Subsynaptosomal distribution, inhibition, and characterization of the binding of (14C) 5-OH-indole-3-acetaldehyde to brain preparations.
The distribution of the monoamine oxidase (MAO) dependent binding of [14C] serotonin as well as of pre-formed [14C] 5-OH-indole-3-acetaldehyde to synaptic subfractions paralleled the gross distribution of MAO. The binding of [14C] serotonin and MAO activity in brain preparations was inhibited by CNS antidepressants (imipramine) or stimulants (caffeine), by hallucinogens (N,N-dimethyltryptamine), sedatives (chlorpromazine), and other drugs. The protein-lipid nature of the binding macromolecule was determined. The chemical nature of the acceptors was also investigated. Experiments with sodium borohydride indicated the partial formation of imines, those with SH-reactive compounds showed partial involvement of acceptor-SH groups in the binding.
Subsynaptosomal distribution, inhibition, and characterization of the binding of (14C) 5-OH-indole-3-acetaldehyde to brain preparations. The distribution of the monoamine oxidase (MAO) dependent binding of [14C] serotonin as well as of pre-formed [14C] 5-OH-indole-3-acetaldehyde to synaptic subfractions paralleled the gross distribution of MAO. The binding of [14C] serotonin and MAO activity in brain preparations was inhibited by CNS antidepressants (imipramine) or stimulants (caffeine), by hallucinogens (N,N-dimethyltryptamine), sedatives (chlorpromazine), and other drugs. The protein-lipid nature of the binding macromolecule was determined. The chemical nature of the acceptors was also investigated. Experiments with sodium borohydride indicated the partial formation of imines, those with SH-reactive compounds showed partial involvement of acceptor-SH groups in the binding.