TRPV2 is required for mechanical nociception and the stretch-evoked response of primary sensory neurons.
Sci Rep
; 8(1): 16782, 2018 11 14.
Article
em En
| MEDLINE
| ID: mdl-30429536
ABSTRACT
Mechanotransduction plays important roles in many sensory processes, including touch, pain, hearing, and proprioception. However, the molecular mechanisms of mechanical nociception have remained unclear. Here, we showed that elimination of transient receptor potential vanilloid 2 (TRPV2) in mice resulted in the deficit of mechanical nociception due to the lack of mechanosensitivity in a subclass of adult primary sensory neurons (PSNs). The PSN-specific TRPV2-deficient mice showed behavioural impairment of mechanical nociception in tail-pressure and von Frey hair tests, without defects in axonal growth and neuronal composition. Conversely, the mice displayed normal behaviour to noxious heat and non-noxious tactile stimuli. Furthermore, based on the stretch-evoked Ca2+ response of cultured PSNs, we characterised two types of stretch-activated neurons in normal mice; fast-decay high-threshold and slow-decay low-threshold mechanosensitive. The cultured neurons from TRPV2-deficient mice lacked stretch-evoked Ca2+ responses by fast-decay neurons normally activated by high-threshold mechanical stimulation. These results demonstrated that TRPV2 has a critical role in mechanical nociception in the adult somatosensory system.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Células Receptoras Sensoriais
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Canais de Cálcio
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Mecanotransdução Celular
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Canais de Cátion TRPV
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Nociceptividade
Limite:
Animals
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article