Disaggregation of brain polysomes by L-5-hydroxytryptophan: Mediation by serotonin

In Vivo Inhibition of Incorporation of [U‐14U]Glucose into Proteins in Experimental Focal Epilepsy

“…Inhibition of protein synthesis in incubated synaptosomes due to exposure to several neurotransmitters has been reported by Goldberg (1972), and mediation of neurotransmitters and related drugs in the polysome disaggregation, which commonly accompanies inhibition of protein synthesis in cell-free systems, has been postulated (Weiss et al, 1971;Weiss et al, 1973;Moskowitz et al, 1975;Baliga et al, 1976;Holbrook and Brown, 1976), though hyperthermia induced by some of the drugs could itself be a causative factor here. In fact very little inhibition of protein labelling occurred in treated and homotopic areas compared with other areas studied, and this might be thought to be due to a greater extent of tissue damage caused by cobalt and freezing, in addition to the longer periods of exposure to hyperactivity.…”

“…Tityustoxin causes massive release, of many neurotransmitters locally in vivo due to its depolarizing action, which can be blocked with tetrodotoxin . Inhibition of protein synthesis in incubated synaptosomes due to exposure to several neurotransmitters has been reported by Goldberg (1972), and mediation of neurotransmitters and related drugs in the polysome disaggregation, which commonly accompanies inhibition of protein synthesis in cell-free systems, has been postulated (Weiss et al, 1971;Weiss et al, 1973;Moskowitz et al, 1975;Baliga et al, 1976;Holbrook and Brown, 1976), though hyperthermia induced by some of the drugs could itself be a causative factor here.…”

“…It could be linked with the accumulation of high concentrations of K+ in the hyperactive cortical tissues. Thus high K+ level alone (104 mM) inhibits protein synthesis in isolated brain preparations (Mase et al, 1962;Austin et al, 1970;Gilbert, 1972;White et al, 1972;Dunlop e t al., 1975), and in the neuronal compartment only of the stellate nerve-ganglion preparation (Pepe et al, 1975). Also general application of K+ (1.34 M ) to the cortex in vivo to cause spreading depression leads to similar effects (Bennett and Edelman, 1969).…”

Effect of Intravenous Administration of d‐Lysergic Acid Diethylamide on Subsequent Protein Synthesis in a Cell‐Free System Derived from Brain

“…It is known that a range of treatments causes a transient disaggregation of brain polysomes to monosomes and frequently a decreased incorporation of amino acid in vivo. These include excess phenylalanine (Aoki and Siegal, 1970;Taub and Johnson, 1975;Roberts and Morelos, 1976), 5-HTP (Weiss et al, 1973;Weiss et al, 1975) L-DOPA (Roe1 et al, 1974;Weiss et al, 1975) and damphetamine (Moskowitz et al, 1975;Widelitz et al, 1975). Physical treatments that result in breakdown of brain polysomes include electroconvulsive shock (Vesco and Giuditta, 1968;Wasterlain, 1972;Dunn, 1973) and intracranial hypertension (Wasterlain, 1974).…”

Characterization of an Initiating Cell‐Free Protein Synthesis System Derived from Rabbit Brain

“…Protein synthesis in the mammalian brain can be disrupted by various means. Such diverse treatments as electroconvulsive shock (Metafora et al, 1977;Wasterlain, 1977), cerebral hypoxia and ischemia (Cooper et al, 1977; Morimoto et al, 1978), amino acid imbalances (Taub and Johnson, 1975;Roberts and Morelos, 1976; Hughes and Johnson, 1977), alterations in catecholamine metabolism (Weiss et al, 1971(Weiss et al, , 1972(Weiss et al, , 1973; Moskowitz et al, 1975Moskowitz et al, , 1977, and intravenous administration of the psychotropic drug lysergic acid diethylamide (LSD) Brown, 1976, 1977;Heikkila et al, 1979) have been shown to result in disaggregation of brain poiysomes and in an inhibition of incor-poration of amino acids into brain proteins. Although it has been suggested that many of these treatments induce a decreased rate of reinitiation of protein synthesis, few precise studies have been carried out on the mechanism of inhibition of brain protein synthesis.…”