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A novel composite is presented as a supercapacitor electrode with a high maximum power rating (990 kW/kg; 396 kW/l) exceeding power performances of other electrodes. The high-power capability of the electrode stemmed from its unique meso-macro pore structure engineered through the utilization of single-walled carbon nanotubes (20 wt %) as scaffolding for single-walled carbon nanohorns (80 wt %). The novel composite electrode also exhibited durable operation (6.5% decline in capacitance over 100 000 cycles) as a result of its monolithic chemical composition and mechanical stability. The novel composite electrode was benchmarked against another high-power electrode made from single-walled carbon nanotubes (Bucky paper electrode). While the composite electrode had a lower surface area compared to the Bucky paper electrode (280 vs 470 m(2)/g from nitrogen adsorption), it had a higher meso-macro pore volume (2.6 vs 1.6 mL/g from mercury porosimetry) which enabled the composite electrode to retain more electrolyte, ensuring facile ion transport, hence achieving a higher maximum power rating (970 vs 400 kW/kg).

Two monoclonal antibodies, bd-17 and bd-24, specific for the beta- and alpha-subunit of the GABAA/benzodiazepine receptor/chloride channel complex, respectively, were used to determine the subcellular distribution of immunoreactivity in the cerebellum by electron microscopy. The 2 antibodies showed similar antigen distribution on the plasma membrane (except in the rat; bd-24 does not recognize the rat antigen), but intracellular immunoreactivity was more prevalent for the alpha-subunit. The plasma membrane of all neuronal types was immunopositive. The degree of immunoreactivity varied greatly between different types of cell, but it was stereotyped among individual cells of the same type. Granule cells showed the strongest immunoreactivity, not only on their dendrites which receive synapses from GABA-containing Golgi cell terminals, but also on their somata which do not receive synapses. Stellate and basket cells were somewhat weaker in immunoreactivity. Purkinje cells were only weakly positive on their somatic membrane but stronger on their dendritic shafts and spines. Golgi cells showed negligible if any immunoreactivity. Neurons of the deep cerebellar nuclei were strongly immunopositive along their plasma membrane. Immunoreactivity was strong in cisternae of the endoplasmic reticulum and in the Golgi saccules of stellate and basket cells, variable in Purkinje cells, while granule cells were rarely immunoreactive intracellularly. It is suggested that these differences reflect differences in the turnover of the receptor complex in the different cell types. The synaptic clefts established by boutons of the GABAergic stellate, basket, and Golgi cells were immunopositive, as were many synapses in the deep cerebellar nuclei. However, immunoreactivity was also present along the nonjunctional plasma membrane, and it was concluded that this reflected the distribution of the antigen. The synaptic clefts at the presumed glutamate-releasing parallel and mossy fiber terminals were almost always immunonegative. No immunoreactivity was detected on axons, nerve terminals, or glial cells. The results demonstrate that different neuronal types express the GABAA/benzodiazepine receptor/chloride channel complex to different degrees. The distribution of the receptor complex suggests that the cellular topography of GABAergic influence is not governed by the precise spatial arrangement of the receptors but by the precise placement of the GABA-releasing terminals, a characteristic of the cerebellar circuit.

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The two monoclonal antibodies, bd-17 and bd-24, are specific for beta- and alpha-subunits of the GABAA/benzodiazepine receptor/chloride channel complex respectively. An abundance of both subunits has been revealed in the visual thalamus of the cat by light microscopic immunocytochemistry using these antibodies. The alpha-subunit specific antibody and electron microscopy were used to determine the subcellular distribution of immunoreactivity with respect to specific cell classes in the dorsal lateral geniculate nucleus. Immunoreactivity was always associated with membranes and the degree of immunoreactivity varied greatly between different types of cell as defined by: (i) immunoreactivity for GABA; (ii) soma area; (iii) presence or absence of cytoplasmic laminated bodies (CLB). GABA negative neurons with the smallest soma area showed the strongest immunoreactivity, mainly in the endoplasmic reticulum and also on the somatic plasma membrane. Cytoplasmic laminated bodies could be found in the majority of these neurons. Large GABA negative cells without CLBs were strongly immunoreactive on the plasma membrane of the soma and dendrites, but showed scant if any intracellular immunoreactivity. GABA-positive cells showed weak intracellular immunoreactivity but negligible if any immunoreactivity at the somatic and proximal dendritic plasma membrane. A similar reaction pattern was found in GABA negative cells which contained no CLBs and which constituted a medium sized cell population. It is suggested that the degree of intracellular receptor immunoreactivity is positively correlated with receptor turnover. The dendrites of projection cells, particularly outside the glomeruli, showed strong immunoreactivity on the plasma membrane. The synaptic junctions formed by many boutons (F terminals) establishing symmetrical synapses with dendrites of relay cells were immunopositive, but no immunoreactivity could be detected at the synapses established by the presynaptic dendrites of the local interneurons. Many axo-somatic F1 junctions were also immunoreactive. However, immunoreactivity for the receptor/channel complex was also widely distribution on nonsynaptic plasma membranes of somata and dendrites. Thus GABA may act at both synaptic and non-synaptic sites. Furthermore, the correlation of immunoreactivity for the GABAA receptor complex with previously published properties of physiologically identified cells suggests that the strongly immunoreactive, small, GABA negative cells with CLBs might correspond to the 'lagged' X-type cells, and the large GABA negative receptor outlined cells without CLBs might correspond to some of the Y-type neurons.

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Two distinct subtypes of angiotensin (Ang) II receptors, type 1 (AT(1)) and type 2 (AT(2)), have been identified. Vascular smooth muscle cells (VSMCs) usually express AT(1) receptor. To elucidate the direct effects of the AT(2) receptor on the AT(1) receptor in VSMCs, we transfected AT(2) receptor gene into cultured rat VSMCs. Overexpression of AT(2) receptor significantly decreased expression of AT(1a) receptor at both the mRNA and protein levels in the presence and absence of Ang II in VSMCs. Overexpression of AT(2) receptor increased expression of bradykinin and inducible NO in the presence and absence of Ang II in VSMCs. Bradykinin B(2) receptor antagonist HOE-140 and NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) inhibited the decreases in AT(1a) receptor expression by the overexpression of AT(2) receptor in VSMCs. L-Arginine augmented the decrease in AT(1a) receptor expression. Overexpression of AT(2) receptor suppressed basal DNA synthesis and proliferation of VSMCs and abolished response of DNA synthesis to Ang II in VSMCs. Our results demonstrate that overexpression of the AT(2) receptor downregulates AT(1a) receptor expression in rat VSMCs in a ligand-independent manner that is mediated by the bradykinin/NO pathway. Downregulation of AT(1a) receptor is a novel mechanism by which the AT(2) receptor regulates growth and metabolism of VSMCs.

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