ABSTRACT
We introduce a type of (2+1)D surface soliton in virtue of the cooperation of nonlocal and local nonlinearities. Furthermore, taking advantage of diffusion and drift nonlinearity this type of surface soliton is demonstrated theoretically and experimentally in a storintium barium nitrate crystal. The dynamics behavior of the excitation and propagation of this type of surface soliton are studied using the beam-propagation method and the nonlinear equation of light rays.
ABSTRACT
Mutant E182 with "narrow leaflet-4 seeded pod" was selected from descendents of EMS-treated seeds of soybean variety Lu Dou No. 4 (LD4) with "ovate leaflet-without 4 seeded pod". Genetic analyses of F2 individuals of crossing between mutant E182 and parent LD4 indicated that segregation ratio between ovate and narrow leaflet was 3:1, so was segregation ratio between "without 4 seeded pod" and "4 seeded pod". Segregation ratios of four character types in F2 population of 1,654 individuals were beyond 9:3:3:1 of two pairs of independent gene, showing linkage inheritance. Reccmbinant ratio between mutant genes of narrow leaflet and 4 seeded pod was 11.24% +/- 0.81%. On the other hand, mutant E182, parent LD4 and F2, F3 individuals of their hybrids were analyzed by means of RAPD technique. The marker OPY6-1300 linked with the mutant gene of narrow leaflet was generated, and genetic distance of the marker and mutant gene was 8 cent Morgan (cM), being 10 cM nearer than RFLP marker of narrow leaflet generated by shoemaker.
Subject(s)
Glycine max/genetics , Mutation , Random Amplified Polymorphic DNA Technique , Genetic Markers , Recombination, GeneticABSTRACT
The effects of Ca2+ on glutamate uptake by synaptosomes were investigated. Glutamate uptake was decreased in the absence of Ca2+ with 2 mM EGTA added to the medium. After a 8-min preincubation, the uptake reduced to the greatest extent (about 64% of the uptake measured in Ca2+ medium). According to the kinetic analysis, lack of Ca2+ resulted in a reduction of the Vmax for glutamate uptake. These results suggested external Ca2+ was necessary for the optimal uptake of glutamate. TTX, an inhibitor of the voltage-dependent Na+ channel, almost reversed the reduction of glutamate uptake, indicating that the uptake might be impaired via the partial activation of the voltage-dependent tetrodotoxin-sensitive Na+ channel. On the other hand, glutamate uptake was decreased by trifluoperazine, a calmodulin antagonist, and KN-62, an inhibitor of Ca2+/calmodulin-dependent protein kinase II, implying that intrasynaptosomal Ca2+ might also have a role in the uptake of glutamate, and Ca2+/calmodulin-dependent processes, such as Ca2+/calmodulin-dependent protein kinase II, might be involved in the modulation of glutamate transporter activity.
Subject(s)
Calcium/pharmacology , Glutamic Acid/pharmacokinetics , Synaptosomes/drug effects , Synaptosomes/metabolism , 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/analogs & derivatives , 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/pharmacology , Animals , Calcium-Calmodulin-Dependent Protein Kinase Type 2 , Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors , Calmodulin/antagonists & inhibitors , Cerebral Cortex/metabolism , Chelating Agents/pharmacology , Egtazic Acid/pharmacology , Electrophysiology , Enzyme Inhibitors/pharmacology , Male , Rats , Rats, Sprague-Dawley , Sodium Channel Blockers , Sodium Channels/physiology , Tetrodotoxin/pharmacology , Trifluoperazine/pharmacologyABSTRACT
The rapid effects of glucocorticoids(GCs) on the Na+dependent, high affinity uptake of 3[H]-L-glutamate(Glu) in rat cerebral cortex synaptosomes(4 min incubation) and human neuroblastoma clone SK-N-SH (10min preincubation and 5 min incubation) were investigated. GCs, including corticosterone, corticosterone-sulfate, hydrocortisone-hemisuccinate and dexamethasone 21-phosphate(DEX) were found stimulating Glu uptake. The uptakes in synaptosomes and SK-N-SH cells were increased to 117-126% and 121-137% respectively of the control by 10(-6)mol/L GCs. The stimulation of GCs was dose-dependent. The maximal effect of DEX in SK-N-SH cells appeared at10(-7)mol/L, and the least effective dose of DEX was at 10(-9)mol/L. Guanosine 5-O-(2-thiodiphosphate), an inhibitor of G-protein activation, could block the stimulation of GCs. The results indicated that GCs rapidly enhance the Na+-dependent high affinity Glu uptake in nerve endings and SK-N-SH cells, even at the concentration of physiological conditions, and the G-protein on synaptic membranes or SK-N-SH cell membranes might be involved in the effect of GCs.
Subject(s)
GTP-Binding Proteins/metabolism , Glucocorticoids/pharmacology , Glutamic Acid/pharmacokinetics , Synaptosomes/drug effects , Synaptosomes/metabolism , Animals , Biological Transport, Active/drug effects , Cerebral Cortex/drug effects , Cerebral Cortex/metabolism , Corticosterone/pharmacology , Dexamethasone/pharmacology , Humans , In Vitro Techniques , Male , Rats , Rats, Sprague-Dawley , Tumor Cells, CulturedABSTRACT
The effects of protein kinase C (PKC) and protein kinase A (PKA) on the high affinity glutamate uptake in rat cerebral cortex synaptosomes, cell lines of human neuroblastoma SK-N-SH and human anaplastic astrocytoma BT-325 were studied by measurement of radioactivity of 3[H]-L-glutamate. The results were as follows: (1) PKC agonist phorbol-12-myristate, 13-acetate (PMA) stimulated the glutamate uptake in the rat cerebral cortex synaptosomes and cell line of BT-325, but not in the cell line of SK-N-SH. This effect of PMA was abolished in the presence of PKC antagonist sphingosine. (2) Glutamate uptake in all these three samples of neural tissues and cells was not affected by PKA agonist adenosine 3',5'-cyclicmonophosphate, N6,O2'-dibutyryl. The above results indicate that it is PKC that stimulates high affinity glutamate uptake in glial cells, although the possibility that neurons are also affected to some extent can not be ruled out.
