Densities of binding sites for the “peripheral-type” benzodiazepine receptor ligand3H-PK11195 are increased in brain 24 hours following portacaval anastomosis

1994 ◽  
Vol 9 (3) ◽  
pp. 267-273 ◽  
Author(s):  
Dorothy K. Leong ◽  
Guy Therrien ◽  
Margaret S. Swain ◽  
Roger F. Butterworth
Keyword(s):  
Binding Sites ◽  
Benzodiazepine Receptor ◽  
Portacaval Anastomosis ◽  
Peripheral Type

Increased expression of the peripheral-type benzodiazepine receptor-isoquinoline carboxamide binding protein mRNA in brain following portacaval anastomosis

1997 ◽  
Vol 758 (1-2) ◽  
pp. 255-258 ◽  
Author(s):  
Paul Desjardins ◽  
Patricia Bandeira ◽  
V.L. Raghavendra Rao ◽  
Stéphane Ledoux ◽  
Roger F. Butterworth
Keyword(s):  
Binding Protein ◽  
Benzodiazepine Receptor ◽  
Portacaval Anastomosis ◽  
Peripheral Type

Peripheral-type benzodiazepine receptor binding sites in platelets of patients with panic disorder associated to separation anxiety symptoms

2005 ◽  
Vol 181 (2) ◽  
pp. 407-411 ◽  
Author(s):  
Stefano Pini ◽  
Claudia Martini ◽  
Marianna Abelli ◽  
Matteo Muti ◽  
Camilla Gesi ◽  
...  
Keyword(s):  
Panic Disorder ◽  
Receptor Binding ◽  
Binding Sites ◽  
Separation Anxiety ◽  
Benzodiazepine Receptor ◽  
Anxiety Symptoms ◽  
Peripheral Type

scholarly journals Increased Densities of Binding Sites for the “Peripheral-Type” Benzodiazepine Receptor Ligand [3H]PK11195 in Vulnerable Regions of the Rat Brain in Thiamine Deficiency Encephalopathy

1994 ◽  
Vol 14 (1) ◽  
pp. 100-105 ◽  
Author(s):  
Dorothy K. Leong ◽  
Oanh Le ◽  
Luis Oliva ◽  
Roger F. Butterworth
Keyword(s):  
Binding Sites ◽  
Thiamine Deficiency ◽  
Neuronal Cell ◽  
Neuronal Loss ◽  
Benzodiazepine Receptor ◽  
Cell Loss ◽  
Brain Regions ◽  
Inferior Olivary Nucleus ◽  
Neuronal Cell Loss ◽  
Peripheral Type

Quantitative receptor autoradiography was used to evaluate the density of high-affinity binding sites for the “peripheral-type” benzodiazepine receptor (PTBR) ligand [3H]PK11195 in brain regions of the rat at different stages of pyrithiamine-induced thiamine deficiency encephalopathy, an experimental model of the Wernicke-Korsakoff syndrome (WKS). Assessment of the density of [3H]PK11195 binding sites in thiamine-deficient animals showing no neurologic signs of thiamine deficiency encephalopathy, and revealed no significant alterations compared with pair-fed control animals in any brain region studied. Densities of [3H]PK11195 binding sites were, however, significantly increased in brain regions of the rat at the symptomatic stage, where increased densities were seen in the inferior colliculus (233% increase, p < 0.001), inferior olivary nucleus (154% increase, p < 0.001) and thalamus (up to 107% increase, p < 0.001). Histologic studies of these same brain regions revealed evidence of neuronal cell loss and concomitant gliosis. Densities of [3H]PK11195 binding sites in nonvulnerable brain regions that showed no histologic evidence of neuronal loss, such as the cerebral cortex, hippocampus, and caudate-putamen, were not significantly different from those in control animals. Increased densities of binding sites for the PTBR ligand probably reflect glial proliferation and are consistent with an excitotoxic mechanism in the pathogenesis of neuronal cell loss in thiamine deficiency encephalopathy. Positron emission tomography (PET) using [11C]PK11195 could offer a potentially useful diagnostic tool in WKS in humans.

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