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At least 19 recordsLinked to original sources
PubMedDate not supplied

Effects of melatonin on hypothalamic gamma-aminobutyric acid, aspartic acid, glutamic acid, beta-endorphin and serotonin levels in male mice.

Effects of melatonin on hypothalamic neurotransmitters in male mice were studied. Exogenous melatonin administered intraperitoneally significantly increased (p < 0.05) hypothalamic concentrations of aspartic acid and gamma-aminobutyric acid by over 29 and 50% respectively. Conversely, hypothalamic beta-endorphin concentration was significantly decreased (p < 0.05) 30 min after melatonin administration with doses between 5- and 100 micrograms/kg. Similarly, melatonin, at a concentration of 100 micrograms/kg, decreased (p < 0.05) the serotonin level in mouse hypothalamus by 46%. Melatonin, however, did not affect the concentration of hypothalamic glutamic acid over a dose range of 0.5-300 micrograms melatonin/kg. Our findings suggested that actions of pineal melatonin in animals such as inhibition on serum corticosterone levels might be mediated by the potentiation of activities of hypothalamic neurons containing gamma-aminobutyric acid and aspartic acid or by the inhibition of the beta-endorphin and serotonin hypothalamic neurons. The neurons containing glutamic acid in the hypothalamus were, however, not influenced by melatonin. Our results are in line with the suggestion that melatonin actions on adrenal corticosterone release or other endocrine secretions may be mediated by way of its actions on hypothalamic neurotransmitter activities.

Animals↗
PubMedDate not supplied

Biochemical changes in progressive muscular dystrophy, XVI. Effect of glutamic acid, aspartic acid and glycine on the amino acid content of skeletal muscle of dystrophic mice.

The effect of exogenous administration of glutamic acid (GL), aspartic acid (A) and glycine (G) on individual amino acids in the free amino acid pool was studied in skeletal muscles of 60- to 70-day-old normal (N) and dystrophic (D) mice. Both N and D mice received either 0.25 ml of saline (S) or 250 mg/kg weight of GL, A or G in 0.25 ml S subcutaneously for 13 days. GL, A, G or S did not cause any significant changes in the body and skeletal muscle weights of either group. Most of the individual amino acids were increased in skeletal muscles of GL-treated mice and were decreased in A- or G-treated animals compared to S administration in the N group. The picture was more dramatic in the D group: GL-induced amino acid elevations were more pronounced than the values of N- or S-treated D controls. A and G elicited amino acid increases in D mice compared to their S-treated counterparts. Most of the individual amino acids in skeletal of the D group were decreased relative to N mice after S, GL or A administration. This was evident when the D/N ratio was calculated for S, GL and A. The situation was very different after G administration since of the individual amino acids were augmented in the skeletal muscle of D mice compared to N animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1990

Substitution of a single amino acid (aspartic acid for histidine) converts the functional activity of human complement C4B to C4A.

The C4B isotype of the fourth component of human complement (C4) displays 3- to 4-fold greater hemolytic activity than does its other isotype C4A. This correlates with differences in their covalent binding efficiencies to erythrocytes coated with antibody and complement C1. C4A binds to a greater extent when C1 is on IgG immune aggregates. The differences in covalent binding properties correlate only with amino acid changes between residues 1101 and 1106 (pro-C4 numbering)--namely, Pro-1101, Cys-1102, Leu-1105, and Asp-1106 in C4A and Leu-1101, Ser-1102, Ile-1105, and His-1106 in C4B, which are located in the C4d region of the alpha chain. To more precisely identify the residues that are important for the functional differences, C4A-C4B hybrid proteins were constructed by using recombinant DNA techniques. Comparison of these by hemolytic assay and binding to IgG aggregates showed that the single substitution of aspartic acid for histidine at position 1106 largely accounted for the change in functional activity and nature of the chemical bond formed (ester vs. amide). Surprisingly, substitution of a neutral residue, alanine, for histidine at position 1106 resulted in an increase in binding to immune aggregates without subsequent reduction in the hemolytic activity. This result strongly suggests that position 1106 is not "catalytic" as previously proposed but interacts sterically/electrostatically with potential acceptor sites and serves to "select" binding sites on potential acceptor molecules.

Animals↗
PubMed1996

Evidence for release of glutamic acid, aspartic acid and substance P but not gamma-aminobutyric acid from primary afferent fibres in rat spinal cord.

In vitro superfusion release experiments and autoradiography were carried out on spinal cords of neonatally capsaicin-treated rats. Electrical and chemical stimulations significantly increased the release of aspartate, glutamate and gamma-aminobutyric acid (GABA) from hemisected dorsal horn slices of vehicle-treated animals. In capsaicin-treated rats, the evoked release of aspartate, glutamate and substance P but not GABA, were significantly lower. Capsaicin (1 microM) stimulated the release of aspartate and glutamate, as reported for substance P, in control slices but this effect was not as apparent in tissues from capsaicin-treated rats. Evoked GABA release was not affected in either case. alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate, dizocilpine and GABAB binding sites were highly localised in the substantia gelatinosa. Capsaicin treatment did not affect the affinity of the binding sites in all four cases but significantly reduced the density of kainate, dizocilpine and GABAB binding sites. The data suggest that capsaicin-sensitive primary afferent fibres release aspartate, glutamate and Substance P following high-intensity stimulations and that this release might be modulated by presynaptic glutamate and GABAB receptors present on these terminals.

Afferent Pathways↗
PubMed1996

The effects of N-methyl-D,L-aspartic acid and aspartic acid on the plasma concentration of gonadotrophins, GH and prolactin in the ewe.

Aspartic acid is a neurotransmitter in the central nervous system that acts via the glutamate receptor and the analogue, N-methyl-D,L-aspartic acid (NMA) is an agonist that stimulates GnRH secretion. Under normal dietary conditions, the plasma concentration of aspartic acid in ewes is low and if increased by improved nutrition may increase the brain concentration of aspartic acid leading to increased gonadotrophin secretion. In two experiments we investigated the effects of NMA on pituitary hormone concentrations and the effects of aspartic acid on ovulation rate and pituitary hormone concentrations. The intravenous injection of NMA into cycling ewes resulted in an immediate (within 15 min) release of a pulse of LH and of GH and a prolonged (up to 1 h) suppression of prolactin secretion. There were marked differences in responsiveness to NMA between individual ewes. The intravenous infusion of aspartic acid for 5 days in the late luteal phase of the oestrous cycle did not affect ovulation rate but reduced the mean LH (P < 0.05) and FSH (P < 0.05) concentrations in plasma. The frequency of LH pulses also tended to be lower (P < 0.1) in ewes infused with aspartic acid. It is suggested that the decrease in gonadotrophin secretion in ewes infused with aspartic acid is due to effects on the hypothalamus or the anterior pituitary gland which are not related to increased levels of ovarian feedback. These changes are likely to involve decreased GnRH secretion.

Animals↗
PubMed1979

Rapid method for the assay of 4-aminobutyric acid (GABA), glutamic acid and aspartic acid in brain tissue and subcellular fractions.

The thin-layer electrophoretic separation at pH 4.8 of brain extracts and a procedure for fluorescent staining of the plates with fluorescamine are described for the rapid routine determination of 4-aminobutyric acid (GABA), glutamic acid and aspartic acid in brain extracts and in particulate fractions of brain tissue. Automated sample application, electrophoretic separation using two chambers, and quantitation by in situ fluorescence scanning allows the assay of 280 samples within three working days. The method is reproducible (S.D. less than 8% of the mean) within the range of 0.2--2 nmole per spot. The staining procedure can be applied to a variety of related analytical problems. The method has proved useful for the determination of the specific radioactivities of GABA, glutamic acid and aspartic acid in metabolic studies.

Aging↗