Carole A. Bartlett

ORCID: 0000-0003-0049-1260
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About
Contact & Profiles
Research Areas
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Axon Guidance and Neuronal Signaling
  • Nerve injury and regeneration
  • Spinal Cord Injury Research
  • Neurogenesis and neuroplasticity mechanisms
  • Traumatic Brain Injury Research
  • Neuroscience and Neuropharmacology Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Laser Applications in Dentistry and Medicine
  • Ion channel regulation and function
  • S100 Proteins and Annexins
  • Glaucoma and retinal disorders
  • Zebrafish Biomedical Research Applications
  • Trace Elements in Health
  • Retinal Development and Disorders
  • Mitochondrial Function and Pathology
  • Photochromic and Fluorescence Chemistry
  • Nicotinic Acetylcholine Receptors Study
  • Angiogenesis and VEGF in Cancer
  • RNA regulation and disease
  • Vagus Nerve Stimulation Research
  • Adenosine and Purinergic Signaling
  • Mass Spectrometry Techniques and Applications
  • Anesthesia and Neurotoxicity Research
  • Connexins and lens biology

The University of Western Australia
2012-2023

Curtin University
2018-2023

Perron Institute for Neurological and Translational Science
2023

Bentley (Canada)
2020

Hudson Institute of Medical Research
2015

The University of Sydney
2015

Inserm
2015

Sorbonne Université
2015

Institut du Cerveau
2015

Centre National de la Recherche Scientifique
2015

A number of intracellular proteins that are protective after brain injury classically thought to exert their effect within the expressing cell. The astrocytic metallothioneins (MT) one example and act via free radical scavenging heavy metal regulation, in particular zinc. Indeed, we have previously established MTs required for successful healing. Here provide evidence a fundamentally different mode action relying upon intercellular transfer from astrocytes neurons, which turn leads...

10.1074/jbc.m708446200 article EN cc-by Journal of Biological Chemistry 2008-03-12

Loss of function following injury to the CNS is worsened by secondary degeneration neurons and glia surrounding initiated oxidative damage. However, it not yet known which cellular populations structures are most vulnerable damage <i>in vivo</i>. Using Nanoscale ion mass spectrometry (NanoSIMS), was semiquantified within subpopulations optic nerve degeneration, a partial transection in adult female PVG rats. Simultaneous assessment revealed oligodendroglia as DNA oxidation injury....

10.1523/jneurosci.1898-17.2018 article EN Journal of Neuroscience 2018-06-18

Secondary degeneration in the central nervous system involves indirect damage to neurons and glia away from initial injury. Partial transection of dorsal optic nerve (ON) results precise spatial separation primary trauma delayed degenerative events ventrally placed axons parent somata. Here we conduct an immunohistochemical survey secondary cellular changes around their retinal ganglion cell (RGC) somata during first 3 days after a restricted, ON transection. This is before loss RGCs...

10.1089/neu.2009.1112 article EN Journal of Neurotrauma 2009-10-23

Purpose.: To examine chronic changes occurring at 6 months following partial optic nerve (ON) transection, assessing axons, myelin, and visual function. Methods.: Dorsal ON axons were transected, leaving ventral vulnerable to secondary degeneration. At 3 toluidine-blue stained sections used assess dimensions of the injury site. Transmission electron microscopy (TEM) images quantify numbers, diameter, area, myelin thickness axons. Immunohistochemistry fluoromyelin staining semiquantitatively...

10.1167/iovs.12-10080 article EN Investigative Ophthalmology & Visual Science 2012-08-12

Purpose.: After partial optic nerve (ON) injury, intact retinal ganglion cells (RGCs) undergo secondary death, but the topographic distribution of this death is unknown, and it unclear which cell pathways are involved. Although calcium channel blocker lomerizine reduces RGC after ON unknown whether drug alleviates necrotic or apoptotic death. Methods.: The dorsal was transected in adult Piebald-Virol-Glaxo (PVG) rats, site determined using anterograde retrograde DiI tracing. assessed at 2 3...

10.1167/iovs.09-3717 article EN Investigative Ophthalmology & Visual Science 2009-11-01

Red/near-infrared irradiation therapy (R/NIR-IT) delivered by laser or light-emitting diode (LED) has improved functional outcomes in a range of CNS injuries. However, translation R/NIR-IT to the clinic for treatment neurotrauma been hampered lack comparative information regarding degree penetration injury site and optimal parameters different We compared efficacy at 670 nm 830 nm, provided narrow-band LED arrays adjusted produce equal irradiance, four vivo rat models injury: partial optic...

10.1371/journal.pone.0104565 article EN cc-by PLoS ONE 2014-08-08

Abstract Cuprizone is a copper-chelating agent that induces pathology similar to within some multiple sclerosis (MS) lesions. The reliability and reproducibility of cuprizone for inducing demyelinating disease depends on the animals ingesting consistent doses cuprizone. Cuprizone-containing pelleted feed convenient way delivering cuprizone, but efficacy these pellets at demyelination has been questioned. This study compared degree between mice fed delivered in powdered formulation an early 3...

10.1038/s41598-021-01963-3 article EN cc-by Scientific Reports 2021-11-19

Following injury to the central nervous system, axons and myelin distinct from initial site undergo changes associated with compromised function. Quantifying such is important understanding pathophysiology of neurotrauma; however, most studies date used 2 dimensional (D) electron microscopy analyse single sections, thereby failing capture along individual axons. We serial block face scanning (SBF SEM) undertake 3D reconstruction myelin, analysing optic nerves normal uninjured female rats...

10.1038/s41598-018-22361-2 article EN cc-by Scientific Reports 2018-02-27

Topographically ordered projections are established by molecular guidance cues and refined neuronal activity. Retinal input to a primary visual center, the superior colliculus (SC), is bilateral with dense contralateral projection sparse ipsilateral one. Both topographically organized, but in opposing anterior–posterior orientations. This arrangement provides functionally coherent each from binocular field, supporting function. When involved topography (ephrin-As) absent, crossed retinal...

10.1523/jneurosci.1135-08.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-07-16

Traumatic injury to the central nervous system (CNS) is accompanied by spreading damage of secondary degeneration, resulting in further loss neurons and function. Partial transection optic nerve (ON) has been used as a model which axons retinal ganglion cells ventral ON are spared from initial dorsal injury, but vulnerable degeneration. We have recently demonstrated that early after partial oxidative stress spreads through degeneration via astrocytes, persists aggregates cellular debris. In...

10.1089/neu.2010.1426 article EN Journal of Neurotrauma 2010-09-07

Abstract The use of nanoparticles for targeted delivery therapeutic agents to sites injury or disease in the central nervous system (CNS) holds great promise. However, biodistribution following vivo administration is often unknown, and concerns have been raised regarding potential toxicity. Using poly(glycidyl methacrylate) (PGMA) coated with polyethylenimine (PEI) containing superparamagnetic iron oxide as a magnetic resonance imaging (MRI) contrast agent rhodamine B fluorophore, whole...

10.1002/smll.201102648 article EN Small 2012-03-13

Abstract CNS injury is often localized but can be followed by more widespread secondary degenerative events that usually result in greater functional loss. Using a partial transection model rat optic nerve (ON). we recently demonstrated vivo increases the oxidative stress‐associated enzyme MnSOD 5 min after injury. However, mechanisms which early stress spreads remain unclear. In present study, assessed ion distributions, additional indicators, and channel immunoreactivity ON first 24 hr...

10.1002/jnr.22784 article EN Journal of Neuroscience Research 2011-10-31

Abstract The highly restrictive blood-brain barrier (BBB) plays a critically important role in maintaining brain homeostasis and is pivotal for proper neuronal function. BBB currently considered the main limiting factor restricting passage of large (up to 200 nm) intravenously administered nanoparticles brain. Breakdown occurs as consequence cerebrovascular diseases traumatic injury. In this article, we report that remote injuries CNS are also associated with dysfunction. particular, show...

10.1038/srep22595 article EN cc-by Scientific Reports 2016-03-04

Following injury to the central nervous system, increased microglia, secretion of pro- and anti-inflammatory cytokines, altered blood-brain barrier permeability, a hallmark degeneration, are observed at immediately adjacent site. However, few studies investigate how regions remote from primary could also suffer inflammation secondary degeneration.Adult female Piebald-Viral-Glaxo (PVG) rats underwent partial transection right optic nerve, with normal, age-matched, unoperated animals as...

10.1186/s12974-018-1227-0 article EN cc-by Journal of Neuroinflammation 2018-07-07

Partial injury to the central nervous system (CNS) is exacerbated by additional loss of neurons and glia via toxic events known as secondary degeneration. Using partial transection rat optic nerve (ON) a model, we have previously shown that myelin decompaction persists during Failure repair abnormalities degeneration may be attributed insufficient OPC proliferation and/or differentiation compensate for oligodendrocyte lineage cells (oligodendroglia). Following ON transection, found...

10.1371/journal.pone.0065710 article EN cc-by PLoS ONE 2013-06-11

Following partial injury to the central nervous system, cells beyond initial site undergo secondary degeneration, exacerbating loss of neurons, compact myelin and function. Changes in Ca2+ flux are associated with metabolic structural changes, but it is not yet clear how through specific ion channels contributes various pathologies. Here, optic nerve transection adult female rats was used model degeneration. Treatment combinations three channel inhibitors as a tool investigate which elements...

10.1186/s12868-017-0380-1 article EN cc-by BMC Neuroscience 2017-08-14

Secondary degeneration is a serious consequence of traumatic injury to the central nervous system (CNS) and involves progressive loss neurons function. However, while disruption myelin has been observed in spared axons, ultrastructural abnormalities that occur axons spatially separated from primary susceptible exclusively secondary are unknown. We used model which dorsal aspect rat optic nerve (ON) was transected leaving central/ventral ON undamaged, but vulnerable degeneration. Transmission...

10.1089/neu.2010.1665 article EN Journal of Neurotrauma 2011-03-07

Secondary degeneration of nerve tissue adjacent to a traumatic injury results in further loss neurons, glia and function, via mechanisms that may involve oxidative stress. However, changes indicators stress have not yet been demonstrated oligodendrocytes vulnerable secondary vivo. We show increases the indicator carboxymethyl lysine at days 1 3 after degeneration. Dihydroethidium staining for superoxide is reduced, indicating endogenous control this particular reactive species injury....

10.1371/journal.pone.0066448 article EN cc-by PLoS ONE 2013-06-19
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