Cell surface localization of the peripheral-type benzodiazepine receptor (PBR) in adrenal cortex

Oke, B. O.; Suárez‐Quian, Carlos A.; Ferrara, Pascual; Papadopoulos, Vassilios

doi:10.1016/0303-7207(92)90248-5

Cited by 80 publications

(45 citation statements)

References 15 publications

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“…It is well established that, in the CNS, PBR are mainly expressed in glial cells (Benavides et al, 1990;Moynagh et al, 1991). Although PBR are primarily located on the mitochondrial membrane (Anholt et al, 1986;Papadopoulos, 1993), it has been shown that PBR are also present at the plasma membrane level in various cell types, including rat skeletal fibroblasts , rat adrenocortical cells (Oke et al, 1992), rat Leydig cells (Garnier et al, 1993), and frog hypothalamic neurons (Do-Régo et al, 1998). In addition, the occurrence of PBR has been demonstrated in a plasma membrane-enriched preparation from rat astrocytes (Itzhak et al, 1993).…”

Section: Ttn Binds To Pbr Located At Plasma Membrane Levelmentioning

confidence: 97%

The triakontatetraneuropeptide TTN increases [Ca²⁺]_i in rat astrocytes through activation of peripheral‐type benzodiazepine receptors

Gandolfo

Louiset

Patte

et al. 2001

Glia

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Astrocytes synthesize a series of regulatory peptides called endozepines, which act as endogenous ligands of benzodiazepine receptors. We have recently shown that one of these endozepines, the triakontatetraneuropeptide TTN, stimulates DNA synthesis in astroglial cells. The purpose of the present study was to determine the mechanism of action of TTN on cultured rat astrocytes. Binding of the peripheral-type benzodiazepine receptor ligand [3H]Ro5-4864 to intact astrocytes was displaced by TTN, whereas its C-terminal fragment (TTN[17-34], the octadecaneuropeptide ODN) did not compete for [3H]Ro5-4864 binding. Microfluorimetric measurement of cytosolic calcium concentrations ([Ca2+]i) with the fluorescent probe indo-1 showed that TTN (10(-10) to 10(-6) M) provokes a concentration-dependent increase in [Ca2+]i in cultured astrocytes. Simultaneous administration of TTN (10(-8) M) and Ro5-4864 (10(-5) M) induced an increase in [Ca2+]i similar to that obtained with Ro5-4864 alone. In contrast, the effects of TTN (10(-8) M) and ODN (10(-8) M) on [Ca2+]i were strictly additive. Chelation of extracellular Ca2+ by EGTA (6 mM) or blockage of Ca2+ channels with Ni2+ (2 mM) abrogated the stimulatory effect of TTN. The calcium influx evoked by TTN (10(-7) M) or by Ro5-4864 (10(-5) M) was not affected by the N- and T-type calcium channel blockers omega-conotoxin (10(-6) M) and mibefradil (10(-6) M), but was significantly reduced by the L-type calcium channel blocker nifedipine (10(-7) M). Patch-clamp studies showed that, at negative potentials, TTN (10(-7) M) induced a sustained depolarization. Reduction of the chloride concentration in the extracellular solution shifted the reversal potential from 0 mV to a positive potential. These data show that TTN, acting through peripheral-type benzodiazepine receptors, provokes chloride efflux, which in turn induces calcium influx via L-type calcium channels in rat astrocytes.

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Section: Ttn Binds To Pbr Located At Plasma Membrane Levelmentioning

confidence: 97%

The triakontatetraneuropeptide TTN increases [Ca²⁺]_i in rat astrocytes through activation of peripheral‐type benzodiazepine receptors

Gandolfo

Louiset

Patte

et al. 2001

Glia

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“…Stimulation of steroidgenesis is mediated through a peripheral-type benzodiazepine receptor, which is subcellularly located at mitochondrial membranes in most tissues (21). Recently, cell surface receptors on the plasma membrane have been demonstrated on adrenal cortical cells and Leydig cells (25,26). (26).…”

Section: Luminal Secretion Of Dbi-like Immunoreactivity Duringmentioning

confidence: 99%

Diazepam binding inhibitor is a potent cholecystokinin-releasing peptide in the intestine.

Herzig

Schön

Tatemoto

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

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authors request that the following correction be noted. On page 7927 in the Abstract, diazepam binding inhibitor [33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50] is mentioned incorrectly and should read: ''Similarly, diazepam binding inhibitor 33-52 also stimulated CCK release and pancreatic secretion in a dosedependent manner although it was 100 times less potent than the whole peptide.'' Also, due to a printer's error, the corresponding author's address should read D-24105 Kiel. CorrectionProc. Natl. Acad. Sci. USA 93 (1996) Proc. Natl. Acad.

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“…The main functions of the PBR include: cholesterol binding and transport essential for biosynthesis of steroids and bile salts; protein import for biogenesis of membranes; porphyrin binding and transport for the biosynthesis of heme; ion transport and immunomodulation [24,25]. Although the PBR is mainly located in the outer mitochondrial membrane, especially at the contact sites of the outer and inner mitochondrial membranes, it can be also found in nuclear fractions of normal and cancerous human liver tissue and in the plasma membrane and membrane of organelles in various cell types [26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

MicroPET/CT Imaging of [¹⁸F]-FEPPA in the Nonhuman Primate: A Potential Biomarker of Pathogenic Processes Associated with Anesthetic-Induced Neurotoxicity

Zhang

Paule

Newport

et al. 2012

ISRN Anesthesiology

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Background. The inhalation anesthetics nitrous oxide (N 2 O) and isoflurane (ISO) are used in surgical procedures for human infants. Injury to the central nervous system is often accompanied by localization of activated microglia or astrocytosis at the site of injury. The tracer that targets to the peripheral benzodiazepine receptor (PBR), [ 18 F]N-2-(2-fluoroethoxy)benzyl)-N-(4-phenoxypyridin-3-yl)acetamide ([ 18 F]-FEPPA), has been reported as a sensitive biomarker for the detection of neuronal damage/inflammation. Methods. On postnatal day (PND) 5 or 6 rhesus monkey neonates were exposed to a mixture of N 2 O/oxygen and ISO for 8 hours and control monkeys were exposed to room air. MicroPET/CT images with [ 18 F]-FEPPA were obtained for each monkey 1 day, one week, three weeks, and 6 months after the anesthetic exposure. Results. The radiotracer quickly distributed into the brains of both treated and control monkeys on all scan days. One day after anesthetic exposure, the uptake of [ 18 F]-FEPPA was significantly increased in the temporal lobe. One week after exposure, the uptake of [ 18 F]-FEPPA in the frontal lobe of treated animals was significantly greater than that in controls. Conclusions. These findings suggest that microPET imaging is capable of dynamic detection of inhaled anesthetic-induced brain damage in different brain regions of the nonhuman primate.

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Cell surface localization of the peripheral-type benzodiazepine receptor (PBR) in adrenal cortex

Cited by 80 publications

References 15 publications

The triakontatetraneuropeptide TTN increases [Ca²⁺]_i in rat astrocytes through activation of peripheral‐type benzodiazepine receptors

The triakontatetraneuropeptide TTN increases [Ca²⁺]_i in rat astrocytes through activation of peripheral‐type benzodiazepine receptors

Diazepam binding inhibitor is a potent cholecystokinin-releasing peptide in the intestine.

MicroPET/CT Imaging of [¹⁸F]-FEPPA in the Nonhuman Primate: A Potential Biomarker of Pathogenic Processes Associated with Anesthetic-Induced Neurotoxicity

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Cell surface localization of the peripheral-type benzodiazepine receptor (PBR) in adrenal cortex

Cited by 80 publications

References 15 publications

The triakontatetraneuropeptide TTN increases [Ca2+]i in rat astrocytes through activation of peripheral‐type benzodiazepine receptors

The triakontatetraneuropeptide TTN increases [Ca2+]i in rat astrocytes through activation of peripheral‐type benzodiazepine receptors

Diazepam binding inhibitor is a potent cholecystokinin-releasing peptide in the intestine.

MicroPET/CT Imaging of [18F]-FEPPA in the Nonhuman Primate: A Potential Biomarker of Pathogenic Processes Associated with Anesthetic-Induced Neurotoxicity

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The triakontatetraneuropeptide TTN increases [Ca²⁺]_i in rat astrocytes through activation of peripheral‐type benzodiazepine receptors

The triakontatetraneuropeptide TTN increases [Ca²⁺]_i in rat astrocytes through activation of peripheral‐type benzodiazepine receptors

MicroPET/CT Imaging of [¹⁸F]-FEPPA in the Nonhuman Primate: A Potential Biomarker of Pathogenic Processes Associated with Anesthetic-Induced Neurotoxicity