Male rats treated 3 wk earlier with streptozotocin showed abnormally high blood levels of leucine, isoleucine, and valine throughout the 24-h period. Serum phenylalanine levels were slightly increased, while those of tryptophan and tyrosine were occasionally reduced. In brain, the level of each branched-chain amino acid was significantly increased above normal at all times. The brain concentration of each aromatic amino acid was always below normal. These changes were restored almost to normal by exogenous insulin therapy. Since the ingestion of protein is normally a major factor influencing blood amino acid levels, the effect of ingesting single, protein-containing meals on the blood and brain levels of these amino acids was also studied. After an overnight fast, the ingestion of a protein-containing meal by diabetic rats increased substantially both blood and brain levels of each branched-chain amino acid. No such increases occurred in normal rats. Ingestion of this meal produced only small changes in the brain and blood levels of the aromatic amino acids in both diabetic and normal rats. The changes in the brain level of each large neutral amino acid in some cases paralleled those in its blood level. More often, they paralleled the changes in the blood ratio of each amino acid to the sum of the other aromatic and branched-chain amino acids. This ratio is often a good predictor of the competitive transport of these amino acids into brain (Fernstrom and Faller, 1978). The observed changes in the brain levels of these amino acids in diabetes may influence the rates at which they are consumed in metabolic pathways within this organ.
The rate of serotonin synthesis in brain was determined in streptozotocin-diabetic and normal rats using two methods. Both the rate of 5-hydroxytryptophan accumulation after aromatic amino acid decarboxylase inhibition, and the decline rate of 5-hydroxyindole acetic acid after pargyline treatment were significantly reduced in diabetic rats. The reduced rate of synthesis may be a direct result of significantly lowered brain tryptophan levels in diabetic rats.
In normal, fasting rats, intubation with glucose did not alter serum tryptophan, but it did reduce serum concentrations of the large neutral amino acids, tryptophan's competitors for brain uptake. The serum ratio of tryptophan to the sum of these competitors, which predicts brain tryptophan uptake, was thus increased. Brain tryptophan, serotonin (which is synthesized from tryptophan), and 5-hydroxyindoleacetic acid levels also increased. Such increases in brain serotonin are potentially important, since serotonin is a neurotransmitter. Changes in its level may indicate altered release by neurons and, thus, modified brain function. In contrast, glucose intubation of fasting streptozotocindiabetic rats elicited only a small increase in the serum tryptophan ratio. Brain tryptophan increased slightly; no changes occurred in brain serotonin or in 5-hydroxyindoleacetic acid. Similar effects were noted when fasting diabetic rats consumed a single, carbohydrate meal. However, brain indoles did increase after carbohydrate ingestion in diabetic rats that received an insulin injection at the time food was presented. Effects of ingesting a protein-containing meal were also studied. In normal rats, consumption of this meal increased the serum tryptophan ratio slightly. Brain tryptophan and serotonin levels were unchanged. In diabetic rats, ingestion of the protein-containing meal often lowered the serum tryptophan ratio. Brain tryptophan also fell in diabetic rats when the serum tryptophan ratio was reduced, but brain 5-hydroxyindoles did not fall. The data demonstrate that the absence of a carbohydrate-induced increment in brain indole levels follows indirectly from the absence of the insulin-induced rise in the serum tryptophan ratio. The diabetic rat's inability to experience normal carbohydrate-induced increments in brain serotonin suggests that brain functions, normally dependent on such neurochemical signals, may be abnormal.
To elucidate the impact of name descriptiveness and aging on learning new names, 26 young and 26 healthy older participants learned visibly-descriptive (e.g., Lengthy for a giraffe), psychologicallydescriptive (e.g., Classy), and non-descriptive (e.g., Sam) proper names for previously-unknown cartoon characters. More visibly-descriptive names were learned than psychologically-or nondescriptive names, which did not differ from each other. There was also a differential benefit for older adults when the name was visibly-descriptive of the referent, such that older adults learned visibly-descriptive names as well as young adults but there were substantial age-related deficits in learning psychologically-and non-descriptive names.Proper names are harder to learn and remember than other types of biographical and semantic information (e.g., Cohen & Burke, 1993;McWeeny, Young, Hay, & Ellis, 1987;Valentine, Brennen, & Brédart, 1996), and aging is associated with substantial, disproportionate declines both in learning new names and in retrieving known names (e.g.,
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