https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Calretinin positive neurons form an excitatory amplifier network in the spinal cord dorsal horn https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45274 Wed 26 Oct 2022 20:10:58 AEDT ]]> Spinoparabrachial projection neurons form distinct classes in the mouse dorsal horn https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46481 Wed 24 May 2023 13:04:59 AEST ]]> Gabapentin modulates HCN4 channel voltage-dependence https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30562 h in brain slice experiments. However, evidence showing that GBP directly modulates HCN channels is lacking. The effect of GBP was tested using two-electrode voltage clamp recordings from human HCN1, HCN2, and HCN4 channels expressed in Xenopus oocytes. Whole-cell recordings were also made from mouse spinal cord slices targeting either parvalbumin positive (PV+) or calretinin positive (CR+) inhibitory neurons. The effect of GBP on Ih was measured in each inhibitory neuron population. HCN4 expression was assessed in the spinal cord using immunohistochemistry. When applied to HCN4 channels, GBP (100 μM) caused a hyperpolarizing shift in the voltage of half activation (V1/2) thereby reducing the currents. Gabapentin had no impact on the V1/2 of HCN1 or HCN2 channels. There was a robust increase in the time to half activation for HCN4 channels with only a small increase noted for HCN1 channels. Gabapentin also caused a hyperpolarizing shift in the V1/2 of Ih measured from HCN4-expressing PV+ inhibitory neurons in the spinal dorsal horn. Gabapentin had minimal effect on Ih recorded from CR+ neurons. Consistent with this, immunohistochemical analysis revealed that the majority of CR+ inhibitory neurons do not express somatic HCN4 channels. In conclusion, GBP reduces HCN4 channel-mediated currents through a hyperpolarized shift in the V1/2. The HCN channel subtype selectivity of GBP provides a unique tool for investigating HCN4 channel function in the central nervous system. The HCN4 channel is a candidate molecular target for the acute analgesic and anticonvulsant actions of GBP.]]> Wed 11 Apr 2018 16:01:42 AEST ]]> The search for novel analgesics: re-examining spinal cord circuits with new tools https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18904 Wed 11 Apr 2018 10:50:42 AEST ]]> Altered Intrinsic Properties and Inhibitory Connectivity in Aged Parvalbumin-Expressing Dorsal Horn Neurons https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45401 Thu 27 Oct 2022 17:29:15 AEDT ]]> Diversity of inhibitory and excitatory parvalbumin interneuron circuits in the dorsal horn https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45783 Sat 05 Nov 2022 12:42:10 AEDT ]]> Calretinin-expressing islet cells are a source of pre- and post-synaptic inhibition of non-peptidergic nociceptor input to the mouse spinal cord https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53289 Mon 27 Nov 2023 15:51:04 AEDT ]]> Channelrhodopsin-2 Assisted Circuit Mapping in the Spinal Cord Dorsal Horn https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50957 Mon 14 Aug 2023 15:10:54 AEST ]]>