Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat cerebral astrocytes from confluent primary cultures were grown for two weeks in medium made hyperosmotic with additional NaCl. At the time the cells were harvested (four weeks in culture), the medium osmolality of experimental cultures was approximately 600 mOsm. Amino acid, protein, and potassium contents and the cell volume were measured. Compared to cells maintained in control medium (approximately 300 mOsm), cells grown in hyperosmotic conditions had over two times the content of taurine and five times the content of glutamine. Alanine, aspartate, glutamate, glycine, and tyrosine contents also were elevated in these hyperosmotic-treated cells, while asparagine contents were unchanged relative to control cells. Cell volume and potassium content were decreased to approximately 50% of control levels by the hyperosmotic treatment while total protein content per cell was unchanged relative to cells from control cultures. Seven min after hyperosmotic-exposed cells were rapidly diluted into PBS with osmolality equal to about 330 mOsm, cell contents of alanine, asparagine, glutamine, glutamate, glycine, taurine, and tyrosine fell toward control levels. The data indicate that significant alterations in intracellular osmolytes occur in astrocytes adapted to hyperosmotic conditions. We suggest that a loss of intracellular potassium is at least partially compensated by accumulation of taurine, glutamine, and perhaps other amino acids acting as intracellular osmolytes.
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PMID:Amino acid content of rat cerebral astrocytes adapted to hyperosmotic medium in vitro. 225 66

Pentobarbital anesthesia has been observed to increase markedly the effectiveness of respiration of oxygen at 3 atmospheres of pressure absolute to increase the response of early generation isotransplants of C3H mouse tumors to two-dose irradiation. A possible mechanism of this phenomenon is suppression of oxygen utilization by the pentobarbital and hence increasing mean pO2 and oxygen diffusion lengths. Measurements of QO2 of suspension of MCaIV and FSaII cells from freshly excised tumor tissue have been measured for cells suspended in PBS, Hank's buffered with HEPES +/- glutamate. The oxygen utilization by these tumor cells in vitro (when measured at congruent to 10 minutes after excision) is low, viz. 1 nmole/min/mg protein as compared with 6-9 nmoles/min/mg protein for established cell lines cultured in vitro. The suppression of QO2 by 2mM pentobarbital is less than 10%. This is a concentration of pentobarbital that is judged to be close to that which obtains in the tissues of the animals in the radiation response assays. Pentobarbital at .2mM did not change the cell survival characteristics of Chinese V79 cell spheroids irradiated in vitro. The results of these experiments do not indicate the suppression of oxygen utilization is an important contributor to the observed phenomenon of the increased response of tumors irradiated in mice respiring oxygen at high pressure. The role of hypothermia produced by the anesthesia is under further study.
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PMID:On the mechanism for enhancement of tumor radiation to hyperbaric oxygen in sodium pentobarbital anesthetized rodents. 653 7

The present experiments investigated the effects of blocking glutamate transmission in the amygdala on the learning and subsequent performance of a discriminated approach response to food, as well as on locomotor activity and a test of neophobia to food. In the appetitive conditioning experiment, three separate groups of rats received intra-amygdala infusions of PBS (phosphate-buffered saline) or 1.0 or 3.0 nmol of AP5, an antagonist at the NMDA glutamate receptor subtype, immediately before each conditioning session. The effects of AP5 on the performance of the discriminated approach response were tested in a fourth group of animals. AP5 dose-dependently impaired the discriminated approach response during the acquisition of the stimulus-reward association but had no effect on the performance of this response after this association was learned. These results suggest that glutamate transmission in the amygdala at the NMDA glutamate receptor subtype is important in the learning process. In separate experiments, intra-amygdala AP5 increased locomotor activity and attenuated the neophobia to food in a novel environment by increasing approaches to the food. Together, these findings parallel the effects of lesions to the basolateral amygdala. In addition, the specific effects on learning are consistent with the hypothesis that NMDA-receptor-mediated LTP underlies specific forms of learning within the amygdala.
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PMID:Intra-amygdala infusion of the N-methyl-D-aspartate receptor antagonist AP5 impairs acquisition but not performance of discriminated approach to an appetitive CS. 791 8

The nucleus of the solitary tract (NTS) was systematically explored in the alpha-chloralose-anesthetized rat for sites that elicited changes in mean arterial pressure (MAP) and heart rate (HR) during microinjections (20 nl) of phosphate-buffered saline (PBS; pH 7.2-7.4) or NaCl solutions containing various concentrations of NaCl (104-326 mM). Decreases in MAP (range 7-83 mmHg) and HR (range 10-70 bpm) were consistently elicited from sites in the caudal medial and commissural subnuclei of NTS. Microinjection of PBS or NaCl into other NTS subnuclei or area postrema did not elicit cardiovascular responses. Microinjection of LiCl in PBS elicited cardiovascular responses that were significantly smaller than those elicited by microinjection of NaCl in PBS at the same NTS site. Injections of either a hyperosmotic (400 mOsm/kg) or a hyposmotic (204 mOsm/kg) solution of mannitol into NaCl-sensitive sites did not elicit cardiovascular responses. Finally, most of the sites in NTS that elicited cardiovascular responses during microinjection of glutamate (1 M) did not respond to microinjections of PBS. Administration of atropine methyl bromide had no effect on the magnitude of the depressor response to injections of PBS into NTS, but significantly attenuated (32%) the HR response. Subsequent administration of the ganglionic blockers hexamethonium bromide or arfonad abolished both the depressor and bradycardic responses. These data suggest that within a restricted region of the caudal NTS there exists a pool of neurons sensitive to changes in extracellular Na+ concentrations that, when activated by the sodium, elicit vasodepressor responses as a result of sympathoinhibition and bradycardia as a result of vagal excitation and sympathoinhibition.
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PMID:Cardiovascular effects of NaCl microinjections into the nucleus of the solitary tract. 805 35

A rapid and reproducible spinal motor neuron death occurs after sciatic nerve transection in neonatal rats. This neuronal death could be due to lack of retrogradely transported target derived neurotrophic factors, such as ciliary neurotrophic factor, brain-derived neurotrophic factor, leukemia inhibitory factor and glial cell line-derived neurotrophic factor. Another hypothesis suggests that glutamate and its receptors has been implicated as possible mechanism for motor neuron death. In order to investigate the effect of N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists on axotomy-induced cell death in the spinal motor neurons of neonatal rats, we have studied neuroprotective effects of these receptor antagonists. Newborn rats were anesthetized with hypothermia. Sciatic nerve was transected near the obturator tendon in the left thigh. Animals were then treated daily with MK-801, APV, and CNQX for 14 days with intraperitoneal injections. Control animals received PBS in the same fashion. After the treatment, the number of spinal motor neurons in the L4-6 was counted. MK-801 and APV did not show any significant neuroprotective effect. By contrast, the number of surviving motor neurons was greater in animals that were treated with 1.0, 2.0 and 4.0 mg/kg of CNQX. This neuroprotective effect was not dose-related. We demonstrate that neuroprotective effect of CNQX on axotomized motor neurons, raises a possibility that such a agent may have therapeutic potential in motor neuronopathy and amyotrophic lateral sclerosis.
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PMID:CNQX prevents spinal motor neuron death following sciatic nerve transection in newborn rats. 874 38

Excitotoxic amino acids, such as glutamate, may play an important role in retinal ischemia/reperfusion damage. In central neurons, excitotoxicity may be mediated by nitric oxide synthase (NOS) causing DNA damage via nitric oxide (NO). The nicked DNA activates poly-adenosine diphosphate (ADP)-ribose polymerase (PARP) and may deplete intracellular ATP resulting in cell death. PARP may also be involved in apoptosis. We used 3-aminobenzamide (3-ABA), a PARP inhibitor, to examine the possible involvement of PARP in a rat model of retinal ischemia. Retinal ischemia was induced by elevating the intraocular pressure (IOP) through the insertion of a needle into the anterior chamber of a rat eye. IOP was raised to 110 mm Hg for 60 minutes. Animals were given intracameral infusion of 0, 1, 3, 10, 30, 100 mM 3-ABA in 0.1 M PBS, pH 7.4 during ischemia. Morphologic and morphometric evaluation at 7 days after reperfusion showed that 3-ABA at 3 mM and above significantly ameliorated the ischemic/reperfusion damage to the retina. In addition, at 10 mM 3-ABA inhibited the characteristic ladder pattern in DNA gel analysis seen in apoptosis of retinal neurons after ischemia/reperfusion. Hence, PARP may be involved in retinal cell loss after ischemia/reperfusion insult probably through the apoptotic pathway.
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PMID:The effect of 3-aminobenzamide, an inhibitor of poly-ADP-ribose polymerase, on ischemia/reperfusion damage in rat retina. 914 32

We previously reported the protective effect of N-carbamoyl-L-glutamate plus L-arginine in rats given a lethal dose (LD99.9) of ammonium acetate (Kim, S. et al., Proc. Natl. Acad. Sci. 69, 3530-3533, 1971; ref.1). The present study was undertaken to find out whether the same compounds could also be effective even after the functional mass of the liver was significantly reduced. Thus, the protective effect of these compounds in 70% partial hepatectomized rats following the injection of sublethal dose of ammonium acetate was assessed. The mixture could significantly decrease blood ammonia level compared with PBS-injected control group. In addition, abnormal behaviors observed in the control rats were significantly improved. The protective effect on the behavioral change seemed to be closely related with their effect on blood ammonia level, showing a strong correlation between the blood ammonia level and the behavioral score. The findings provide a rational basis for the clinical use of N-carbamoyl-L-glutamate plus L-arginine in the prevention and treatment of hyperammonemia encountered in liver diseases.
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PMID:N-carbamoyl-L-glutamate plus L-arginine can protect ammonia intoxication in rats with reduced functional liver mass. 967 47

Work with varicella-zoster virus has been seriously hampered by the difficulty of preparing high-titre cell free virus, and by the instability of such virus when frozen and thawed. We have evaluated the use of a range of protocols and demonstrate that relatively high titres of 19,000 plaque forming units per millilitre may be recovered after freezing in PBS-sucrose-glutamate-serum buffer (PSGC). In addition, we have shown that the virus obtained by this method gives similar results in neutralisation and antiviral susceptibility assays to that freshly prepared from infected cells, allowing the use of high titre, titrated virus stocks in such assays.
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PMID:High-titre, cryostable cell-free varicella zoster virus. 968 73

The diblock polymer poly(l-leucine-block-l-glutamate), bLE, was synthesized by acid hydrolysis of the ester poly(l-leucine-block-l-methyl glutamate). During the hydrolysis reaction the leucine block precipitates from the reaction mixture, forming nanosized particulate structures. These particles can be purified and further suspended in water or in 0.15 M phosphate saline buffer (PBS) to give stable, colloidal dispersions. TEM analysis shows the predominant particle form to be that of platelets with a diameter of 200 nm. Smaller cylindrical or spherical particles form a relatively minor fraction of the sample. After fractionation, analysis shows the platelets to be compositionally rich in leucine, while the spheres are glutamate-rich. (1)H NMR, CD, and X-ray diffraction indicate that the core of the platelets is composed of crystalline, helical leucine segments. The poly(l-glutamate) polyelectrolyte brush extending out from the two faces of the disk stabilizes individual particles from flocculation. At pH 7.4, the nanoparticles (platelets and cylinders) spontaneously adsorb proteins, such as insulin, directly from solution. Partial desorption of the protein in its native configuration can be induced by simple dilution. The reversibility of the insulin-nanoparticle complex is the basis for a potential new delivery system. Copyright 1999 Academic Press.
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PMID:Macromolecular Colloids of Diblock Poly(amino acids) That Bind Insulin. 1046 44

Transection of the sciatic nerve in neonatal rats results discernable loss of motor neurons in the spinal cord. This neuronal death could be due to lack of retrogradely transported target derived neurotrophic factors, since some of these factors have been shown to be effective in injury induced motor neuron death. Another hypothesis suggests that glutamate and its receptors has been implicated as possible mechanism for motor neuron death, because inhibitor of glutamate release and antagonists of glutamate receptors are effective in preventing axotomized motor neuron death. To investigate the effect of insulin-like growth factor-I (IGF-I) and riluzole, a drug that inhibits glutamate release, on axotomy induced motor neuron death. Newborn rats were anesthetized with hypothermia. Sciatic nerve was cut near the obturator tendon in the left thigh. Animals were then treated daily with different doses of IGF-I and riluzole for 14 days with intraperitoneal injections. Control rats received PBS in the same fashion. After the treatment, the number of surviving motor neurons and the motor neuron diameter in the L(4) was assessed. Both IGF-I (1.0 mg/kg) and riluzole (5.0 mg/kg) rescued motor neuron death in a similar way. Co-administration of IGF-I (1.0 mg/kg) and riluzole (5.0 mg/kg) was more effective than either agent alone and there was a statistically significant difference between co-administration and IGF-I alone. However there was no significant difference between simultaneous treatment and riluzole alone. As for diameter of motor neurons, riluzole (5.0 mg/kg) preserved the motor neuron diameter in the lesion side. Nonetheless, no further increase in motor neuron diameter was seen when riluzole (5 mg/kg) and IGF-I (1.0 mg/kg) were applied in combination. Both agents did not affect diameter of motor neurons in the non-axotomy side. Riluzole is available in amyotrophic lateral sclerosis (ALS) and the positive results of clinical trials with IGF-I suggests that combination treatment of IGF-I and riluzole in ALS remains to be determined.
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PMID:Prevention by insulin-like growth factor-I and riluzole in motor neuron death after neonatal axotomy. 1054 24


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