Specific immunolysis of serotonergic nerve terminals using an antiserum against tryptophan hydroxylase.
An antiserum to tryptophan hydroxylase purified from whole rat brain when incubated with rat striatal synaptosomes in the presence of complement caused release of 18% of LDH, 20% loss of potassium and 60% loss of tryptophan hydroxylase. Uptake of 5-HT was reduced by 60%. Anti-tryptophan hydroxylase alone, or complement alone were without action. The antiserum plus complement had no effect on DA uptake and did not release TH or GAD. These results suggest selective lysis of serotonergic nerve terminals had occurred. The antiserum plus complement reduced choline uptake by 45%. However, this did not seem due to lysis of cholinergic terminals, as ChAT was not released.
D000818:Animals; D001921:Brain / Q000201:enzymology; D002794:Choline / Q000378:metabolism; D003165:Complement System Proteins / Q000276:immunology; D003342:Corpus Striatum / Q000648:ultrastructure*; D007106:Immune Sera / Q000276:immunology / Q000494:pharmacology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009411:Nerve Endings / Q000276:immunology*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012701:Serotonin / Q000502:physiology*; D013574:Synaptosomes / Q000276:immunology* / Q000378:metabolism; D014365:Tryptophan Hydroxylase / Q000276:immunology* / Q000378:metabolism
D007106:Immune Sera; D012701:Serotonin; D003165:Complement System Proteins; D007770:L-Lactate Dehydrogenase; D014365:Tryptophan Hydroxylase; D002794:Choline; D011188:Potassium