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Inflammation is known to be responsible for the sensitization of peripheral sensory neurons, leading to spontaneous pain and invalidating pain hypersensitivity. Given its role in regulating neuronal excitability, the voltage-gated Nav1.9 channel is a potential target for the treatment of pathological pain, but its implication in inflammatory pain is yet not(More)
Voltage-gated Na(+) channels (Nav) are the targets of a variety of scorpion toxins. Here, we investigated the effects of Amm VIII, a toxin isolated from the venom of the scorpion Androctonus mauretanicus mauretanicus, on pain-related behaviours in mice. The effects of Amm VIII were compared with the classic scorpion α-toxin AaH II from Androctonus(More)
Physical contact with the external world occurs through specialized neural structures called mechanoreceptors. Cutaneous mechanoreceptors provide information to the central nervous system (CNS) about touch, pressure, vibration, and skin stretch. The physiological function of these mechanoreceptors is to convert physical forces into neuronal signals. Key(More)
Cold-triggered pain is essential to avoid prolonged exposure to harmfully low temperatures. However, the molecular basis of noxious cold sensing in mammals is still not completely understood. Here, we show that the voltage-gated Nav1.9 sodium channel is important for the perception of pain in response to noxious cold. Nav1.9 activity is upregulated in a(More)
(A) Latency to flinches or paw rubbing observed in Nav1.9 +/+ and Nav1.9-/-mice littermates placed on a cold plate set at 0 or 6°C. n = 7 at 0°C, n = 10 at 6°C. (B) Number of flinches observed in Nav1.9 +/+ and Nav1.9-/-mice littermates placed on a cold plate set at 0°C for 5 min. n = 6 (+/+), n = 8 (-/-), unpaired t test. Error bars correspond to standard(More)
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