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Biochemical modulation of blood-brain barrier permeability.

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Standard

Biochemical modulation of blood-brain barrier permeability. / Gjedde, A; Crone, C.

I: Acta neuropathologica. Supplementum, Bind 8, 1983, s. 59-74.

Publikation: Bidrag til tidsskriftReviewForskning

Harvard

Gjedde, A & Crone, C 1983, 'Biochemical modulation of blood-brain barrier permeability.', Acta neuropathologica. Supplementum, bind 8, s. 59-74.

APA

Gjedde, A., & Crone, C. (1983). Biochemical modulation of blood-brain barrier permeability. Acta neuropathologica. Supplementum, 8, 59-74.

Vancouver

Gjedde A, Crone C. Biochemical modulation of blood-brain barrier permeability. Acta neuropathologica. Supplementum. 1983;8:59-74.

Author

Gjedde, A ; Crone, C. / Biochemical modulation of blood-brain barrier permeability. I: Acta neuropathologica. Supplementum. 1983 ; Bind 8. s. 59-74.

Bibtex

@article{eb1281b0b31411debc73000ea68e967b,
title = "Biochemical modulation of blood-brain barrier permeability.",
abstract = "Hydrophilic substrates necessary for brain function cross the capillary by facilitated diffusion. The facilitation has many features in common with enzyme-catalyzed reactions and is probably subserved by protein entities in the endothelial wall. The proteins act as receptors, recognizing substrate molecules, and as translocators, giving the molecules access to an aqueous path through the endothelium. These receptor-translocators can be saturated, and the transport is subject to competitive inhibition by substrate analogs. Thus, amino acids inhibit the transport of each other, and galactose can inhibit glucose transport in suckling rats. The proteins can be induced, as in the case of ketone transport in starvation, and repressed, as in the case of glucose transport in hyperglycemia. In rats with hyperglycemia for three weeks, the maximum glucose transport capacity of the blood-brain barrier decreased from 400 to 290 mumol/hg/min. An important result of the description is the understanding that rigid distinctions between the function of receptors, translocators, and enzymes is impossible. Understanding of the biochemical properties of facilitated diffusion may help explain a variety of symptoms in many 'inborn errors of metabolism'. This understanding has followed greater, recent insights into the general properties of the blood-brain barrier (45,46,47).",
author = "A Gjedde and C Crone",
year = "1983",
language = "English",
volume = "8",
pages = "59--74",
journal = "Acta Neuropathologica",
issn = "0001-6322",
publisher = "Springer",

}

RIS

TY - JOUR

T1 - Biochemical modulation of blood-brain barrier permeability.

AU - Gjedde, A

AU - Crone, C

PY - 1983

Y1 - 1983

N2 - Hydrophilic substrates necessary for brain function cross the capillary by facilitated diffusion. The facilitation has many features in common with enzyme-catalyzed reactions and is probably subserved by protein entities in the endothelial wall. The proteins act as receptors, recognizing substrate molecules, and as translocators, giving the molecules access to an aqueous path through the endothelium. These receptor-translocators can be saturated, and the transport is subject to competitive inhibition by substrate analogs. Thus, amino acids inhibit the transport of each other, and galactose can inhibit glucose transport in suckling rats. The proteins can be induced, as in the case of ketone transport in starvation, and repressed, as in the case of glucose transport in hyperglycemia. In rats with hyperglycemia for three weeks, the maximum glucose transport capacity of the blood-brain barrier decreased from 400 to 290 mumol/hg/min. An important result of the description is the understanding that rigid distinctions between the function of receptors, translocators, and enzymes is impossible. Understanding of the biochemical properties of facilitated diffusion may help explain a variety of symptoms in many 'inborn errors of metabolism'. This understanding has followed greater, recent insights into the general properties of the blood-brain barrier (45,46,47).

AB - Hydrophilic substrates necessary for brain function cross the capillary by facilitated diffusion. The facilitation has many features in common with enzyme-catalyzed reactions and is probably subserved by protein entities in the endothelial wall. The proteins act as receptors, recognizing substrate molecules, and as translocators, giving the molecules access to an aqueous path through the endothelium. These receptor-translocators can be saturated, and the transport is subject to competitive inhibition by substrate analogs. Thus, amino acids inhibit the transport of each other, and galactose can inhibit glucose transport in suckling rats. The proteins can be induced, as in the case of ketone transport in starvation, and repressed, as in the case of glucose transport in hyperglycemia. In rats with hyperglycemia for three weeks, the maximum glucose transport capacity of the blood-brain barrier decreased from 400 to 290 mumol/hg/min. An important result of the description is the understanding that rigid distinctions between the function of receptors, translocators, and enzymes is impossible. Understanding of the biochemical properties of facilitated diffusion may help explain a variety of symptoms in many 'inborn errors of metabolism'. This understanding has followed greater, recent insights into the general properties of the blood-brain barrier (45,46,47).

M3 - Review

C2 - 6346779

VL - 8

SP - 59

EP - 74

JO - Acta Neuropathologica

JF - Acta Neuropathologica

SN - 0001-6322

ER -

ID: 14942339