Australian and New Zealand universities commenced a new academic year in February/March 2020 largely with “business as usual.” The subsequent Covid‐19 pandemic imposed unexpected disruptions to anatomical educational practice. Rapid change occurred due to government‐imposed physical distancing regulations from March 2020 that increasingly restricted anatomy laboratory teaching practices. Anatomy educators in both these countries were mobilized to adjust their teaching approaches. This study on anatomy education disruption at pandemic onset within Australia and New Zealand adopts a social constructivist lens. The research question was “What are the perceived disruptions and changes made to anatomy education in Australia and New Zealand during the initial period of the Covid‐19 pandemic, as reflected on by anatomy educators?.” Thematic analysis to elucidate “the what and why” of anatomy education was applied to these reflections. About 18 anatomy academics from ten institutions participated in this exercise. The analysis revealed loss of integrated “hands‐on” experiences, and impacts on workload, traditional roles, students, pedagogy, and anatomists' personal educational philosophies. The key opportunities recognized for anatomy education included: enabling synchronous teaching across remote sites, expanding offerings into the remote learning space, and embracing new pedagogies. In managing anatomy education's transition in response to the pandemic, six critical elements were identified: community care, clear communications, clarified expectations, constructive alignment, community of practice, ability to compromise, and adapt and continuity planning. There is no doubt that anatomy education has stepped into a yet unknown future in the island countries of Australia and New Zealand.

Duchenne muscular dystrophy (DMD) is the second most commonly occurring genetically inherited disease in humans. It is an X-linked condition that affects approximately one in 3300 live male births. It is caused by the absence or disruption of the protein dystrophin, which is found in a variety of tissues, most notably skeletal muscle and neurones in particular regions of the CNS. Clinically DMD is characterized by a severe pathology of the skeletal musculature that results in the premature death of the individual. An important aspect of DMD that has received less attention is the role played by the absence or disruption of dystrophin on CNS function. In this review we concentrate on insights into this role gained from investigation of boys with DMD and the genetically most relevant animal model of DMD, the dystrophin-deficient mdx mouse. Behavioural studies have shown that DMD boys have a cognitive impairment and a lower IQ (average 85), whilst the mdx mice display an impairment in passive avoidance reflex and in short-term memory. In DMD boys, there is evidence of disordered CNS architecture, abnormalities in dendrites and loss of neurones, all associated with neurones that normally express dystrophin. In the mdx mouse, there have been reports of a 50% decrease in neurone number and neural shrinkage in regions of the cerebral cortex and brainstem. Histological evidence shows that the density of GABA(A) channel clusters is reduced in mdx Purkinje cells and hippocampal CA1 neurones. At the biochemical level, in DMD boys the bioenergetics of the CNS is abnormal and there is an increase in the levels of choline-containing compounds, indicative of CNS pathology. The mdx mice also display abnormal bioenergetics, with an increased level of inorganic phosphate and increased levels of choline-containing compounds. Functionally, DMD boys have EEG abnormalities and there is some preliminary evidence that synaptic function is affected adversely by the absence of dystrophin. Electrophysiological studies of mdx mice have shown that hippocampal neurones have an increased susceptibility to hypoxia. These recent findings on the role of dystrophin in the CNS have implications for the clinical management of boys with DMD.

We demonstrated that the susceptibility of skeletal muscle to injury from lengthening contractions in the dystrophin-deficient mdx mouse is directly linked with the extent of fiber branching within the muscles and that both parameters increase as the mdx animal ages. We subjected isolated extensor digitorum longus muscles to a lengthening contraction protocol of 15% strain and measured the resulting drop in force production (force deficit). We also examined the morphology of individual muscle fibers. In mdx mice 1-2 mo of age, 17% of muscle fibers were branched, and the force deficit of 7% was not significantly different from that of age-matched littermate controls. In mdx mice 6-7 mo of age, 89% of muscle fibers were branched, and the force deficit of 58% was significantly higher than the 25% force deficit of age-matched littermate controls. These data demonstrated an association between the extent of branching and the greater vulnerability to contraction-induced injury in the older fast-twitch dystrophic muscle. Our findings demonstrate that fiber branching may play a role in the pathogenesis of muscular dystrophy in mdx mice, and this could affect the interpretation of previous studies involving lengthening contractions in this animal.

The human brain contains two major cell populations, neurons and glia. While neurons are electrically excitable and capable of discharging short voltage pulses known as action potentials, glial cells are not. However, astrocytes, the prevailing subtype of glia in the cortex, are highly connected and can modulate the excitability of neurons by changing the concentration of potassium ions in the extracellular environment, a process called K clearance. During the past decade, astrocytes have been the focus of much research, mainly due to their close association with synapses and their modulatory impact on neuronal activity. It has been shown that astrocytes play an essential role in normal brain function including: nitrosative regulation of synaptic release in the neocortex, synaptogenesis, synaptic transmission and plasticity. Here, we discuss the role of astrocytes in network modulation through their K clearance capabilities, a theory that was first raised 50 years ago by Orkand and Kuffler. We will discuss the functional alterations in astrocytic activity that leads to aberrant modulation of network oscillations and synchronous activity.

In the last decade several groups have been developing vision prostheses to restore visual perception to the profoundly blind. Despite some promising results from human trials, further understanding of the neural mechanisms involved is crucial for improving the efficacy of these devices. One of the techniques involves placing stimulating electrodes in the subretinal space between the photoreceptor layer and the pigment epithelium to evoke neural responses in the degenerative retina. This study used cell-attached and whole cell current-clamp recordings to investigate the responses of rabbit retinal ganglion cells (RGCs) following subretinal stimulation with 25-mum-diameter electrodes. We found that direct RGC responses with short latency (

With increasing research advances and clinical trials of visual prostheses, there is significant demand to better understand the perceptual and psychophysical aspects of prosthetic vision. In prosthetic vision a visual scene is composed of relatively large, isolated, spots of light so-called "phosphenes", very much like a magnified pictorial print. The utility of prosthetic vision has been studied by investigators in the form of virtual-reality visual models (simulations) of prosthetic vision administered to normally sighted subjects. In this review, the simulations from these investigations are examined with respect to how they visually render the phosphenes and the virtual-reality apparatus involved. A comparison is made between these simulations and the actual descriptions of phosphenes reported from human trials of visual prosthesis devices. For the results from these simulation studies to be relevant to the experience of visual prosthesis recipients, it is important that, the simulated phosphenes must be consistent with the descriptions from human trials. A standardized simulation and reporting framework is proposed so that future simulations may be configured to be more realistic to the experience of implant recipients, and the simulation parameters from different investigators may be more readily extracted, and study results more fittingly compared.

This paper presents the results of the first investigations into the use of bipolar electrical stimulation of the retina with a suprachoroidal vision prosthesis, and the effects of different electrode configurations on localization of responses on the primary visual cortex. Cats were implanted with electrodes in the suprachoroidal space, and electrically evoked potentials were recorded on the visual cortex. Responses were elicited to bipolar and monopolar stimuli, with each stimulating electrode coupled with either six-return electrodes, two-return electrodes, or a single-return electrode. The average charge threshold to elicit a response with bipolar stimulation and six-return electrodes was 76.47+/-8.76 nC. Bipolar stimulation using six-return electrodes evoked responses half the magnitude of those elicited with a single or two-return electrodes. Monopolar stimulation evoked a greater magnitude, and area of cortical activation than bipolar stimulation. This study showed that suprachoroidal, bipolar stimulation can elicit localized activity in the primary visual cortex, with the extent of localization and magnitude of response dependent on the electrode configuration.

Human subjects were required to differentiate grating surfaces of alternating grooves and ridges by moving a finger back and forth across the surface. Their discriminative capacities were measured, as well as the movement and force profiles that they selected. To measure discrimination, a forced choice paradigm was used in which three surfaces were presented on each trial. Two surfaces were the same (standards) and the subject was required to indicate which of the three surfaces (the comparison) differed from the other two. Two series of surfaces were used with standards whose spatial periods were 770 and 1002 mu, respectively. Subjects were able to discriminate, at the 75% correct level, two gratings which differed in spatial period by the order of 5%. When tangential movement between the surface and the finger was eliminated, and only radial contact permitted, discrimination was degraded and the 75% correct levels increased to the order of 10%. Subjects were free to choose their own patterns of finger movement and of contact force between finger and surface. Movement was measured cinematographically. For all subjects movement patterns were close to sinusoidal, with frequencies in the range of 4.0 Hz and with mean velocities of the order of 160 mm/s. Patterns of contact force were measured by a force transducer. For all subjects the force varied rhythmically in synchrony with movement, but the patterns and magnitudes varied with the subject. Gratings were scaled for perceived roughness by a magnitude estimation technique: the relationship between perceived roughness and grating period was monotonic.