Regulation of expression and enzymatic activities of tyrosine and tryptophan hydroxylases in rat brain after acute electroconvulsive shock.

Acute electroconvulsive shock (ECS) causes a significant increase of protein synthesis in depressive patients and such an increase raises the possibility that the regulation of specific proteins and enzymatic activities in the brain might be one of the mechanisms required for the induction of long-term adaptive neurochemical changes after electroconvulsive therapy. In current studies, we investigated and compared simultaneously the short- and long-term effects of an acute ECS on the expression and enzymatic activities of both tyrosine and tryptophan hydroxylases (TH and TpOH, respectively) in different rat brain areas. Our results demonstrated that an acute ECS produced: (1) a long-lasting decrease in TH and TpOH protein levels in locus ceruleus (LC), ventral tegmental area (VTA) and in TpOH protein level in the raphe centralis (RC), maximal at 72 h, with concomitant changes in mRNA levels and enzymatic activities in the LC only; (2) large increase of TpOH protein levels in the frontal cortex (Cxf) (+145%) and increase of TH protein levels in the hippocampus (Hip) (+207%), maximal at 72 h and 7 days which was not accompanied by corresponding increase of in vivo enzymatic activities.

Biochemical and autoradiographic measurements of brain serotonin synthesis rate in the freely moving rat: a reexamination of the alpha-methyl-L-tryptophan method.

Biochemical approaches were used in freely moving rats to determine, under steady-state conditions, the brain/arterial plasma partition coefficients of L-tryptophan and alpha-[3H]methyl-L-tryptophan, from which the lumped constant for the alpha-methyl-L-tryptophan method of estimating the rate of brain serotonin synthesis is calculated. The lumped constants were significantly different in the various structures examined: 0.149 +/- 0.

Early and prolonged widespread increase in brain protein synthesis following a single electroconvulsive shock in free-moving rats.

The autoradiographic method with l-[35S] methionine ([35S]Met) was used to determine the effect of a single electroconvulsive shock (ECS) on local rates of protein synthesis in the adult rat brain in free-moving conditions. We have estimated the relative contribution of methionine derived from protein breakdown to the intracellular precursor amino acid pool (tRNA pool) for protein synthesis. In steady-state conditions, we showed a large contribution (around 60%) of Met recycling into the precursor pool (lambda=0.

Paradoxical metabolic response of the human brain to a single electroconvulsive shock.

Regional brain protein synthesis was evaluated with positron emission tomography (PET) and L-(S-[11C]methyl)methionine ([11C]MET) in depressive patients, before and 3 h after an electroconvulsive shock (ECS), when energy supply is restored, and in healthy volunteers. Depressive patients presented apparent lower protein synthesis than normals, in agreement with known reduction of cerebral activity. In contrast, ECS resulted in a significant increase (56%, P < 0.

Widespread increase in brain protein synthesis following acute immobilization stress in adult rat brain.

The autoradiographic method with [L-35S]methionine was used to determine the effects of a 2 h acute immobilization stress followed by a 4 h recovery on local rates of protein synthesis in the adult rat brain. Methionine incorporation into proteins was significantly increased (from 17 to 86%) in 37 out of the 39 analyzed brain structures. These results show that the stress-induced activation of the overall rate of brain protein synthesis may persist for at least 4 h after cessation of the stimulus even though the stress-related physiological variables have returned to basal levels.