https://nova.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:41131 Wed 27 Jul 2022 11:10:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45274 Wed 26 Oct 2022 20:10:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:46481 Wed 24 May 2023 13:04:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:429 Wed 22 Mar 2023 16:05:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:31446 Wed 11 Apr 2018 17:23:06 AEST ]]> 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 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://nova.newcastle.edu.au/vital/access/manager/Repository/uon:30241 Wed 11 Apr 2018 14:56:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:27947 Wed 11 Apr 2018 14:50:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:27443 Wed 11 Apr 2018 14:01:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14215 Wed 11 Apr 2018 13:17:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:13807 2 wk after inflammation). Blinded outcomes were used in 42% studies, randomization in 10%, and evidence of visceral inflammation in 54%. Only 3 studies fulfilled our criteria for high methodological quality, and no study reported sample size calculations. Conclusions: The included studies provide strong evidence for CNS plasticity following GIT inflammation, specifically in the spinal cord dorsal horn. This evidence includes altered visceromotor responses and indices of referred pain, elevated neural activation and peptide content, and increased neuronal excitability. This evidence supports continued use of this approach for preclinical studies; however, there is substantial scope to improve study design.]]> Wed 11 Apr 2018 12:29:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:15919 Wed 11 Apr 2018 10:53:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:7526 Wed 11 Apr 2018 10:11:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:11242 Wed 11 Apr 2018 10:02:02 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:34069 in vivo preparation and patch-clamp electrophysiology to test whether the synaptic and intrinsic properties of superficial dorsal horn (SDH) neurons are altered 5 days after the induction of mild colitis in adult male mice (i.e. during acute inflammation of the colon). Whole-cell recordings were made from lumbosacral (L6-S1) superficial dorsal horn neurons (SDH), in animals under isoflurane anesthesia. Noxious colorectal distension (CRD) was used to identify SDH neurons with colonic inputs, while stimulation of the hind paw and tail was employed to assess convergent cutaneous input. Following inflammation, a significantly increased proportion of SDH neurons received both colonic and cutaneous inputs, compared to neurons in naïve animals. In addition, the nature and magnitude of responses to CRD and cutaneous stimulation differed in inflamed animals, as was spontaneous excitatory synaptic drive. Conversely, several measures of intrinsic excitability were altered in a manner that would decrease SDH network excitability following colitis. We propose that during inflammation, sensitization of colonic afferents results in increased signaling to the SDH. This is accompanied by plasticity in SDH neurons whereby their intrinsic properties are changed to compensate for altered afferent activity.]]> Wed 06 Feb 2019 09:51:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:47016 Tue 13 Dec 2022 12:23:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45401 Thu 27 Oct 2022 17:29:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:7485 Sat 24 Mar 2018 08:40:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:1748 Sat 24 Mar 2018 08:27:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:12708 Sat 24 Mar 2018 08:16:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:11388 Sat 24 Mar 2018 08:10:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:20373 Sat 24 Mar 2018 07:58:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:5822 Sat 24 Mar 2018 07:48:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:5804 Sat 24 Mar 2018 07:44:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:28641 Sat 24 Mar 2018 07:37:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:181 FOG > SO, and slow-twitch always > slow-tonic. In terms of weighted cross-sectional area, which provides a coarse-grain measure of each fiber type's potential contribution to whole muscle force, all five muscles exhibited a higher Fg and lower SO contribution to cross-sectional area than suggested by their corresponding fiber-type prevalence. This was also the case for the slow-twitch vs. slow-tonic fibers. We conclude that slow-tonic fibers are widespread in turtle muscle. The weighted cross-sectional area evidence suggested, however, that their contribution to force generation is minor except in highly oxidative muscles, with a special functional role, like TeC4. There is discussion of: 1) the relationship between the present results and previous work on homologous neck and hindlimb muscles in other nonmammalian species, and 2) the potential motoneuronal innervation of slow-tonic fibers in turtle hindlimb muscles. (c) 2005 Wiley-Liss, Inc.]]> Mon 24 Sep 2018 16:14:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:36538 Fri 29 May 2020 17:22:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:46131 Fri 11 Nov 2022 15:28:57 AEDT ]]>