Monoclonal Antibodies to Rat Brain Acetylcholinesterase: Comparative Affinity for Soluble and Membrane-Associated Enzyme and for Enzyme from Different Vertebrate Species

1986 ◽  
Vol 46 (1) ◽  
pp. 280-287 ◽  
Author(s):  
Zoltán Rakonczay ◽  
Stephen Brimijoin
Keyword(s):  
Monoclonal Antibodies ◽  
Rat Brain ◽  
Vertebrate Species ◽  
Brain Acetylcholinesterase

scholarly journals Binding of 125I-fasciculin to rat brain acetylcholinesterase. The complex still binds diisopropyl fluorophosphate

1993 ◽  
Vol 268 (17) ◽  
pp. 12458-12467
Author(s):  
P. Marchot ◽  
A. Khélif ◽  
Y.H. Ji ◽  
P. Mansuelle ◽  
P.E. Bougis
Keyword(s):  
Rat Brain ◽  
Diisopropyl Fluorophosphate ◽  
Brain Acetylcholinesterase

Oximes-induced reactivation of rat brain acetylcholinesterase inhibited by VX agent

2004 ◽  
Vol 23 (4) ◽  
pp. 167-171 ◽  
Author(s):  
Kamil Kuča ◽  
Jiří Kassa
Keyword(s):  
Rat Brain ◽  
Brain Homogenate ◽  
Hi 6 ◽  
Brain Acetylcholinesterase

A comparison of one mono- and seven bisquaternary acetylcholinesterase (AChE) reactivators of acetylcholinesterase inhibited by VX agent was performed. As a source of the acetylcholinesterase, a rat brain homogenate was taken. There were significant differences in reactivation potency of all tested oximes. The oxime TO205 seems to be the most efficacious followed by TO046, HI-6, HS-6, K027, obidoxime, MMC and 2-PAM. In addition, the results of this study showed that the reactivation potency of the tested reactivators depends on many factors-such as the number of pyridinium rings, the number of oxime groups and their position, as well as the length and the shape of linkage bridge between two pyridinium rings.

scholarly journals Monoclonal antibodies against a C-terminal peptide of human brain acetylcholinesterase distinguish between erythrocyte and brain acetylcholinesterases

1996 ◽  
Vol 42 (1) ◽  
pp. 19-23 ◽  
Author(s):  
N Boschetti ◽  
U Brodbeck ◽  
S P Jensen ◽  
C Koch ◽  
B Nørgaard-Pedersen
Keyword(s):  
Monoclonal Antibodies ◽  
Human Brain ◽  
Solid Phase ◽  
Bovine Brain ◽  
Mammalian Brain ◽  
Dot Blot ◽  
Electric Eel ◽  
Terminal Amino ◽  
Dot Blot Analysis ◽  
Brain Acetylcholinesterase

Abstract Monoclonal antibodies (mAbs) were raised against a peptide of the 10 C-terminal amino acids of human brain acetylcholinesterase (AChE): H-Tyr-Ser-Lys-Gln-Asp-Arg-Cys-Ser-Asp-Leu-OH. Two positive clones (mAbs 190-1 and 190-2) were selected and tested for their ability to distinguish between mammalian brain and erythrocyte AChEs. In a solid-phase enzyme antigen immunoassay as well as by Western- and dot-blot analysis, both antibodies showed clear binding to AChE from human and bovine brain but not to AChE from erythrocytes. MAbs 190-1 and 190-2 reacted with neither AChE from electric eel nor butyrylcholinesterase from human serum. Both antibodies were used in a quantitative assay for AChE in amniotic fluids, where AChE activity could be found only in samples from open neural tube-defect pregnancies, but not in fluids from normal pregnancies or in artificially blood-contaminated samples.

scholarly journals Immunocytochemical Study of an Early Microglial Activation in Ischemia

1992 ◽  
Vol 12 (2) ◽  
pp. 257-269 ◽  
Author(s):  
Jochen Gehrmann ◽  
Petra Bonnekoh ◽  
Takahito Miyazawa ◽  
Konstantin-Alexander Hossmann ◽  
Georg W. Kreutzberg
Keyword(s):  
Monoclonal Antibodies ◽  
Distribution Pattern ◽  
Rat Brain ◽  
Mhc Class Ii ◽  
Neuronal Damage ◽  
Dorsal Hippocampus ◽  
Neuronal Cell ◽  
Microglial Cells ◽  
Vessel Occlusion ◽  
Temporal And Spatial Distribution

Transient arrest of the cerebral blood circulation results in neuronal cell death in selectively vulnerable regions of the rat brain. To elucidate further the involvement of glial cells in this pathology, we have studied the temporal and spatial distribution pattern of activated microglial cells in several regions of the ischemic rat brain. Transient global ischemia was produced in rats by 30 min of a four-vessel occlusion. Survival times were 1, 3, and 7 days after the ischemic injury. The microglial reaction was studied immunocytochemically using several monoclonal antibodies, e.g., against CR3 complement receptor and major histocompatibility complex (MHC) antigens. Two recently produced monoclonal antibodies against rat microglial cells, designated MUC 101 and 102, were also used to identify microglial cells. Following ischemia, the microglial reaction was correlated with the development of neuronal damage. The earliest presence of activated microglial cells was observed in the dorsolateral striatum, the CA1 area, and the dentate hilus of the dorsal hippocampus. However, the microglial reaction was not confined to areas showing selective neuronal damage, but also occurred in regions that are rather resistant to ischemia, such as the CA3 area. Particularly in the frontoparietal cortex, the appearance of MHC class II–positive microglial cells provided an early indication of the subsequent distribution pattern of neuronal damage. The microglial reaction would thus seem to be an early, sensitive, and reliable marker for the occurrence of neuronal damage in ischemia.

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