A Central Amygdala Input to the Parafascicular Nucleus Controls Comorbid Pain in Depression.
Cell Rep
; 29(12): 3847-3858.e5, 2019 12 17.
Article
en En
| MEDLINE
| ID: mdl-31851918
ABSTRACT
While comorbid pain in depression (CP) occurs at a high rate worldwide, the neural connections underlying the core symptoms of CP have yet to be elucidated. Here, we define a pathway whereby GABAergic neurons from the central nucleus of the amygdala (GABACeA) project to glutamatergic neurons in the parafascicular nucleus (GluPF). These GluPF neurons relay directly to neurons in the second somatosensory cortex (S2), a well-known area involved in pain signal processing. Enhanced inhibition of the GABACeAâGluPFâS2 pathway is found in mice exhibiting CP symptoms. Reversing this pathway using chemogenetic or optogenetic approaches alleviates CP symptoms. Together, the current study demonstrates the putative importance of the GABACeAâGluPFâS2 pathway in controlling at least some aspects of CP.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Dolor
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Corteza Somatosensorial
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Núcleos Talámicos Intralaminares
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Depresión
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Neuronas GABAérgicas
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Núcleo Amigdalino Central
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Vías Nerviosas
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
En
Año:
2019
Tipo del documento:
Article