The effect of caffeine on some mouse brain free amino acid levels.

Changes in free amino acids were examined in the central nervous system of mice treated with caffeine for three weeks. Caffeine was administered in the drinking water, and at the end of three weeks the level of caffeine in the cerebral cortex was 113 +/- 19 micrograms/g. When amino acid levels in cerebral hemispheres, midbrain, pons and medulla, and cerebellum were measured a significant increase in glutamine levels was found in all four regions.

Effects of caffeine on amino acid transport in the brain.

Chronic administration of caffeine to mice did not alter cellular (low-affinity) transport as measured in brain slices of the amino acids ?-aminobutyric acid, glutamic acid, and glycine. Chronic caffeine administration did, however, increase the long-term (60-min) uptake of ?-aminoisobutyric acid and valine into brain slices. A similar tendency, although not statistically significant, towards increased amino acid uptake was also seen in the transport of phenylalanine and lysine across the blood-brain barrier in chronically treated rats.

Depolarization of brain cortex slices and synaptosomes by lithium. Determination of K+-equilibrium potential in cortex slices.

K+-equilibrium potential was determined in brain cortex slices of rat by measuring 86Rb+ distribution between the extra- and intracellular space. The ratio of internal to external Rb+ concentration was 39 +/- 1.8, corresponding to a resting membrane potential of 93.

Modulation of the serotonin S2-receptor in brain after chronic lithium.

In vivo effects of chronic lithium administration on dopaminergic and serotonergic receptor binding were studied in the striatum and cerebral cortex of the rat. [3H]Domperidone was used as the ligand for the dopaminergic receptor, and [3H]ketanserin for the serotonergic system. Long-term ingestion of lithium (2-3 months) resulted in high levels of lithium in the cerebral cortex and significantly higher potassium levels; the sodium content remained at normal levels.

Dietary lithium during development: changes in amino acid levels, ionic content, and [3H]spiperone binding in the brain of rats.

We found that chronic lithium diet affects the sensitivity of neuroleptic receptors and the content of amino acids in the brain, and that the changes in adult animals differ from those in young rats. Pregnant rats were kept on lithium diet (pellets with 0.21% Li2CO3 and 0.

Effects of cations and temperature on the binding of [3H]spiperone to sheep caudate nucleus.

The specific [3H]spiperone binding by sheep caudate nucleus homogenate is increased by divalent cations. The effect of Ca2+ or Mn2+ (5 mM) is temperature-dependent, and it is optimal at about 37 degrees, but is relatively low below 15 degrees and above 50 degrees. In the absence of added Ca2+ or Mn2+, the maximal specific [3H]spiperone binding is observed at about 25 degrees, and the cations shift the optimum to about 37 degrees.

Influence of chronic lithium administration on binding to benzodiazepine- and histamine H1-receptors in rat brain.

In rat, chronic lithium treatment lowered the Kd of [3H]-mepyramine in midbrain, and reduced the Bmax in midbrain and pons-medulla. Binding of [3H]flunitrazepam in cerebellum and midbrain was not altered. The suggestion that some actions of lithium may occur by way of central nervous system receptors is further supported by these observations that lithium's effects on neurotransmitter systems are regional and specific.

Lithium: effect on [3H]spiperone binding, ionic content, and amino acid levels in the brain of rats.

After prolonged treatment of rats with lithium (pellets, 0.21% lithium carbonate, or 0.5 mg/ml lithium chloride in drinking water) for three months, the level of lithium in plasma was 0.

Effect of lithium and sodium ions on opiate- and dopamine-receptor binding.

The effects of lithium and sodium were studied in the corpus striatum and cerebral cortex of rats. Lithium was inhibitory at low concentrations but at 20 mM it increased the binding of [G-3H]naloxone (specific activity 15.6 Ci/mmol).

Distribution of opiate-like substances in rat tissues.

Rat tissues were tested for their ability to inhibit the binding of [3H]dihydromorphine or [3H]naloxone to membrane-bound opiate receptors. By this criterion, morphine-like substances were found in lung, heart, liver, and kidney as well as in brain. The relative activity of the extracts, based on initial tissue weight, differed with the radioactive lignand employed.

The effects of morphine on the accumulation of homovanillic and 5-hydroxyindoleacetic acids in the choroid plexus of rats.

1 Choroid plexus obtained from the lateral ventricles of the rat actively accumulated homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA). 2 Morphine 5 X 10(-6) M to 5 X 10(-4)M potentiated 5-HIAA accumulation but did not affect HVA accumulation. Levorphanol and dextorphan had little effect.

The influence of 3,4-dihydroxyphenylacetic acid on the accumulation of 5-hydroxyindoleacetic acid in the choroid plexus and kidney cortex slices of rats.

In vitro, the choroid plexus of rats accumulates 5-hydroxyindoleacetic acid (5-HIAA) by active transport. In the experiments presented here, the kidney cortex slices also showed active accumulation of this organic acid, which proved to be inhibited by most of the organic acids tested. In the choroid plexus 3,4-dihydroxyphenylacetic acid (DOPAC), a metabolite of dopamine, stimulated the accumulation of 5-HIAA, whereas in the kidney slices DOPAC was inhibitory.

Isotopic labeling of synaptosomes that accumulate choline and the effect of narcotic drugs.

Subcellular studies of choline uptake of rat striatum indicated a correspondence between the Na(+)-dependent uptake and choline acetyltransferase (ChAc), whereas there was a lack of correspondence between the Na(+)-independent uptake and ChAc. Subcellular studies also showed a correspondence between the Na(+)-dependent uptake and hemicholinium-3 inhibition, and more important, particles that accumulate choline were shown to consist of at least two subcellular populations. A comparison was made of kinetic data from three areas of the rat brain: corpus striatum, cerebral cortex, and hypothalamus.

The amphetamine-induced inhibition of dopamine biosynthesis in rat striatum.

The dopamine biosynthetic machinery of intact synaptosomes of rat striatum showed a 5-fold increase in development from 3-day-old neonates to adults, and it was fully developed between 2-3 weeks after birth. Concurring with this development was the appearance 2 weeks after birth of a regulatory mechanism(s) through which amphetamine in vivo induced an inhibition of dopamine biosynthesis. The inhibition was not appreciably reversed when haloperidol, in addition to amphetamine, was administered.

Morphine-induced kinetic alterations of choline acetyltransferase of the rat caudate nucleus.

1. In order to explain the decrease of choline acetyltransferase (2.3.

Effects of morphone on choline acetyltransferase levels in the caudate nucleus of the rat.

1. Choline acetyltransferase (choline-o-acetyltransferase 2.3.