https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45274 Wed 26 Oct 2022 20:10:58 AEDT ]]> https://ogma.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 I_h 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 (V_1/2) thereby reducing the currents. Gabapentin had no impact on the V_1/2 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 V_1/2 of I_h measured from HCN₄-expressing PV⁺ inhibitory neurons in the spinal dorsal horn. Gabapentin had minimal effect on I_h 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 V_1/2. 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 ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41419 Wed 03 Aug 2022 11:59:22 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34545 GlyT2^GFP and GAD67^GFP mice showed the majority of inhibitory LDPNs project either ipsilaterally or adjacent to the midline. Additionally, we used several transgenic mouse lines to define the developmental provenance of LDPNs and found that V2b positive neurons form a subset of ipsilaterally projecting LDPNs. Finally, a population of Neurobiotin (NB) labelled LDPNs were assessed in detail to examine morphology and plot the spatial distribution of contacts from a variety of neurochemically distinct axon terminals. These results provide important baseline data in mice for future work on their role in locomotion and recovery from SCI.]]> Tue 03 Sep 2019 18:26:15 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45038 Thu 27 Oct 2022 13:52:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45783 Sat 05 Nov 2022 12:42:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53289 Mon 27 Nov 2023 15:51:04 AEDT ]]>