S.R. White

Newfoundland and Labrador Centre for Applied Health Research

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G.K. Samathanam

Washington State University

D. Bieger

Memorial University of Newfoundland

Darrell A. Jackson

Washington State University Spokane

Fredric P. White

Washington State University

Simon J. Fung

VA Greater Los Angeles Healthcare System

Charles D. Barnes

Manhattan College

R.S. Neuman

Memorial University of Newfoundland

Kevin M. Imel

Washington State University

O. Pompeiano

University of Pisa

Philip E. Duffy

Trinity College Dublin

Cooperative Institutions

Washington State University

Memorial University of Newfoundland

The Ohio State University

University College London

Harvard University

University of California, Los Angeles

University of Pennsylvania

University of Massachusetts Amherst

American Academy of Child and Adolescent Psychiatry

Neurological Surgery

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Facilitation of spinal motoneurone excitability by 5-hydroxytryptamine and noradrenaline

Brain Research (1980)

S.R. White R.S. Neuman

Facilitation

Iontophoresis

10.1016/0006-8993(80)90561-2

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Citations (485)

Role of Muscarinic Receptors in the Cerebellar Control of the Vestibulospinal Reflex Gain: Cellular Mechanisms

Acta Oto-Laryngologica (1995)

P. André O. Pompeiano S.R. White

Most of the inhibitory Purkinje (P-) cells of the cerebellar anterior vermis fire out-of-phase with respect to the excitatory vestibulospinal neurons during roll tilt of the animal, thus exerting a positive influence on the gain of the vestibulospinal reflex (VSR). The responses of these P-cells depend on activation of glutamatergic excitatory mossy fibers-granule cells, but they are likely to be shaped by GABAergic inhibitory interneurons. The cerebellar cortex contains cholinergic fibers and both muscarinic and nicotinic receptors. In decerebrate cats intravermal injection of the muscarinic agonist bethanechol increased the VSR gain. The cellular mechanisms underlying these gain changes were studied in anesthetized Sprague-Dawley rats by microiontophoresis. Application of bethanechol (10-60 nA, 300 s) increased the response of vermal P-cells to pulses of glutamate (22/33 cells) or GABA (23/25 cells). These effects, which were blocked by the muscarinic antagonist scopolamine, lasted up to 15-40 min and occurred regardless of whether bethanecol altered the basal firing rate of the cells. We propose that the increase of P-cell responses to both excitatory and inhibitory neurotransmitters following activation of muscarinic receptors enhances the amplitude of modulation of these neurons to animal tilt, thus increasing the gain of the VSR.

Muscarinic agonist

Muscarinic antagonist

10.3109/00016489509125197

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Citations (10)

Prazosin suppresses development of axonal damage in rats inoculated for experimental allergic encephalomyelitis

Journal of Neuroimmunology (1992)

S.R. White Patrick Black G.K. Samathanam K.C. Paros

Monoaminergic

Encephalomyelitis

10.1016/0165-5728(92)90255-j

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Citations (24)

GW433908/ritonavir once daily in antiretroviral therapy-naive HIV-infected patients

AIDS (2004)

S. MacManus Phillip J. Yates Robert C. Elston S.R. White Naomi Richards

Objectives: To investigate the emergence of resistance to GW433908 (908), a protease inhibitor (PI) with demonstrated antiviral efficacy, safety and tolerability, when administered once daily (q.d.) with low dose ritonavir (908/r). Design: A 48-week Phase III open-label study (SOLO, APV30002) in which antiretroviral therapy-naive patients (n = 649) were treated with 908/r, (1400 mg/200 mg, q.d.) or nelfinavir [1250 mg, twice daily (b.i.d.)] with two nucleoside reverse transcriptase inhibitors (NRTI), abacavir (300 mg, b.i.d.) and lamivudine (150 mg, b.i.d.). Methods: Viral genotype and phenotype were analysed at baseline and on treatment up to 48 weeks and beyond. Results: Emergence of genotypic resistance was significantly different between the 908/r q.d. and the nelfinavir b.i.d. treatment arms for both PIs (0 versus 50%; P < 0.001) and the NRTI (13% versus 69%; P < 0.001) received. In the nelfinavir arm the key protease mutations D30N and/or L90M were frequently observed. The absence of protease resistance mutations and reduced incidence of NRTI resistance mutations in the 908/r q.d. arm was confirmed by phenotyping, which showed a lack of PI cross-resistance. Conclusions: The absence of resistance to 908 or cross-resistance to other PIs, and reduced NRTI resistance, following a 908/r q.d. regimen supports the use of this boosted PI early in therapy.

Nelfinavir

Ritonavir

Protease inhibitor (pharmacology)

Abacavir

Tolerability

Regimen

Indinavir

Resistance mutation

Reverse-transcriptase inhibitor

10.1097/00002030-200403050-00009

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Citations (67)

The synthesis of stress proteins by cerebral tissue is developmentally regulated in rats

International Journal of Developmental Neuroscience (1985)

Frederic P. White W.R. Currie S.R. White

White (mutation)

10.1016/0736-5748(85)90208-4

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Citations (0)

Damage to bulbospinal serotonin‐, tyrosine hydroxylase‐, and TRH‐containing axons occurs early in the development of experimental allergic encephalomyelitis in rats

Journal of Neuroscience Research (1990)

S.R. White G.K. Samathanam Robert M. Bowker Martin W. Wessendorf

Abstract Spinal cord monoaminergic and peptidergic axonal damage occurring during the development of experimental allergic encephalomyelitis (EAE) was assessed using immunohistochemistry. Spinal cord axons immunoreactive for serotonin, catecholamines, or a thyrotropin‐releasing hormone marker peptide were found to be markedly swollen and distorted by the earliest stage of detectable paralysis during EAE development (the flaccid tail stage). As clinical signs progressed to complete hindlimb paralysis, axonal damage became increasingly extensive. Axonal damage was equally pronounced whether EAE was induced by inoculation with purified myelin basic protein or with whole spinal cord homogenate, suggesting that the damage did not result from an immune attack directed against specific monoaminergic and/or peptidergic antigens present in the inoculant. However, two observations suggested that mechanical or chemical factors associated with the inflammatory foci contribute to the axonal damage: first, distorted axons were nearly always located adjacent to blood vessels or the pial surface, sites at which inflammation occurs during EAE. Second, the severity of axonal damage correlated with the severity of the inflammation. The early onset of axonal damage during development of EAE and the close correlation that was found between the severity of axonal damage and the severity of clinical signs suggested that the axonal damage may contribute to the clinical signs of the disease.

Monoaminergic

Encephalomyelitis

Brain damage

10.1002/jnr.490270114

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Citations (15)

Elevated MMP-9 in the Lumbar Cord Early after Thoracic Spinal Cord Injury Impedes Motor Relearning in Mice

Journal of Neuroscience (2013)

Christopher N. Hansen Lesley C. Fisher Rochelle J. Deibert Lyn B. Jakeman HaoYang Zhang

Spinal cord injury results in distant pathology around putative locomotor networks that may jeopardize the recovery of locomotion. We previously showed that activated microglia and increased cytokine expression extend at least 10 segments below the injury to influence sensory function. Matrix metalloproteinase-9 (MMP-9) is a potent regulator of acute neuroinflammation. Whether MMP-9 is produced remote to the injury or influences locomotor plasticity remains unexamined. Therefore, we characterized the lumbar enlargement after a T9 spinal cord injury in C57BL/6 (wild-type [WT]) and MMP-9-null (knock-out [KO]) mice. Within 24 h, resident microglia displayed an activated phenotype alongside increased expression of progelatinase MMP-3 in WT mice. By 7 d, increases in active MMP-9 around lumbar vasculature and production of proinflammatory TNF-α were evident. Deletion of MMP-9 attenuated remote microglial activation and restored TNF-α expression to homeostatic levels. To determine whether MMP-9 impedes locomotor plasticity, we delivered lumbar-focused treadmill training in WT and KO mice during early (2–9 d) or late (35–42 d) phases of recovery. Robust behavioral improvements were observed by 7 d, when only trained KO mice stepped in the open field. Locomotor improvements were retained for 4 weeks as identified using state of the art mouse kinematics. Neither training nor MMP-9 depletion alone promoted recovery. The same intervention delivered late was ineffective, suggesting that lesion site sparing is insufficient to facilitate activity-based training and recovery. Our work suggests that by attenuating remote mechanisms of inflammation, acute treadmill training can harness endogenous spinal plasticity to promote robust recovery.

Proinflammatory cytokine

Lumbar Spinal Cord

10.1523/jneurosci.1576-13.2013

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Citations (61)

A comparison of the effects of serotonin, substance P and thyrotropin-releasing hormone on excitability of rat spinal motoneurons in vivo

Brain Research (1985)

S.R. White

Tachyphylaxis

Iontophoresis

10.1016/0006-8993(85)90276-8

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