ORCID Profile
0000-0003-3285-0168
Current Organisation
University of Tasmania
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Publisher: Institute of Electrical and Electronics Engineers (IEEE)
Date: 2021
Publisher: SAGE Publications
Date: 04-1997
DOI: 10.3109/00048679709073830
Abstract: Objective: To provide an overview of the progress and prospects of transcranial magnetic stimulation as a psychiatric therapy for depression. Method: Published and unpublished studies of the usefulness of transcranial magnetic stimulation as a therapy for depression were assessed, and characterised in terms of a consistent measure of dosage. Additional information was obtained through correspondence, personal meetings and visits to facilities. Results: Transcranial magnetic stimulation, a means for inducing small regional currents in the brain, has been used in clinical neurology for some time, and can be used on conscious subjects with minimal side-effects. Early researchers noticed transient mood effects on people receiving this treatment, which prompted several inconclusive investigations of its effects on depressed patients. More recently, knowledge of functional abnormalities associated with depression has led to trials using repetitive transcranial magnetic stimulation to stimulate underactive left prefrontal regions, an approach which has produced short-term benefits for some subjects. The higher dosage delivered by high-frequency repetitive transcranial magnetic stimulation appears to produce greater benefits scope exists for more conclusive studies based on extended treatment periods. Conclusions: Repetitive transcranial magnetic stimulation is a promising technology. The reviewed evidence indicates that it may be useful in the treatment of depression, and perhaps other disorders which are associated with regional hypometabolism. Should repetitive transcranial magnetic stimulation prove an effective, non-invasive, drug-free treatment for depression, a range of disorders could be similarly treatable.
Publisher: Elsevier BV
Date: 09-2002
DOI: 10.1016/S0891-0618(02)00043-1
Abstract: The cellular localisation of neurofilament triplet subunits was investigated in the rat neocortex. A subset of mainly pyramidal neurons showed colocalisation of subunit immunolabelling throughout the neocortex, including labelling with the antibody SMI32, which has been used extensively in other studies of the primate cortex as a selective cellular marker. Neurofilament-labelled neurons were principally localised to two or three cell layers in most cortical regions, but dramatically reduced labelling was present in areas such as the perirhinal cortex, anterior cingulate and a strip of cortex extending from caudal motor regions through the medial parietal region to secondary visual areas. However, quantitative analysis demonstrated a similar proportion (10-20%) of cells with neurofilament triplet labelling in regions of high or low labelling. Combining retrograde tracing with immunolabelling showed that cellular content of the neurofilament proteins was not correlated with the length of projection. Double labelling immunohistochemistry demonstrated that neurofilament content in axons was closely associated with myelination. Analysis of SMI32 labelling in development indicated that content of this epitope within cell bodies was associated with relatively late maturation, between postnatal days 14 and 21. This study is further evidence of a cell type-specific regulation of neurofilament proteins within neocortical neurons. Neurofilament triplet content may be more closely related to the degree of myelination, rather than the absolute length, of the projecting axon.
Publisher: Elsevier BV
Date: 10-2016
DOI: 10.1016/J.JCHEMNEU.2016.05.006
Abstract: The physical structure of neurons - dendrites converging on the soma, with an axon conveying activity to distant locations - is uniquely tied to their function. To perform their role, axons need to maintain structural precision in the soft, gelatinous environment of the central nervous system and the dynamic, flexible paths of nerves in the periphery. This requires close mechanical coupling between axons and the surrounding tissue, as well as an elastic, robust axoplasm resistant to pinching and flattening, and capable of sustaining transport despite physical distortion. These mechanical properties arise primarily from the properties of the internal cytoskeleton, coupled to the axonal membrane and the extracellular matrix. In particular, the two large constituents of the internal cytoskeleton, microtubules and neurofilaments, are braced against each other and flexibly interlinked by specialised proteins. Recent evidence suggests that the primary function of neurofilament sidearms is to structure the axoplasm into a linearly organised, elastic gel. This provides support and structure to the contents of axons in peripheral nerves subject to bending, protecting the relatively brittle microtubule bundles and maintaining them as transport conduits. Furthermore, a substantial proportion of axons are myelinated, and this thick jacket of membrane wrappings alters the form, function and internal composition of the axons to which it is applied. Together these structures determine the physical properties and integrity of neural tissue, both under conditions of normal movement, and in response to physical trauma. The effects of traumatic injury are directly dependent on the physical properties of neural tissue, especially axons, and because of axons' extreme structural specialisation, post-traumatic effects are usually characterised by particular modes of axonal damage. The physical realities of axons in neural tissue are integral to both normal function and their response to injury, and require specific consideration in evaluating research models of neurotrauma.
Publisher: Elsevier BV
Date: 10-2013
DOI: 10.1016/J.NEUROBIOLAGING.2013.04.010
Abstract: Amyloid-β (Aβ) plaque accumulation in Alzheimer's disease (AD) is associated with glutamatergic synapse loss, but less is known about its effect on inhibitory synapses. Here, we demonstrate that vesicular γ-aminobutyric acid (GABA) transporter (VGAT) presynaptic bouton density is unaffected in human preclinical and end-stage AD and in APP/PS1 transgenic (TG) mice. Conversely, excitatory vesicular glutamate transporter 1 (VGlut1) boutons are significantly reduced in end-stage AD cases and less reduced in preclinical AD cases and TGs. Aged TGs also show reduced protein levels of VGlut1 and synaptophysin but not VGAT or glutamate decarboxylase (GAD). These findings indicate that GABAergic synapses are preserved in human AD and mouse TGs. Synaptosomes isolated from plaque-rich TG cortex had significantly higher GAD activity than those from plaque-free cerebellum or the cortex of wild-type littermates. Using tissue fractionation, this increased activity was localized to glial synaptosomes, suggesting that Aβ plaques stimulate increased astrocyte GABA synthesis.
Publisher: Public Library of Science (PLoS)
Date: 17-02-2012
Publisher: Springer Science and Business Media LLC
Date: 2011
Publisher: Mary Ann Liebert Inc
Date: 06-2019
Abstract: Traumatic brain injury (TBI) has been identified as a risk factor for Alzheimer's disease (AD). However, how such neural damage contributes to AD pathology remains unclear specifically, the relationship between the timing of a TBI relative to aging and the onset of AD pathology is not known. In this study, we have examined the effect of TBI on subsequent beta-amyloid (Aβ) deposition in APP/PS1 (APP
Publisher: IOP Publishing
Date: 04-2008
DOI: 10.1088/1741-2560/5/2/003
Abstract: Using a multi-channel platinum surface electrode array, recordings from cat primary visual cortex were obtained in response to visual stimuli, and electrical stimuli delivered using the elements of the array itself. Neural responses to electrical stimuli were consistent, regardless of stimulus polarity or leading phase (biphasic), although thresholds were lower for monophasic than biphasic pulses. Both visual and electrical stimuli reliably evoked responses with characteristic components, which interacted with each other in a nonlinear summation showing first facilitation then suppression during the window of interaction. The chronaxie for eliciting threshold cortical responses was about 100 mus, and the charge density with a pulse width of 50-100 mus was around 55 muC cm(-2). These data form the basis of understanding the types of cortical responses to stimuli delivered by devices suitable for chronic implantation.
Publisher: Ubiquity Press, Ltd.
Date: 06-11-2017
DOI: 10.5334/JORS.172
Publisher: Elsevier BV
Date: 2016
DOI: 10.1016/J.EXPNEUROL.2015.09.019
Abstract: Amyotrophic lateral sclerosis (ALS) is an adult onset neurodegenerative disease that results in motor dysfunction and death, generally from respiratory failure. 90% of ALS cases are sporadic with no known cause. Familial cases have been linked with mutations in several disparate classes of genes, including those involved in DNA/RNA metabolism, protein misfolding, oxidative stress and the cytoskeleton, leading to the proposition that ALS could be a multi-factorial disease. However, alterations in excitability have been reported in all types of ALS cases, and may be a common disease mechanism predisposing neurons to degeneration. Excitotoxicity has long been suspected as a mediator in the disease process, and may arise from changes in synaptic inputs, or alterations in the excitability of the neurons being stimulated. Although the glutamatergic system is widely recognised as a therapeutic avenue with the potential to extend lifespan and delay disease onset, the causes of altered excitability in ALS are currently unclear and warrant further investigation. This article reviews current evidence of alterations to excitatory and inhibitory signalling in the cortex and spinal cord, and in the intrinsic excitability of motor neurons, in ALS.
Publisher: Springer Science and Business Media LLC
Date: 03-03-2010
DOI: 10.1007/S00401-010-0657-2
Abstract: We have investigated alterations in myelin associated with Abeta plaques, a major pathological hallmark of Alzheimer's disease (AD), in human tissue and relevant transgenic mice models. Using quantitative morphological techniques, we determined that fibrillar Abeta pathology in the grey matter of the neocortex was associated with focal demyelination in human presenilin-1 familial, sporadic and preclinical AD cases, as well as in two mouse transgenic models of AD, compared with age-matched control tissue. This demyelination was most pronounced at the core of Abeta plaques. Furthermore, we found a focal loss of oligodendrocytes in sporadic and preclinical AD cases associated with Abeta plaque cores. In human and transgenic mice alike, plaque-free neocortical regions showed no significant demyelination or oligodendrocyte loss compared with controls. Dystrophic neurites associated with the plaques were also demyelinated. We suggest that such plaque-associated focal demyelination of the cortical grey matter might impair cortical processing, and may also be associated with aberrant axonal sprouting that underlies dystrophic neurite formation.
Publisher: Frontiers Media SA
Date: 17-12-2014
Publisher: Elsevier BV
Date: 10-2009
DOI: 10.1016/J.BRAINRESBULL.2009.08.004
Abstract: There has been growing interest in the axon as the initial focus of pathological change in a number of neurodegenerative diseases of the central nervous system. This review concentrates on three major neurodegenerative conditions--amyotrophic lateral sclerosis, multiple sclerosis and Alzheimer's disease--with emphasis on key cellular changes that may underlie early axonal dysfunction and pathology and, potentially, the degeneration of neurons. In particular, this review will address recent data that indicate that the main pathological stimuli for these conditions, though often not definitively determined, result in an initial perturbation of the axon and its cytoskeleton, which then results in slow neuronal degeneration and loss of connectivity. The identification of a degenerative process initiated in the axon may provide new therapeutic targets for early intervention to inhibit the grim outcomes related to the progression of these diseases.
Publisher: Elsevier BV
Date: 10-2017
DOI: 10.1016/J.MCN.2017.05.010
Abstract: Intermediate filaments are critical for the extreme structural specialisations of neurons, providing integrity in dynamic environments and efficient communication along axons a metre or more in length. As neurons mature, an initial expression of nestin and vimentin gives way to the neurofilament triplet proteins and α-internexin, substituted by peripherin in axons outside the CNS, which physically consolidate axons as they elongate and find their targets. Once connection is established, these proteins are transported, assembled, stabilised and modified, structurally transforming axons and dendrites as they acquire their full function. The interaction between these neurons and myelinating glial cells optimises the structure of axons for peak functional efficiency, a property retained across their lifespan. This finely calibrated structural regulation allows the nervous system to maintain timing precision and efficient control across large distances throughout somatic growth and, in maturity, as a plasticity mechanism allowing functional adaptation.
Publisher: Wiley
Date: 04-2007
DOI: 10.1111/J.1365-2826.2006.01527.X
Abstract: The 3alpha-hydroxy,5alpha-reduced pregnane steroids, allopregnanolone and allotetrahydrodeoxycorticosterone, are the most potent endogenous positive modulators of GABA(A) receptor-mediated inhibition. This study presents the first immunohistochemical examination of the cellular distribution of 3alpha-hydroxy,5alpha-reduced pregnane steroids across the brain. We found a widespread distribution in the adult rat, with dense immunolabelling in the olfactory bulb, striatum and cerebral cortex, and lower density labelling in the brainstem reticular formation. In general terms, this distribution accords with the regional concentrations of 3alpha-hydroxy,5alpha-reduced steroids determined, in other laboratories, by brain region s ling and either gas chromatography-mass fragmentography or radioimmunoassay. However, immunohistochemistry allowed for a more detailed examination of regional distribution and cellular specificity. All immunoreactivity was confined to the cell bodies and thick dendrites of neurones no identifiable glia were labelled. In most brain areas, the location and morphology of labelled cells identified them as excitatory neurones. In addition, cell populations known to be projecting GABAergic neurones (e.g. cerebellar Purkinje cells) were immunoreactive, whereas local inhibitory neurones generally were not. The cellular distribution of 3alpha-hydroxy,5alpha-reduced steroids suggests that sensory, motor, limbic and homeostatic systems can be influenced by neurosteroids at multiple stages of processing.
Publisher: Cambridge University Press (CUP)
Date: 06-2007
DOI: 10.1111/J.1601-5215.2007.00204.X
Abstract: To critically examine the relationship between evolutionary and developmental influences on human neocortex and the properties of the conscious mind it creates. Using PubMed searches and the bibliographies of several monographs, we selected 50 key works, which offer empirical support for a novel understanding of the organization of the neocortex. The cognitive gulf between humans and our closest primate relatives has usually been taken as evidence that our brains evolved crucial new mechanisms somehow conferring advanced capacities, particularly in association areas of the neocortex. In this overview of neocortical development and comparative brain morphometry, we propose an alternative view: that an increase in neocortical size, alone, could account for novel and powerful cognitive capabilities. Other than humans’ very large brain in relation to the body weight, the morphometric relations between neocortex and all other brain regions show remarkably consistent exponential ratios across the range of primate species, including humans. For an increase in neocortical size to produce new abilities, the developmental mechanisms of neocortex would need to be able to generate an interarchy of functionally erse cortical domains in the absence of explicit specification, and in this respect, the mammalian neocortex is unique: its relationship to the rest of the nervous system is unusually plastic, allowing great changes in cortical organization to occur in relatively short periods of evolution. The fact that even advanced abilities like self-recognition have arisen in species from different mammalian orders suggests that expansion of the neocortex quite naturally generates new levels of cognitive sophistication. Our cognitive and behavioural sophistication may, therefore, be attributable to these intrinsic mechanisms’ ability to generate complex interarchies when the neocortex reaches a sufficient size. Our analysis offers a parsimonious explanation for key properties of the human mind based on evolutionary influences and developmental processes. This view is perhaps surprising in its simplicity, but offers a fresh perspective on the evolutionary basis of mental complexity.
Publisher: Elsevier BV
Date: 09-2016
DOI: 10.1016/J.BRAINRESBULL.2016.07.012
Abstract: Neurofilaments are major protein constituents of the brain, but are particularly abundant in specific subpopulations of neurons and likely have a key role in the regulation of axonal calibre. Neurofilament proteins may also be involved in the transformation of the neuronal cytoskeleton leading to substantial tau pathology in axons damaged by Aβ, subsequently leading to neurofibrillary pathology in their cell bodies of origin. An understanding of neurofilamentous changes in axons and subsequent tau pathology may provide insight into how Aβ pathology may stimulate an aberrant plasticity-related response of damaged neurons, leading to the progressive and degenerative changes in the neuronal cytoskeleton that result in synapse loss and neuronal degeneration.
Publisher: Wiley
Date: 07-2010
Publisher: Bentham Science Publishers Ltd.
Date: 04-02-2019
DOI: 10.2174/1567205016666181212152622
Abstract: Images of amyloid-β pathology characteristic of Alzheimer’s disease are difficult to consistently and accurately segment, due to diffuse deposit boundaries and imaging variations. We evaluated the performance of ImageSURF, our open-source ImageJ plugin, which considers a range of image derivatives to train image classifiers. We compared ImageSURF to standard image thresholding to assess its reproducibility, accuracy and generalizability when used on fluorescence images of amyloid pathology. ImageSURF segments amyloid-β images significantly more faithfully, and with significantly greater generalizability, than optimized thresholding. In addition to its superior performance in capturing human evaluations of pathology images, ImageSURF is able to segment image sets of any size in a consistent and unbiased manner, without requiring additional blinding, and can be retrospectively applied to existing images. The training process yields a classifier file which can be shared as supplemental data, allowing fully open methods and data, and enabling more direct comparisons between different studies.
Publisher: Frontiers Media SA
Date: 2013
Publisher: Elsevier BV
Date: 05-2015
DOI: 10.1016/J.EXPNEUROL.2015.02.034
Abstract: Traumatic brain injury is a risk factor for Alzheimer's disease (AD), however the effect of such neural damage on the onset and progression of beta-amyloid (Aβ) plaque pathology is not well understood. This study utilized an in vivo model of focal brain injury to examine how localized damage may acutely affect the onset and progression of Aβ plaque deposition as well as inflammatory and synaptic changes, in the APP/PS1 (APPSWE, PSEN1dE9) transgenic model of AD relative to wild-type (Wt) mice. Acute focal brain injury in 3- and 9-month-old APP/PS1 and Wt mice was induced by insertion of a needle into the somatosensory neocortex, as compared to sham surgery, and examined at 24h and 7d post-injury (PI). Focal brain injury did not induce thioflavine-S stained or (pan-Aβ antibody) MOAB-2-labeled plaques at either 24h or 7d PI in 3-month-old APP/PS1 mice or Wt mice. Nine-month-old APP/PS1 mice demonstrate cortical Aβ plaques but focal injury had no statistically significant (p>0.05) effect on thioflavine-S or MOAB-2 plaque load surrounding the injury site at 24h PI or 7d PI. There was a significant (p 0.05). For both Wt and APP/PS1 mice alike, synaptophysin puncta near the injury site were significantly reduced 24h PI (compared to sites distant to the injury and the corresponding area in sham mice p 0.05). There was no significant effect of genotype on this response (p>0.05). These results indicate that focal brain injury and the associated microglial response do not acutely alter Aβ plaque deposition in the APP/PS1 mouse model. Furthermore the current study demonstrated that the brains of both Wt and APP/PS1 mice are capable of recovering lost synaptophysin immunoreactivity post-injury, the latter in the presence of Aβ plaque pathology that causes synaptic degeneration.
Publisher: Wiley
Date: 04-04-2013
DOI: 10.1002/CNE.23261
Abstract: The neurofilament light (NFL) subunit is considered as an obligate subunit polymer for neuronal intermediate filaments comprising the neurofilament (NF) triplet proteins. We examined cytoskeletal protein levels in the cerebral cortex of NFL knockout (KO) mice at postnatal day 4 (P4), 5 months, and 12 months of age compared with age-matched wild-type (WT) mice of a similar genetic background (C57BL/6). The absence of NFL protein resulted in a significant reduction of phosphorylated and dephosphorylated NFs (NF-P, NF-DP), the medium NF subunit (NFM), and the intermediate filament α-internexin (INT) at P4. At 5 months, NF-DP, NFM, and INT remained significantly lower in knockouts. At 12 months, NF-P was again significantly decreased, and INT significantly increased, in KOs compared with wild type. In addition, protein levels of class III neuron-specific β-tubulin and microtubule-associated protein 2 were significantly increased in NFL KO mice at P4, 5 months, and 12 months, whereas β-actin levels were significantly decreased at P4. Immunocytochemical studies demonstrated that NF-DP accumulated abnormally in the perikarya of cortical neurons by 5 months of age in NFL KO mice. Neurons that lacked NF triplet proteins, such as calretinin-immunolabeled nonpyramidal cells, showed no alterations in density or cytoarchitectural distribution in NFL KO mice at 5 months relative to WT mice, although calretinin protein levels were decreased significantly after 12 months in NFL KO mice. These findings suggest that a lack of NFL protein alters the expression of cytoskeletal proteins and disrupts other NF subunits, causing intracellular aggregation but not gross structural changes in cortical neurons or cytoarchitecture. The data also indicate that changes in expression of other cytoskeletal proteins may compensate for decreased NFs.
Publisher: The Company of Biologists
Date: 02-2021
DOI: 10.1242/DMM.047548
Abstract: Mislocalization of the TAR DNA-binding protein 43 (TDP-43 encoded by TARDBP) from the nucleus to the cytoplasm is a common feature of neurodegenerative conditions such as amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). The downstream in vivo cellular effects of this mislocalization are not well understood. To investigate the impact of mislocalized TDP-43 on neuronal cell bodies, axons and axonal terminals, we utilized the mouse visual system to create a new model of TDP-43 proteinopathy. Mouse (C57BL/6J) retinal ganglion cells (RGCs) were transduced with GFP-tagged human wild-type TDP-43 (hTDP-WT-GFP) and human TDP-43 with a mutation in the nuclear localization sequence (hTDP-ΔNLS-GFP), to cause TDP-43 mislocalization, with ∼60% transduction efficiency achieved. Expression of both hTDP-WT-GFP and hTDP-ΔNLS-GFP resulted in changes to neurofilament expression, with cytoplasmic TDP-43 being associated with significantly (P& .05) increased neurofilament heavy expression in the cell soma, and both forms of altered TDP-43 leading to significantly (P& .05) decreased numbers of neurofilament-positive axons within the optic nerve. Alterations to neurofilament proteins were associated with significantly (P& .05) increased microglial density in the optic nerve and retina. Furthermore, expression of hTDP-WT-GFP was associated with a significant (P& .05) increase in pre-synaptic input into RGCs in the retina. The current study has developed a new model that allows detailed examination of alterations to TDP-43 and will contribute to the knowledge of TDP-43-mediated neuronal alterations and degeneration.
Publisher: Elsevier BV
Date: 02-2015
DOI: 10.1016/J.NEUROBIOLAGING.2014.10.001
Abstract: The transactive response DNA-binding protein 43 (TDP-43) has been identified as a neurofilament light (NF-L) messenger RNA (mRNA)-binding protein. Abnormally increased levels of TDP-43 are detected in patients with amyotrophic lateral sclerosis and a downregulation of NF-L mRNA. However, links between NF-L and TDP-43 expressions are unclear. In this study, we investigated whether the deficiency of NF-L protein can result in alterations in TDP-43 localization or protein expression and whether this is altered with aging. There was a significant increase in TDP-43 protein levels in the cortex and lumbar spinal cord in 12-month-old NF-L knockout (NF-L KO) mice, compared with wild-type (WT) C57BL/6 mice. However, there was no difference in either the phosphorylation of TDP-43 between WT and NF-L KO mice or the abnormal mislocalization of TDP-43 to the cytoplasm in NF-L KO animals. Our findings suggest that NF-L protein or mRNA may negatively affect the expression of TDP-43 in the central nervous system. However, altered phosphorylation of TDP-43 may be more highly associated with aging than the levels of TDP-43 expression.
Publisher: Elsevier BV
Date: 10-2022
DOI: 10.1016/J.SLEH.2022.06.001
Abstract: The physiological impact of transitioning from full-time study to work in occupations that involve high-stress environments and shift work may plausibly impact sleep patterns and quality. There are limited studies focusing on the transition to shift work in graduate paramedics. This study aimed to assess early metabolic markers of health, activity, and sleep quality during the first 5 months of rostered shift work in a cohort of 28 graduate paramedics. Participants were tested for 4-week blocks before starting shift work (baseline), and during their first and fifth month of shift work. In each block, sleep and activity levels were monitored 24 h/day (workdays and nonworking days) using a wrist-worn actigraph. During shift work, the number of sleep episodes increased by 16.7% (p = .02) and self-reporting of poor sleep quality increased by 35.4% (p = .05) however, overall sleep quantity and sleep efficiency did not differ. Sleep metrics recorded during nonwork days were not different to baseline with exception of reduced sleep duration recorded the night before returning to work (5.99 ± 1.66 hours Month 1 5.72 ± 1.06 hours Month 5). Sedentary behavior increased by 4.8% across the study, attributable to a significant decline in light exercise (p = .05). No changes were recorded in vigorous physical activity, average steps recorded per day, fasting blood glucose levels, systolic and diastolic blood pressure, weight, or waist circumference. These results warrant further large-scale and longitudinal studies to gauge any physiological implications for ongoing paramedic health.
Publisher: Springer Science and Business Media LLC
Date: 27-06-2021
DOI: 10.1007/S00429-021-02327-3
Abstract: The calcium binding protein parvalbumin is expressed in interneurons of two main morphologies, the basket and chandelier cells, which target perisomatic domains on principal cells and are extensively interconnected in laminar networks by synapses and gap junctions. Beyond its utility as a convenient cellular marker, parvalbumin is an unambiguous identifier of the key role that these interneurons play in the fundamental functions of the cortex. They provide a temporal framework for principal cell activity by propagating gamma oscillation, providing coherence for cortical information processing and the basis for timing-dependent plasticity processes. As these parvalbumin networks mature, they are physically and functionally stabilised by axonal myelination and development of the extracellular matrix structure termed the perineuronal net. This maturation correlates with the emergence of high-speed, highly energetic activity and provides a coherent foundation for the unique ability of the cortex to cross-correlate activity across sensory modes and internal representations.
No related grants have been discovered for Matthew Kirkcaldie.