In humans, a similar method could be applied to
block pain neurons from releasing microRNA - 21 in particles, which would prevent neuropathic pain from ocurring.
Not exact matches
When the researchers selectively
blocked prostaglandin synthesis in
neurons, mice displayed reduced aversive responses to inflammation - induced
pain.
Therefore we hope that these induced sensory
neurons will allow our group and others to identify new compounds that
block pain and itch and to better understand and treat neurodegenerative disease and spinal cord injury.»
The model showed that the sodium channels 1.6 in the feeling sensory
neurons were
blocked with 670 microamperes, but the
pain neuron's sodium channels 1.7 were
blocked at only 290 microamperes.
Fridman and Guan realized that the
pain and «feeling» sensory
neurons each contained different kinds of sodium channels and that it may be possible to
block one kind of channel and not the others to prevent patients from feeling
pain but not other sensations.
The current at 0.8 milliamperes completely
blocked the response of the
pain - transmitting
neurons.
After the current was stopped, the signal from the
pain - transmitting
neurons remained
blocked for another two minutes, whereas the signal from the feeling sensory
neurons quickly came back.
«We also found that because the
pain neurons take longer to come back on line, we may be able to conserve energy and not have to deliver this electrical current constantly to keep them
blocked.»
The authors showed that when they
blocked DRG
pain neurons from releasing microRNA - 21 in particles, this had an anti-inflammatory effect at a cellular level, which prevented neuropathic
pain from occurring in mice.
Knockdown of sodium channel Na < sub > V 1.6
blocks mechanical
pain and abnormal bursting activity of afferent
neurons in inflamed sensory ganglia.