AMINO ACID AND PROTEIN METABOLISM OF THE BRAIN-VII THE PENETRATION OF CHOLINESTERASE INHIBITORS INTO THE NERVOUS SYSTEM OF THE FROG

1961 ◽  
Vol 8 (3-4) ◽  
pp. 189-200 ◽  
Author(s):  
Doris H. Clouet ◽  
Heinrich Waelsch
1976 ◽  
Vol 22 (5) ◽  
pp. 649-660 ◽  
Author(s):  
Héctor Maldonado ◽  
Alfonso Tablante ◽  
Norberto Balderrama

1958 ◽  
Vol 2 (2-3) ◽  
pp. 216-225 ◽  
Author(s):  
S. Furst ◽  
A. Lajtha ◽  
H. Waelsch

2013 ◽  
Vol 110 (7) ◽  
pp. 1567-1582 ◽  
Author(s):  
Andrew D. Bolton ◽  
Marnie A. Phillips ◽  
Martha Constantine-Paton

N-methyl-d-aspartate receptors (NMDARs) have been linked to schizophrenia because agents that bind the receptor, like ketamine and phencyclidine, are capable of inducing schizophrenia-like symptoms. Here we show that the amino acid homocysteine (HCY), which is increased in the blood of schizophrenia patients, reduces desensitization of NMDARs in cultured mouse neurons, human embryonic kidney cells transfected with GluN1 + GluN2A, GluN2B, or GluN2D subunits, and hippocampal slices. HCY also alters the peak amplitude of NMDAR currents, depending on the GluN2 subunit the receptor contains; GluN1 + GluN2A-containing NMDARs show an increase in peak amplitude when exposed to HCY, while GluN1 + GluN2B-containing NMDARs show a decrease in peak amplitude. Both peak amplitude and desensitization effects of HCY can be occluded by saturating the NMDAR with glycine. Since glycine concentrations are not saturating in the brain, HCY could play an NMDAR-modulating role in the nervous system. We also show that HCY shares characteristics with glutamate and suggest that HCY affects both the agonist and co-agonist site of the NMDAR.


1957 ◽  
Vol 1 (3) ◽  
pp. 289-300 ◽  
Author(s):  
A. Lajtha ◽  
S. Furst ◽  
A. Gerstein ◽  
H. Waelsch

1982 ◽  
Vol 7 (12) ◽  
pp. 1515-1522 ◽  
Author(s):  
H. Sershen ◽  
M. E. A. Reith ◽  
M. Banay-Schwartz ◽  
A. Lajtha

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