Effects of Fluoxetine on Sodium Currents in Rat Sensory Neurons
Journal of the Korean Neurological Association
;
: 754-763, 2000.
Artículo
en Coreano
| WPRIM
| ID: wpr-193159
ABSTRACT
BACKGROUND:
Fluoxetine, a widely used antidepressant drug, has been described as a selective serotonin reuptake inhibitor. In addition to its antidepressant action it has been demonstrated to be effective in alleviating pain associated with various diseases. Dorsal root ganglion (DRG) neurons are primary sensory neurons and transmit peripheral information to central nervous system. Two types of sodium channels are expressed in DRG neurons based on their sensitivity to tetrodotoxin. They are involved in the generation and conduction of nociception. The effects of fluoxetine on sodium currents in DRG neurons were examined to elucidate the analgesic mechanism of the drug.METHODS:
DRG neurons wereacutely dissociated from rats (2~6 days postnatal) by enzymatic digestion. The whole-cell configuration of patch clamp technique was used to record tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) sodium currents.RESULTS:
Fluoxetine inhibited TTX-S and TTX-R sodium currents with Kd values of 60 microM and 59 microM, respectively, at the holding potential of -80 mV. For both types of sodium channels the steady-state inactivation curves were shifted in the hyperpolarizing direction and the conductance-voltage relationship curves were shifted in the depolarizing direction by fluoxetine. These effects combined together would greatly reduce the neuronal excitability.CONCLUSIONS:
The blockade of sodium currents in sensory neurons is considered as a possible mechanism for the analgesic action of fluoxetine.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Células Receptoras Sensoriales
/
Sodio
/
Tetrodotoxina
/
Canales de Sodio
/
Serotonina
/
Sistema Nervioso Central
/
Fluoxetina
/
Grupos Diagnósticos Relacionados
/
Digestión
/
Nocicepción
Límite:
Animales
Idioma:
Coreano
Revista:
Journal of the Korean Neurological Association
Año:
2000
Tipo del documento:
Artículo
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