Thiamine Deficiency Limits Glucose Utilization and Glial Proliferation in Brain Lesions of Symptomatic Rats

Sharp, Frank R.; Bolger, Eric; Evans, Kathleen

doi:10.1038/jcbfm.1982.20

Cited by 15 publications

(2 citation statements)

References 13 publications

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“…Inversely, it can excite distant neurons via polysynaptic activation (Stoney et al, 1968) likely through cortico-cortical networks. Deoxyglucose, a metabolic marker, is increased in other cortical areas interconnected with the site of stimulation (Sharp and Ryan, 1984) but not in subcortical structures (Sharp et al, 1982). Most importantly, ICMS can be used to generate rapid cortical reorganization of motor representation in rats (Nudo et al, 1990).…”

Section: Fundamental Rational For the Use Of Stimulation To Favor Recmentioning

confidence: 99%

Shaping plasticity to enhance recovery after injury

Dancause

Nudo

2011

Progress in Brain Research

171

127

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The past decade of neuroscience research has provided considerable evidence that the adult brain can undergo substantial reorganization following injury. For example, following an ischemic lesion, such as occurs following a stroke, there is a cascade of molecular, genetic, physiological and anatomical events that allows the remaining structures in the brain to reorganize. Often, these events are associated with recovery, suggesting that they contribute to it. Indeed, the term plasticity in stroke research has had a positive connotation historically. But more recently, efforts have been made to differentiate beneficial from detrimental changes. These notions are timely now that neurorehabilitative research is developing novel treatments to modulate, increase, or inhibit plasticity in targeted brain regions. We will review basic principles of plasticity and some of the new and exciting approaches that are currently being investigated to shape plasticity following injury in the central nervous system.

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Section: Fundamental Rational For the Use Of Stimulation To Favor Recmentioning

confidence: 99%

Shaping plasticity to enhance recovery after injury

Dancause

Nudo

2011

Progress in Brain Research

171

127

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“…A likely explanation for these variable and high levels came after inspection of the Nissl-stained sections from these experiments; namely, inflammatory cells had invaded the infusion sites in the SCN to a variable extent. Microglia, astrocytes, and macrophages may lead to an increased glucose utilization, which accompanies healing (Sharp et al, 1982;Cooper et al, 1984).…”

Section: Discussionmentioning

confidence: 99%

Further Evaluation of the Tetrodotoxin-Resistant Circadian Pacemaker in the Suprachiasmatic Nuclei

Schwartz

1991

J Biol Rhythms

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We previously reported the results of an experimental paradigm in which tetrodotoxin (TTX) was chronically infused by miniosmotic pump into the rat suprachiasmatic nuclei (SCN) (Schwartz et al., 1987). Although TTX reversibly blocked photic entrainment and overt expression of the circadian drinking rhythm, the circadian pacemaker in the SCN continued to oscillate unperturbed by the toxin, and we concluded that Na(+)-dependent action potentials are not a part of the SCN pacemaker's internal timekeeping mechanism. In the research reported in the present paper, we used our paradigm to chronically infuse other agents, in order to evaluate the validity of this interpretation further. (1) Infusion of 50% procaine into the SCN of blinded rats resulted in a disorganized circadian drinking rhythm during the infusion, after which behavioral rhythmicity returned without apparent phase shift. In intact rats, procaine reduced the phase-resetting action of a reversed light-dark cycle imposed during the infusion. Thus, the effects of voltage-dependent Na+ channel blockade by a local anesthetic resemble those produced by TTX. (2) Infusion of high (20 mM) K+ or 100 microM veratridine into the SCN of blinded rats resulted in an apparent phase advance of the circadian drinking rhythm by over 4 hr. The phase-shifting effect of veratridine was blocked by simultaneous infusion of 1 microM TTX. Thus, membrane depolarization or direct activation of voltage-dependent Na+ channels can affect the pacemaker's oscillation. Our infusion paradigm can detect alterations of rhythm phase, and the lack of phase shift after TTX or procaine infusion is not an artifact of an insensitive method.

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Wernicke—Korsakoff Syndrome

Greenberg

Diamond

1985

Alcohol and the Brain

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Thiamine Deficiency Limits Glucose Utilization and Glial Proliferation in Brain Lesions of Symptomatic Rats

Cited by 15 publications

References 13 publications

Shaping plasticity to enhance recovery after injury

Shaping plasticity to enhance recovery after injury

Further Evaluation of the Tetrodotoxin-Resistant Circadian Pacemaker in the Suprachiasmatic Nuclei

Wernicke—Korsakoff Syndrome

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