Abstract
Chronic pain affects 1 in 5 New Zealanders costing our society approximately $14 billion in 2016. Opioids are used to treat chronic pain but show poor long-term efficacy and high rates of addiction. Innovations for effective, personalised chronic pain treatments are desperately needed. Aberrant pain signalling, arising from disinhibition of spinal cord pain projection neurons, is proposed to underlie chronic pain. Altered chloride transporter expression in these neurons disrupts their chloride balance eroding the effectiveness of inhibitory input. We propose that expressing and activating the light-activated chloride channel Guillardia theta anion channel rhodopsin 2 (GtACR2) in spinal cord pain projection neurons will restore their chloride balance, re-establish inhibition, and reduce pain. Here, we produced a lentiviral vector encoding a red fluorescence tagged GtACR2 construct and confirmed its expression and function in vitro.