9 research outputs found

    Virtual Reality in Higher Education

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    Virtual reality (VR) is an interactive experience which immerses the user in a digital environment through a sense of presence. In the context of providing an active learning experience, virtual reality has the potential to improve learning outcomes for biomedical science students as it allows the visualisation of and interaction with digital representations of dynamic objects and complex concepts. Studies in bioscience and medical education have shown mixed results pertaining to the benefits of VR as a learning tool. This review aims to consolidate how VR succeeded or failed in improving learning outcomes, and assesses the issue of VR scalability for the ever-growing cohorts in tertiary bioscience courses

    Neurokinin-1 receptors modulate the excitability of expiratory neurons in the ventral respiratory group

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    We studied the role of neurokinin-1 receptors (NK1-R) on the excitability of expiratory (E) neurons (tonic discharge, E(TONIC); augmenting, E(AUG); decrementing, E(DEC)) throughout the ventral respiratory group, including B�tzinger Complex (B�tC) using extracellular single-unit recording combined with pressurized picoejection in decerebrate, arterially perfused juvenile rats. Responses evoked by picoejection of the NK1-R agonist, [Sar9-Met(O2)11]-substance P (SSP) were determined before and after the selective NK1-R antagonist, CP99,994. SSP excited 20 of 35 expiratory neurons by increasing the number of action potentials per burst (+33.7 +/- 6.5% of control), burst duration (+20.6 +/- 7.9% of control), and peak firing frequency (+16.2 +/- 4.8% of control; means +/- SE). Pretreatment with CP99,994 completely blocked SSP-evoked excitation in a subset of neurons tested, supporting the notion that SSP excitation was mediated through NK1-R activation. Because we had previously shown that E(AUG) neurons were crucial to locomotor-respiratory coupling (LRC), we reasoned that blockade of NK1-R would alter LRC by preventing somatic-evoked excitation of E(AUG) neurons. Blockade of NK1-Rs by CP99,994 in the B�tC severely disrupted LRC and prevented somatic-evoked excitation of E(AUG) neurons. These findings demonstrate that LRC is dependent on endogenous SP release acting via NK1-Rs on E(AUG) neurons of the B�tC. Taken together with our earlier finding that inspiratory off-switching by the Hering-Breuer Reflex requires endogenous activation of NK1-Rs through activation of NK1-Rs on E(DEC) neurons, we suggest that endogenous release of substance P in the B�tC provides a reflex pathway-dependent mechanism to selectively modulate respiratory rhythm.15 page(s

    Neurokinin-1 receptor activation in the Botzinger complex evokes bradypnea and is involved in mediating the Hering-Breuer reflex

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    The role of substance P (SP) and its receptor, the neurokinin-1 (NK1R), in the generation of respiratory rhythm has received considerable attention, particularly at the Pre-Bötzinger Complex of the ventral respiratory group (VRG). However, the functional role of SP and NK1R in other VRG regions has not been explored in detail. We review the current literature and describe recent data demonstrating that selective activation of NK1R in the Bötzinger Complex (BötC) of the VRG evoked bradypnea by lengthening expiratory period. In addition, endogenous activation of NK1R in the BötC participates in the expiratory lengthening effect of the Hering-Breuer reflex. These data suggest that NK1R expressing neurons in different subregions of the VRG have functionally diverse roles and provide new insight on the modulatory role of SP on respiratory reflexes.5 page(s

    Expression of Group I metabotropic glutamate receptors on phenotypically different cells within the nucleus of the solitary tract in the rat

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    Group I metabotropic glutamate receptors (mGluRs) are G-coupled receptors that modulate synaptic activity. Previous studies have shown that Group I mGluRs are present in the nucleus of the solitary tract (NTS), in which many visceral afferents terminate. Microinjection of selective Group I mGluR agonists into the NTS results in a depressor response and decrease in sympathetic nerve activity. There is, however, little evidence detailing which phenotypes of neurons within the NTS express Group I mGluRs. In brainstem slices, we performed immunohistochemical localization of Group I mGluRs and either glutamic acid decarboxylase 67 kDa isoform (GAD67), neuronal nitric oxide synthase (nNOS) or tyrosine hydroxylase (TH). Fluoro-Gold (FG, 2%; 15 nl) was microinjected in the caudal ventrolateral medulla (CVLM) of the rat to retrogradely label NTS neurons that project to CVLM. Group I mGluRs were distributed throughout the rostral-caudal extent of the NTS and were found within most NTS subregions. The relative percentages of Group I mGluR expressing neurons colabeled with the different markers were FG (6.9+/-0.7) nNOS (5.6+/-0.9), TH (3.9+/-1.0), and GAD67 (3.1+/-1.4). The percentage of FG containing cells colabeled with Group I mGluR (13.6+/-2.0) was greater than the percent colabeled with GAD67 (3.1+/-0.5), nNOS (4.7+/-0.5), and TH (0.1+/-0.08). Cells triple labeled for FG, nNOS, and Group I mGluRs were identified in the NTS. Thus, these data provide an anatomical substrate by which Group I mGluRs could modulate activity of CVLM projecting neurons in the NTS.16 page(s
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