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At least 721 records · Page 40Linked to original sources
PubMed1988

Blood-brain barrier transport of 1-aminocyclohexanecarboxylic acid, a nonmetabolizable amino acid for in vivo studies of brain transport.

Regional transport of 1-aminocyclohexanecarboxylic acid (ACHC), a nonmetabolizable amino acid, across the blood-brain barrier was studied in pentobarbital-anesthetized rats using an in situ brain perfusion technique. The concentration dependence of influx was best described by a model with a saturable and a nonsaturable component. Best-fit values for the kinetic constants of the frontal cortex equaled 9.7 X 10(-4) mumol/s/g for Vmax, 0.054 mumol/ml for Km, and 1.0 X 10(-4) ml/s/g for KD in the absence of competing amino acids. Saturable influx could be reduced by greater than 85% by either L-phenylalanine or 2-aminobicyclo[2.2.1]heptane-2-carboxylic acid, consistent with transport by the cerebrovascular neutral amino acid transport system. The transport Km for ACHC was one-fifth that for the more commonly used homologue, 1-aminocyclopentanecarboxylic acid, and was similar to values for several natural amino acids, such as L-methionine, L-isoleucine, and L-tyrosine. The results indicate that ACHC may be a useful probe for in vivo studies of amino acid transport into brain.

Amino Acids↗
PubMed1978

Management of late corneal graft problems.

Immediately after an operation the corneal graft is taken care of by the surgeon, but after a certain period of time the control lies in the hands of the general ophthalmologist. Examples of the management of different kinds of postoperative complications are presented. Early correct treatment of any graft problem is of decisive importance. Careful slit-lamp examination and measurement of graft thickness is stressed and the prompt use of systemic and subconjunctival steroids is recommended for incipient graft failure. Systemic tranexamic acid may also be useful.

Adrenal Cortex Hormones↗
PubMed1999

Structural requirement of the calcium-channel subunit alpha2delta for gabapentin binding.

Gabapentin [Neurontin, 1-(aminomethyl)cyclohexaneacetic acid] is a novel anticonvulsant drug with a high binding affinity for the Ca(2+)-channel subunit alpha(2)delta. In this study, the gabapentin-binding properties of wild-type and mutated porcine brain alpha(2)delta proteins were investigated. Removal of the disulphide bonds between the alpha(2) and the delta subunits did not result in a significant loss of gabapentin binding, suggesting that the disulphide linkage between the two subunits is not required for binding. Singly expressed alpha(2) protein remained membrane associated. However, alpha(2) alone was unable to bind gabapentin, unless the cells were concurrently transfected with the expression vector for delta, suggesting that both alpha(2) and delta are required for gabapentin binding. Using internal deletion mutagenesis, we mapped two regions [amino acid residues 339-365 (DeltaF) and 875-905 (DeltaJ)] within the alpha(2) subunit that are not required for gabapentin binding. Further, deletion of three other individual regions [amino acid residues 206-222 (DeltaD), 516-537 (DeltaH) and 583-603 (DeltaI)] within the alpha(2) subunit disrupted gabapentin binding, suggesting the structural importance of these regions. Using alanine to replace four to six amino acid residues in each of these regions abolished gabapentin binding. These results demonstrate that region D, between the N-terminal end and the first putative transmembrane domain of alpha(2), and regions H and I, between the putative splicing acceptor sites (Gln(511) and Ser(601)), may play important roles in maintaining the structural integrity for gabapentin binding. Further single amino acid replacement mutagenesis within these regions identified Arg(217) as critical for gabapentin binding.

Acetates↗
PubMed1975

Purification and characterization of catabolic dehydroquinase, an enzyme in the inducible quinic acid catabolic pathway of Neurospora crassa.

Catabolic dehydroquinase which functions in the inducible quinic acid catabolic pathway in Neurospora crassa has been purified 8000-fold. The enzyme was purified by two methods. One used heat denaturation of contaminating proteins; the other used antibody affinity chromatography. The preparations obtained by these two methods were identical by all criteria. The purified enzyme is extremely resistant to thermal denaturation as well as denaturation 0y urea and guanidine hydrochloride at 25 degrees. It is irreversibly inactivated, although not efficiently dissociated, by sodium dodecyl sulfate and guanidine hydrochloride at 55 degrees. At pH 3.0, the enzyme is reversibly dissociated into inactive subunits. At high concentrations catabolic dehydroquinase aggregates into an inactive, high molecular weight complex. The native enzyme, which has a very high specific activity, has a molecular weight of approximately 220,000 and is composed of identical subunits of 8,000 to 12,000 molecular weight each. The native enzyme and the subunit are both asymmetric.

Amino Acids↗
PubMed2003

[Effect of anticonvulsant gabapentin on visceral nociception and its relationship with amino acid neurotransmitters released from spinal cord].

OBJECTIVE: To test whether gabapentin, an anticonvulsant, is able to inhibit responses to peritoneal irritation-induced visceral pain and to examine the effect of gabapentin on spinal cord amino acid release. METHODS: Forty-eight SD rats randomly received intraperitoneal (i.p.) injection of saline or gabapentin (50, 100, or 200 mg.kg-1), and 40 minutes later, 0.6% acetic acid (4 ml.kg-1) was administrated intraperitoneally. The acetic acid-induced writhing assay was used to determine the degree of nociception. The beam balance task was employed to test a possible inhibitory or sedative effect of the central nervous system. Cerebrospinal fluid dialysate was collected by microdialysis from the spinal subarachnoid space in anesthetized rats. Concentrations of amino acids in the dialysate, including glutamate, aspartate, serine, glutamine and glycine, following i.p. injection of acetic acid were evaluated. The effects of pretreatment with saline or gabapentin (100 mg.kg-1 i.p.) on amino acid release were compared. RESULTS: Gabapentin reduced writhing responses in a dose-related fashion. Beam-balance time was significantly shortened after pretreatment with 200 mg.kg-1 of gabapentin. Dialysate concentrations of glutamate, aspartate and serine increased significantly-following i.p. injection of acetic acid, while glutamine and glycine concentrations were not. When compared to saline-treated rats, animals pre-treated with 100 mg.kg-1 of gabapentin showed suppression of the acetic acid-induced increases in glutamate, aspartate and serine concentrations. CONCLUSION: These data demonstrate that gabapentin effectively inhibited acetic acid-induced nociception, and the antinociceptive effect of gabapentin might correlate with the suppression of noxious-evoked release of excitatory amino acids in the spinal cord.

Acetates↗