexico
Murcia-Ramirez, Jimena:
Laboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico
Univ Nacl Autonoma Mexico, Lab Neuroendocrinol, Dept Fisiol, Fac Med, Mexico City, DF, Mexico
Martinez-Tapia, Ricardo Jesus:
Laboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico
Univ Nacl Autonoma Mexico, Lab Neuroendocrinol, Dept Fisiol, Fac Med, Mexico City, DF, Mexico
Noriega-Navarro, Roxana:
Laboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico
Univ Nacl Autonoma Mexico, Lab Neuroendocrinol, Dept Fisiol, Fac Med, Mexico City, DF, Mexico
Navarro, Luz:
Laboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico
Univ Nacl Autonoma Mexico, Lab Neuroendocrinol, Dept Fisiol, Fac Med, Mexico City, DF, Mexico
Green Published, gold, Gold, Green
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