G. Campbell

ORCID: 0000-0003-4828-421X
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • Multiple Sclerosis Research Studies
  • Neurogenesis and neuroplasticity mechanisms
  • Neurobiology and Insect Physiology Research
  • Metabolism and Genetic Disorders
  • Amyotrophic Lateral Sclerosis Research
  • Peripheral Neuropathies and Disorders
  • Neuroscience and Neuropharmacology Research
  • Neuropeptides and Animal Physiology
  • Ion channel regulation and function
  • Alzheimer's disease research and treatments
  • Hereditary Neurological Disorders
  • Physiological and biochemical adaptations
  • Receptor Mechanisms and Signaling
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Nerve injury and regeneration
  • Neurological diseases and metabolism
  • Genetic Neurodegenerative Diseases
  • Adenosine and Purinergic Signaling
  • Drug Transport and Resistance Mechanisms
  • Olfactory and Sensory Function Studies
  • Diet and metabolism studies
  • Advanced Chemical Sensor Technologies
  • Neuroscience of respiration and sleep
  • ATP Synthase and ATPases Research

Institute for Neurosciences of Montpellier
2018-2024

Inserm
2018-2024

University of Edinburgh
2012-2022

Université de Montpellier
2018-2022

Hôpital Saint Eloi
2021

Sussex Partnership NHS Foundation Trust
2019

Biomedical Primate Research Centre
2017

Medical University of Vienna
2012-2017

Amsterdam UMC Location Vrije Universiteit Amsterdam
2017

University Medical Center Groningen
2017

Summary . Stimulation of the vagal non‐adrenergic inhibitory innervation caused release adenosine and inosine into vascular perfusates from stomachs guinea‐pigs toads. portions Auerbach's plexus isolated turkey gizzard triphosphate (ATP), diphosphate (ADP) monophosphate (AMP). ATP, added to solutions perfused through toad stomach vasculature, was broken down adenosine, adenine. Of a series purine pyrimidine derivatives tested for activity on guinea‐pig taenia coli, ATP ADP were most potent....

10.1111/j.1476-5381.1970.tb10646.x article EN British Journal of Pharmacology 1970-12-01

1. Stimulation of the vagal non-adrenergic inhibitory innervation caused release adenosine and inosine into vascular perfusates from stomachs guinea-pigs toads.2. portions Auerbach's plexus isolated turkey gizzard triphosphate (ATP), diphosphate (ADP) monophosphate (AMP).3. ATP, added to solutions perfused through toad stomach vasculature, was broken down adenosine, adenine.4. Of a series purine pyrimidine derivatives tested for activity on guinea-pig taenia coli, ATP ADP were most potent.5....

10.1111/j.1476-5381.1997.tb06815.x article EN British Journal of Pharmacology 1997-02-01

Multiple sclerosis is the most common cause of non-traumatic neurological impairment in young adults. An energy deficient state has been implicated degeneration axons, pathological correlate disease progression, multiple sclerosis. Mitochondria are efficient producers and play an important role calcium homeostasis. We analysed density function mitochondria using immunohistochemistry histochemistry, respectively, chronic active inactive lesions progressive As shown before acute pattern III...

10.1093/brain/awp046 article EN Brain 2009-03-17

Abstract Objective Cerebral atrophy is a correlate of clinical progression in multiple sclerosis (MS). Mitochondria are now established to play part the pathogenesis MS. Uniquely, mitochondria harbor their own mitochondrial DNA (mtDNA), essential for maintaining healthy central nervous system. We explored respiratory chain activity and mtDNA deletions single neurons from secondary progressive MS (SPMS) cases. Methods Ninety‐eight snap‐frozen brain blocks 13 SPMS cases together with complex...

10.1002/ana.22109 article EN other-oa Annals of Neurology 2010-11-08

1. The inhibitory innervation of the taenia guinea‐pig caecum has been studied, after blocking responses to stimulation excitatory cholinergic nerves with atropine. 2. Stimulation perivascular supplying caused relaxations. These had properties which were typical sympathetic post‐ganglionic adrenergic nerves. relaxations by maximal at frequencies above 30 pulses/sec and they abolished bretylium, guanethidine 1,1‐dimethyl‐4‐phenylpiperazinium iodide (DMPP). 3. is also innervated intramural...

10.1113/jphysiol.1966.sp007834 article EN The Journal of Physiology 1966-02-01

Mitochondrial content within axons increases following demyelination in the central nervous system, presumably as a response to changes energy needs of imposed by redistribution sodium channels. Myelin sheaths can be restored demyelinated and remyelination some multiple sclerosis lesions is extensive, while others it incomplete or absent. The effects on axonal mitochondrial sclerosis, particularly whether completely reverses that follow demyelination, are currently unknown. In this study, we...

10.1093/brain/awr110 article EN Brain 2011-06-23

Neurons and glial cells exchange energy-rich metabolites it has been suggested, originally based on in vitro data, that astrocytes provide lactate to glutamatergic synapses (“lactate shuttle”). Here, we have studied lack mitochondrial respiration vivo . A novel mouse mutant ( GLAST CreERT2 :: Cox10 flox/flox ) was generated, which the administration of tamoxifen causes fail assembly cytochrome c oxidase (COX). Focusing cerebellar Bergmann glia (BG) cells, exhibit highest rate Cre-mediated...

10.1523/jneurosci.0756-16.2017 article EN cc-by-nc-sa Journal of Neuroscience 2017-03-17

Single, large-scale deletions of mitochondrial DNA are a common cause disease and broad phenotypic spectrum ranging from mild myopathy to devastating multi-system syndromes such as Kearns-Sayre syndrome. Studies date have been inconsistent on the value putative predictors clinical phenotype progression mutation load size or location deletion. Using cohort 87 patients with single, we demonstrate that variety outcome measures COX-deficient fibre density, age-at-onset symptoms burden, measured...

10.1093/brain/awt321 article EN cc-by Brain 2013-11-25

Abstract Axonal loss is the key pathological substrate of neurological disability in demyelinating disorders, including multiple sclerosis (MS). However, consequences demyelination on neuronal and axonal biology are poorly understood. The abundance mitochondria demyelinated axons MS raises possibility that increased mitochondrial content serves as a compensatory response to demyelination. Here, we show upon move from cell body axon, increasing content, which term (ARMD). following degenerate...

10.1007/s00401-020-02179-x article EN cc-by Acta Neuropathologica 2020-06-22

1. A comparison was made between the inhibitory responses of isolated atropinized guinea‐pig stomach to stimulation vagus and perivascular nerves. 2. When low frequencies were used, vagi more effective than nerves in causing relaxation stomach. 3. The vagal faster onset nerve stimulation. 4. Responses abolished by concentrations bretylium, whereas only slight reduced. Vagal strongly reduced higher bretylium. 5. Amphetamine relieved blockade which caused but never reduction responses. 6. It...

10.1113/jphysiol.1966.sp008004 article EN The Journal of Physiology 1966-08-01

Abstract Oligodendrocyte lineage cells are susceptible to a variety of insults including hypoxia, excitotoxicity, and reactive oxygen species. Demyelination is well‐recognized feature several CNS disorders multiple sclerosis, white matter strokes, progressive multifocal leukoencephalopathy, due mitochondrial DNA mutations. Although mitochondria have been implicated in the demise oligodendrocyte cells, consequences respiratory chain defects not examined. We determine vitro impact established...

10.1002/glia.21052 article EN other-oa Glia 2010-07-21

Mitochondria are critical for the function and maintenance of myelinated axons notably through Adenosine triphosphate (ATP) production. A direct by-product this ATP production is reactive oxygen species (ROS), which highly deleterious neurons. While shortage ROS levels increase involved in several neurodegenerative diseases, it still unclear whether real-time dynamics both axonal mitochondria altered by or demyelinating neuropathies. To answer question, we imaged quantified mitochondrial...

10.1186/s40478-019-0740-4 article EN cc-by Acta Neuropathologica Communications 2019-06-11

Abstract Charcot-Marie-Tooth disease 1 A (CMT1A) results from a duplication of the PMP22 gene in Schwann cells and deficit myelination peripheral nerves. Patients with CMT1A have reduced nerve conduction velocity, muscle wasting, hand foot deformations drop walking. Here, we evaluate safety efficacy recombinant adeno-associated viral vector serotype 9 (AAV2/9) expressing GFP shRNAs targeting Pmp22 mRNA animal models A. Intra-nerve delivery AAV2/9 sciatic allowed widespread transgene...

10.1038/s41467-021-22593-3 article EN cc-by Nature Communications 2021-04-21

1. A study was made of the responses isolated taenia guinea‐pig caecum to stimulation intramural nerves. 2. Four types response are described, up a contraction and/or relaxation occurring during and an after‐contraction when is stopped. 3. delayed which sometimes occurred at end also described. 4. Atropine usually abolished contractions stimulation. After‐contractions either appeared or were increased in amplitude presence atropine, relaxations abolished. 5. The anti‐cholinesterase drug...

10.1113/jphysiol.1966.sp007977 article EN The Journal of Physiology 1966-07-01

Background Tardive dyskinesia (TD) may be mediated through free radical damage to neurons. Plasma lipid peroxide levels are a measure of fats. Vitamin E is scavenger. Method One hundred and twenty-eight schizophrenic patients were examined for TD using the Abnormal Involuntary Movements Scale. Blood samples taken plasma peroxide, serum vitamin cholesterol, Exholesterol ratios. Twenty-four also in October 1993, January 1994, April 1994. Biochemical results compared 81 79 normal subjects....

10.1192/bjp.167.5.610 article EN The British Journal of Psychiatry 1995-11-01
Coming Soon ...