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- W2219713874 endingPage "183" @default.
- W2219713874 startingPage "143" @default.
- W2219713874 abstract "This chapter discusses the presynaptic regulation of release in the central nervous system (CNS). The presynaptic receptors near noradrenergic nerve endings may mediate inhibition by prostaglandins, endorphins, and histamine and facilitation by acetylcholine and γ-amino butyric acid (GABA). The inhibition of catecholamine release by neighbouring neurotransmitters may be a biochemical phenomenon parallel to the electrophysiological phenomenon called “presynaptic” or “remote” inhibition. In some cases of inhibition of synaptic transmission, the inhibitory compound acts not on the postsynaptic cell to make it less excitable but rather on the presynaptic excitatory nerve terminals to reduce the release of transmitter. The interpretation of the electrophysiological “presynaptic inhibition” is controversial. However, it cannot be excluded that the biochemical and electrophysiological studies, performed on different neuron systems, in fact basically deal with the same phenomenon. Biochemical studies support a GABAergic inhibition of dopamine neurons in vivo. After intracerebroventricular or systemic administration of amino-oxyacetic acid or high doses of GABA, the brain content of dopamine increases while its utilization declines. The effect of GABA is antagonized by picrotoxin. Interestingly, the biosynthesis of dopamine is simultaneously increased, presumably because with decreasing release and decreasing extracellular concentration of dopamine, the receptor-mediated feedback inhibition of tyrosine hydroxylase ceases." @default.
- W2219713874 created "2016-06-24" @default.
- W2219713874 creator A5049724951 @default.
- W2219713874 date "1979-01-01" @default.
- W2219713874 modified "2023-09-27" @default.
- W2219713874 title "PRESYNAPTIC REGULATION OF RELEASE IN THE CENTRAL NERVOUS SYSTEM" @default.
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