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Notes: Abstract Stable, yellow anodic films of parathiocyanogen (SCN) x were formed on a platinum electrode from 2.8 M KSCN in methanol at 45 °C at a constant current of 20–40 mA cm−2 for 15–30 min. Loosely bound orange crystals of a more amorphous character were removed by rinsing to leave an adherent yellow film with sharp Raman bands under 647.1 nm laser excitation at 627 cm−1 (vCS), 1152 cm−1 and 1236–1261 cm−1 (vNN and vCN). The lack of electroactivity and short-lived photocurrents pointed to an insulating film at potentials up to 1.0 V (SHE). At more positive potentials, longer-lasting photocurrents were obtained, consistent with breakdown of the insulating film. XPS scans confirmed N:C:S ratios close to 1:1:1, with a deficiency of S of some 10% due to S lost as sulfate at the film surface. Oxidation of SeCN− in neutral aqueous solution led to the formation of a less-stable orange paraselenocyanogen film with a Raman band at 1256–1267 cm−1, which decomposed within a day to grey selenium.

Notes: The high-affinity uptake of L-[3H]glutamate and L-[3H]aspartate into synaptosomes prepared from rat cerebral cortical, hippocampal, and cerebellar tissue was reduced by a number of structural analogues of L-glutamate and L-aspartate. thero-3-Hydroxy-L-aspartic acid was a more potent inhibitor of L-glutamate uptake than of L-aspartate uptake in the cerebral cortex, but not in the hippocampus or cerebellum. A similar pattern of selectivity was observed for cis-l-aminocyclobutane-1,3-dicarboxylic acid. Dihydrokainate was also more potent against L-glutamate than against L-aspartate in the cerebral cortex, but in the hippocampus, it was more potent against L-aspartate than against L-glutamate. By contrast, L-α-aminoadipate was significantly more potent in the cerebellum than in the cerebral cortex and hippocampus as an antagonist of both L-glutamate and L-aspartate. These results support other evidence that there is regional heterogeneity in acidic amino acid uptake sites and that the amino acids L-glutamate and L-aspartate may be taken up by a number of transport systems with overlapping substrate specificity but different inhibitor profiles.

Notes: Inherited congenital myoclonus (ICM) of Poll Hereford cattle is a neurological disease in which there are severe alterations in spinal cord glycine-mediated neurotransmission. There is a specific and marked decrease, or defect, in glycine receptors and a significant increase in neuronal (synaptosomal) glycine uptake. Here we have examined the characteristics of the cerebral γ-aminobutyric acid (GABA) receptor complex, and demonstrate that the malfunction of the spinal cord inhibitory system is accompanied by a change in the major inhibitory system in the cerebral cortex. In synaptic membrane preparations from ICM calves, both high- and low-affinity binding sites for the GABA agonist [3H]muscimol were found (KD= 9.3 ± 1.5 and 227 ± 41 nM, respectively), whereas only the high-affinity site was detectable in controls (KD= 14.0 ± 3.1 nM). The density and affinity of benzodiazepine agonist binding sites labelled by [3H]diazepam were unchanged, but there was an increase in GABA-stimulated benzodiazepine binding. The affinity for t-[3H]butylbicyclo-o-benzoate, a ligand that binds to the GABA-activated chloride channel, was significantly increased in ICM brain membranes (KD= 148 ± 14 nM) compared with controls (KD= 245 ± 33 nM). Muscimol-stimulated 36Cl- uptake was 12% greater in microsacs prepared from ICM calf cerebral cortex, and the uptake was more sensitive to block by the GABA antagonist picrotoxin. The results show that the characteristics of the GABA receptor complex in ICM calf cortex differ from those in cortex from unaffected calves, a difference that is particularly apparent for the low-affinity, physiologically relevant GABA receptors. Study of the GABA receptor complex in ICM calves may provide a greater insight into the interactions of the various binding sites on the GABA-benzodiazepine receptor protein molecule.

Notes: Abstract: The binding of [35S]t-butylbicyclophosphorothionate ([35S]TBPS), a γ-aminobutyric acid (GABA)-activated chloride ionophore ligand; [3H]diazepam, a benzodiazepine agonist; and [3H]muscimol, a GABA receptor probe, were used to assess the effects at 100 μM of deltamethrin, dichlorodiphenyltrichloroethane (DDT), and three experimental insecticides—a DDT-pyrethroid hybrid, GH414 (cycloprothrin), and two DDT-analogues, GH266 and GH149 (EDO), on GABA receptor ionophore complexes in a rat brain membrane preparation. GH266 and GH149 were found to inhibit a greater percentage of [35S]TBPS binding than the same concentration of deltamethrin or DDT, although GH414 had little effect. GH266 and GH149 enhanced [3H]diazepam binding by nearly 200%, in contrast to the inhibitory effects of deltamethrin, DDT, and GH414. GH266 and GH149 also caused a dramatic enhancement of [3H]muscimol binding, 367 and 236% of control, respectively, whereas DDT and deltamethrin caused only a moderate enhancement. The effects of the insecticides on binding affinity and density were examined for each of the ligands. The results show a differential interaction of the insecticides on the various ligand binding sites.

Notes: Abstract: Cerebral cortex tissue was obtained at autopsy from neonatal Poll Hereford calves with clinically confirmed maple syrup urine disease (MSUD), neonatal Holstein-Friesian calves with clinically confirmed citrullinemia, and matched controls. From this, synaptosomes were prepared for studies of neurotransmitter amino acid uptake and stimulus-induced release, and synaptic plasma membranes were obtained for studies of associated postsynaptic receptor binding sites. As well as having abnormal brain tissue concentrations of the pathognomic plasma amino acids (markedly increased levels of the branched-chain compounds valine, isoleucine, and leucine in MSUD; marked elevation of citrulline levels in citrullinemia), both groups of diseased animals showed reduced, brain tissue concentrations of each of the transmitter amino acids glutamate, aspartate, and γ-aminobutyric acid (GABA). Nontransmitter amino acids were generally unaffected in either disease. Citrullinemic calves showed a marked increase in brain glutamine concentration; in calves with MSUD, the glutamine concentration was raised, but to a much lesser extent. The Na+-dependent synaptosomal uptake of both glutamate and GABA was markedly reduced (to 〈50% of control values in both cases) in citrullinemic calves but was unaltered in calves with MSUD. Whereas synaptosomes from normal calves showed the expected stimulus-coupled release of transmitter amino acids, especially glutamate and aspartate, and no response to stimulus of nontransmitter amino acids, there was no increased release of transmitter amino acids in response to depolarization in synaptosomes from citrullinemic calves. This was in part because the extracellular concentrations of these compounds in citrullinemic control incubations were already high, especially for glutamate—basal extrasynaptosomal glutamate concentrations were some 20-fold higher than those found with synaptosomes from normal calves—so that further stimuluscoupled enhancement was not possible. Calves with MSUD showed a marked loss in number of postsynaptic GABAA receptors (to ∼-50% of normal values), as assessed from [3H]diazepam binding studies. In contrast, there was no loss of this receptor site in citrullinemic calves. Calves with citrullinemia showed a marked reduction in the affinity and density of postsynaptic glutamate N-methyl-D-aspartate receptors as assessed from [3H]MK-801 binding studies. In contrast, calves with MSUD showed no change in this parameter. These studies show that two major recessively inherited diseases of cattle have similar, but distinct, neurochemical pathologies. The MSUD encephalopathy appears to be driven by a diminution of GABA-mediated inhibitory neurotransmission, whereas in citrullinemia the equivalent proconvulsive state may be driven by a relative increase in glutamate-mediated excitatory activity.

Notes: Abstract: Up to 60% of γ-[3H]aminobutyric acid ([3H]GABA) bound specifically to rat cerebellar membranes in the absence of Ca2+ was insensitive to the GABAA antagonist bicuculline and to the GABAB agonist baclofen. This indicates that a significant component of specifically bound [3H]GABA is associated with non-GABAA, non-GABAB binding sites. The presence of this binding component appeared seasonal, peaking in the month of September (early spring) each year over a 4-year period. The calcium independence and bicuculline and baclofen insensitivity of the binding indicate that this binding is not to the classical GABAA and GABAB binding sites. High concentrations of muscimol and isoguvacine inhibited non-GABAA, non-GABAB binding. Scatchard analysis of the non-GABAA, non-GABAB binding sites indicated two kinetic components: KDI= 42 nM and KD2= 9.2 μM; Bmaxi= 1.6 pmol/mg of protein and Bmax2= 28 pmol/mg of protein.

Notes: Abstract: The effects of lead on the uptake and release of γ-[3H]aminobutyric acid ([3H]GABA) from rat brain slices were examined in solutions buffered with Tris-HCl, sodium phosphate, and sodium bicarbonate. Lead acetate (10–250 μM) inhibited uptake and potassium-stimulated release and facilitated spontaneous efflux only in solutions buffered with Tris-HCl. Calcium-independent binding of [3H]GABA was unaffected by lead acetate (1–100 μM) in Tris-citrate buffer but was significantly inhibited by 3 μM lead acetate in Tris-HCl solution. At the rat soleus neuromuscular junction, lead caused a dose-dependent reduction of end-plate potential amplitude at concentrations of 10–100 μM lead acetate in HEPES-buffered solution but had no effect at these concentrations in phosphate-buffered solution. Stability constants of lead complexes indicate that buffers containing carbonate and phosphate are unlikely to contain a significant concentration of Pb2+, as complexing by these anions would reduce the availability of free Pb2+. This study indicates that the choice of buffer is important when investigating the effects of lead on biological systems and that negative findings may result from the use of inappropriate buffers. It also has important clinical implications suggesting that some effects of lead poisoning may result from its ability to affect neurotransmitter systems directly and that local changes in pH and complexing anion concentrations in the CNS may influence its biological availability and, hence, variable biological responses.

Notes: The angular dependence of the elastic scattering of helium atoms from a low coverage (aitch-thetaCO=0.03) of randomly distributed isolated CO molecules adsorbed on a Pt(111) surface has been measured over a wide range of incident helium atom beam energies between Ei=5.25 and 62.1 meV. The results are compared with a close-coupling theory for a realistic He–CO potential. From a best fit of the experimental results the distance of the molecule from the surface and a modified gas phase He–CO potential are obtained. © 2000 American Institute of Physics.

Notes: The adsorption of xenon on the sodium chloride (001) surface has been studied using high-resolution helium atom scattering. From the temperature dependence of the specular intensity in the range between 27 and 70 K under isobaric conditions the heat of adsorption of the Xe monolayer was determined to be Eads=19.2±2 kJ/mol. At monolayer coverage, helium atom diffraction measurements reveal that a strained quasi-hexagonal superstructure is formed, which differs from the well-known hexagonal structure of the Xe bulk, and has a c(10×2) symmetry. The perpendicular frustrated translation vibrational energy was measured with helium atom time-of-flight spectroscopy to be 2.5 meV and showed an avoided crossing with the NaCl surface Rayleigh mode. A further dispersive mode of the monolayer has been assigned to a longitudinal in-plane mode of the Xe layer. As found for Xe monolayers on several low index copper surfaces the best fit radial force constant for this mode is a factor of four smaller than deduced from the Xe–Xe gas-phase potential. © 1998 American Institute of Physics.