https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28034 Wed 11 Apr 2018 16:26:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17099 Wed 11 Apr 2018 12:33:25 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:33101 Wed 09 Feb 2022 15:58:21 AEDT ]]> 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:48765 Wed 05 Apr 2023 13:55:44 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7708 Sat 24 Mar 2018 08:41:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7900 Sat 24 Mar 2018 08:35:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7625 Sat 24 Mar 2018 08:34:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7695 Sat 24 Mar 2018 08:33:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1388 Sat 24 Mar 2018 08:28:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15635 +) or drug non-availability (S⁻). Once a stable level of responding was reached, lever pressing was extinguished. Animals were then tested for reinstatement and sacrificed immediately following the presentation of either the S⁻ or S⁺ discriminative stimuli, and Fos-protein expression was assessed in thalamic and epithalamic regions. Interestingly, significant variation was observed in reinstatement behaviour, allowing a comparison between high-reinstating (HR), low-reinstating (LR) and control animals. Compared with LR animals, HR animals exhibited increased Fos-protein expression in the PVT, intermediodorsal thalamus and the medial and lateral divisions of the habenula. Our data provide evidence that activation of thalamic and epithalamic nuclei is associated with propensity to reinstate to cocaine-seeking elicited by drug-related cues. We also build upon existing data highlighting the importance of the PVT in reinstatement behaviour.]]> Sat 24 Mar 2018 08:23:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11329 Sat 24 Mar 2018 08:12:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11513 Sat 24 Mar 2018 08:11:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10380 Sat 24 Mar 2018 08:08:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11118 Sat 24 Mar 2018 08:07:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20245 200 cpm) from 25 ± 3% to 9 ± 2% (p = 0.004). Thus, reduction of the mean respiratory rate by LiCl was predominantly due to reduced contribution of high-frequency breathing that is normally associated with motor activity and/or arousal. Non-linear multifractal analysis of respiratory signals revealed that post-LiCl, respiration becomes less random and more orderly. 5-HT3 antagonist ondansetron prevented respiratory changes elicited by LiCl. We conclude that the observed changes likely reflect effects of LiCl on animals’ motion, and that this effect is mediated via 5-HT3 receptors. Providing that the effects observed in our study were quite robust, we suggest that simple and non-invasive respiratory monitoring may be a promising approach for studying emesis in rodents.]]> Sat 24 Mar 2018 07:59:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20260 Sat 24 Mar 2018 07:59:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25275 Sat 24 Mar 2018 07:38:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22704 Sat 24 Mar 2018 07:15:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24319 in vivo preparation to make patch-clamp recordings from superficial dorsal horn (SDH) neurons receiving colonic inputs in naïve male mice. Recordings were made in the lumbosacral spinal cord (L6-S1) under isoflurane anesthesia. Noxious colorectal distension (CRD) was used to determine whether SDH neurons received inputs from mechanical stimulation/distension of the colon. Responses to hind paw/tail cutaneous stimulation and intrinsic and synaptic properties were also assessed, as well as action potential discharge properties. Approximately 11% of lumbosacral SDH neurons in the cohort of neurons sampled responded to CRD and a majority of these responses were subthreshold. Most CRD-responsive neurons (80%) also responded to cutaneous stimuli, compared with <50% of CRD-non-responsive neurons. Furthermore, CRD-responsive neurons had more hyperpolarized resting membrane potentials, larger rheobase currents, and reduced levels of excitatory drive, compared to CRD-non-responsive neurons. Our results demonstrate that CRD-responsive neurons can be distinguished from CRD-non-responsive neurons by several differences in their membrane properties and excitatory synaptic inputs. We also demonstrate that SDH neurons with colonic inputs show predominately subthreshold responses to CRD and exhibit a high degree of viscerosomatic convergence.]]> Sat 24 Mar 2018 07:14:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23144 mut), a model of a rare type of hereditary hemochromatosis, relative to wildtype control mice. The results were compared with our previous findings in dietary iron-supplemented wildtype mice and Hfe^−/− mice, a model of a common type of hereditary hemochromatosis. For transcripts showing significant changes relative to controls across all three models, there was perfect (100%) directional concordance (i.e. transcripts were increased in all models or decreased in all models). Comparison of the two models of hereditary hemochromatosis, which showed more pronounced changes than the dietary iron-supplemented mice, revealed numerous common molecular effects. Pathway analyses highlighted changes for genes relating to long-term depression (6.8-fold enrichment, p = 5.4 × 10⁻⁷) and, to a lesser extent, long-term potentiation (3.7-fold enrichment, p = 0.01), with generalized reductions in transcription of key genes from these pathways, which are involved in modulating synaptic strength and efficacy and are essential for memory and learning. The agreement across the models suggests the findings are robust and strengthens previous evidence that iron loading disorders affect the brain. Perturbations of brain phenomena such as long-term depression and long-term potentiation might partly explain neurologic symptoms reported for some hemochromatosis patients.]]> Sat 24 Mar 2018 07:10:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43587 Mon 26 Sep 2022 13:48:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43040 Mon 12 Sep 2022 12:10:20 AEST ]]>