Various π-conjugated copolymers constituted of π-excessive thiophene, selenophene, or furan units (Ar) and π-deficient pyridine or quinoxaline (Ar‘) units have been prepared in high yields by the following organometallic polycondensation methods:  (i) n X−Ar−Ar‘−X + n Ni(0)Lm → (-Ar−Ar‘)- n (X = halogen, Ni(0)Lm = zerovalent nickel complex), (ii) n X−Ar−X + n Me3Sn−Ar‘−SnMe3 → (-Ar−Ar‘)- n (palladium catalyzed), and (iii) a X−Ar−X + b X−Ar‘−X + (a + b)Ni(0)Lm → (-Ar) x (Ar‘)- y . Powder X-ray diffraction analysis confirms an alternative structure of a polymer prepared by the method ii. The copolymers have a molecular weight of 5.4 × 103 to 3.3 × 105 and an [η] value of 0.37 to 4.4 dL g-1. π−π* absorption bands of the copolymers generally show red shifts from those of the corresponding homopolymers, (-Ar)- n and (-Ar‘)- n , and the red shifts are accounted for by charge-transferred CT structures of the copolymers. For example, an alternative copolymer of thiophene and 2,3-diphenylquinoxaline gives rise to an absorption band at λmax = 603 nm, whereas homopolymers of thiophene and 2,3-diphenylquinoxaline exhibit absorption peaks at about 460 and 440 nm, respectively. The CT copolymers are electrochemically active in both oxidation and reduction regions, showing oxidation (or p-doping) peaks in a range of 0.39 to 1.32 V vs Ag/Ag+ and reduction (or n-doping) peaks in a range of −1.80 to −2.22 V vs Ag/Ag+, respectively. Copolymers of pyridine give unique cyclic voltammograms exhibiting p-undoping peaks at potentials much different (about 2−3 V lower) from the corresponding p-doping potentials, and this large difference between p-doping and p-undoping potentials is explained by an EC mechanism. They are converted into semiconductors by chemical and electrochemical oxidation and reduction. Copolymers of thiophene with pyridine and quinoxaline show the third-order nonlinear optical susceptibility χ(3) of about 5 × 10-11 esu at the three-photon resonant wavelength, which is 5−7 times larger than those of the corresponding homopolymers and related to the CT structure in the copolymers.

The importance of voltage-dependent Ca2+ channels (VDCCs) in pain transmission has been noticed gradually, as several VDCC blockers have been shown to be effective in inhibiting this process. In particular, the N-type VDCC has attracted attention, because inhibitors of this channel are effective in various aspects of pain-related phenomena. To understand the genuine contribution of the N-type VDCC to the pain transmission system, we generated mice deficient in this channel by gene targeting. We report here that mice lacking N-type VDCCs show suppressed responses to a painful stimulus that induces inflammation and show markedly reduced symptoms of neuropathic pain, which is caused by nerve injury and is known to be difficult to treat by currently available therapeutic methods. This finding clearly demonstrates that the N-type VDCC is essential for development of neuropathic pain and, therefore, controlling the activity of this channel can be of great importance for the management of neuropathic pain.

␣1 subunit of the voltage-dependent Ca 2؉ channel is essential for channel function and determines the functional specificity of various channel types. ␣1E subunit was originally identified as a neuron-specific one, but the physiological function of the Ca 2؉ channel containing this subunit (␣1E Ca 2؉ channel) was not clear compared with other types of Ca 2؉ channels because of the limited availability of specific blockers. To clarify the physiological roles of the ␣1E Ca 2؉ channel, we have generated ␣1E mutant (␣1E؊͞؊) mice by gene targeting. The lacZ gene was inserted in-frame and used as a marker for ␣1E subunit expression. ␣1E؊͞؊ mice showed reduced spontaneous locomotor activities and signs of timidness, but other general behaviors were apparently normal. As involvement of ␣1E in pain transmission was suggested by localization analyses with 5-bromo-4-chloro-3-indolyl ␤-D-galactopyranoside staining, we conducted several pain-related behavioral tests using the mutant mice. Although ␣1E؉͞؊ and ␣1E؊͞؊ mice exhibited normal pain behaviors against acute mechanical, thermal, and chemical stimuli, they both showed reduced responses to somatic inflammatory pain. ␣1E؉͞؊ mice showed reduced response to visceral inflammatory pain, whereas ␣1E؊͞؊ mice showed apparently normal response compared with that of wild-type mice. Furthermore, ␣1E؊͞؊ mice that had been presensitized with a visceral noxious conditioning stimulus showed increased responses to a somatic inflammatory pain, in marked contrast with the wild-type mice in which long-lasting effects of descending antinociceptive pathway were predominant. These results suggest that the ␣1E Ca 2 ؉ channel controls pain behaviors by both spinal and supraspinal mechanisms.V oltage-dependent calcium channels (VDCCs) are classified into several distinct groups termed L-, N-, P-, Q-, R-, and T-types (1, 2). These types of VDCCs play important roles in various neuronal activities, including the control of neurotransmitter release, membrane excitability, and gene expression (3), but exact roles of each channel type are not necessarily clarified. In particular, functions of the R-type Ca 2ϩ channel are least understood. The R-type Ca 2ϩ channel was originally defined as a channel ''Resistant'' to blockers for L-, N-, P-, and Q-type Ca 2ϩ channels (4); therefore, it is possible that the R-type current is a mixture of several different drug-resistant Ca 2ϩ currents. Although the R-type Ca 2ϩ channel is suggested to play a critical role in the release of neurotransmitters and somatodendritic excitability in a certain set of neurons (4-6), the physiological functions of this channel remain to be clarified.VDCCs are heteromultimers composed of ␣ 1 , ␣ 2 -␦, ␤, and ␥ subunits. ␣ 1 subunit is essential for channel function and determines the type of each Ca 2ϩ channel. So far, 10 different ␣ 1 cDNAs (␣ 1A-I and ␣ 1S ) have been cloned from a variety of tissues, and extensive studies have been made to clarify the relationship between each cloned ␣ 1 subunit and native Ca 2ϩ channels (2)....

Palladium-catalyzed polycondensation between dihalo aromatic compounds X-Ar-X (3hexyl-2,5-diiodothiophene, 2,5-dibromoselenophene, and 3,4-dinitro-2,5-dibromothiophene) and diethynyl aromatic compounds HC=C-Ar'-C=CH (2,5-diethynylpyridine, 3-hexyl-2,5-diethynylthiophene, and p-diethynylbenzene) in the presence of triethylamine gives soluble -conjugated poly(aryleneethynylene) (PAE) type polymers (-Ar-C=C-Ar'-C=C-)" when Ar and/or Ar' contains the long alkyl substituent and/or pyridine ring. The PAE type polymers are obtained in high yields (86-100 %), have molecular weights of 9.6 X 10 59 X 104 and pv (degree of depolarization) values of 0.005-0.034 as determined by the light scattering method, and show absorption bands in the range 350-462 nm, which are shifted from the absorption bands of the corresponding aromatic units (HArH and HAr'H), indicating the occurrence of -conjugation along the polymer chain. The polymers exhibit fluorescence in solutions, and the position of the fluorescence is shifted to a longer wavelength in films of the polymers, suggesting the formation of excimer-like adducts in the solid state. The polymer films give a (3) (third-order nonlinear optical susceptibility) value of about 5 x 10"u esu when the Ar group has the hexyl group. Cyclic voltammetry of the PAE type polymers indicates that they receive reduction (n-doping) at about -2 V vs Ag/Ag+ whereas oxidation (p-doping) of the polymer is difficult presumably due to the electron-withdrawing effect of the -C=Cgroup. HBr addition to the -C=Cgroup of the polymer gives a polymer having a -CH=CH(Br)group, which can be further converted into ester and amide groups.

oxides for this reaction appears to correlate with basicity, with no dependence on variable cation valencies or lattice oxygen mobilities as appears to be significant for some other reactions, such as CO oxidation, on these materials.49 Accordingly, in a mechanistic study by Minachev et it was proposed that hydrogen dissociation can occur due to the polarizing action of a rare-earth cation and an oxygen ion and is the rate-limiting step in C2H4 hydrogenation on these materials. On the basis of a series of isotopic studies on Dy203 at 220 K, Minachev et al. further proposed that ethylene is associatively adsorbed on the oxide surface and that the reaction proceeds via a semihydrogenated C2H4 (adsorbed) complex. This catalytic activity of the rare-earth oxides toward C2H4 hydrogenation does not necessarily contradict our observation of the absence of molecular adsorption of C2H4 on oxidized Gd under UHV conditions, because the correlation between the strength of adsorption and hydrogenation activity is unknown.Accordingly, two areas for further investigation are indicated. First, studies of the catalytic activity of rare earth oxide surfaces toward acetylene hydrogenation are necessary for comparison with studies of ethylene hydrogenation. Second, investigations by other techniques, especially vibrational spectroscopy, of the structure of the C2H2 moiety adsorbed on oxidized rare-earth surfaces at low temperature will be valuable for comparison with our UPS results. These studies will provide a clearer understanding of the adsorption selectivity of these rare earth oxide surfaces to C2Hz and CzH4 and of the possible correlation between adsorption selectivity and hydrogenation activity. V. Summary and ConclusionsThe adsorption of C2H2 and C2H4 has been studied on both the metallic Gd(0001) surface6 and on the oxidized surface of Gd(0001). Adsorption of both species is dissociative on the metallic surface at 165 K, and there is no detectable adsorption selectivity for these species on the metallic surface. In contrast, the Gd surface after oxidation preferentially adsorbs acetylene over ethylene at a substrate temperature of 165 K. The adsorption probability for acetylene under these conditions is estimated as 0.02 by using measurements of the carbon Auger signal versus exposure. The adsorption probability for ethylene on the oxidized Gd surface at 165 K is, at the very least, a factor of 3 lower and is probably lower by as much as a factor of 100. On the basis of the available UPS data, it is suggested that acetylene adsorbs molecularly on the oxidized surface at low temperature. The molecularly adsorbed CzH2 decomposes below 350 K, leaving carbon on the oxidized Gd surface. The enhanced selectivity of the oxidized Gd surface toward acetylene over ethylene adsorption is unique. This work suggests that studies of the hydrogenation of C2H2 and C2H4 on gadolinium oxide would be useful to probe the possible extension of the selectivity for adsorption into selectivity for hydrogenation.Two new types of highly soluble n...

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Intrathecal (i.t.) administration of pituitary adenylate cyclase-activating polypeptide (PACAP) induces long-lasting nociceptive behaviors for more than 60 min in mice, while the involvement of PACAP type1 receptor (PAC1-R) has not been clarified yet. The present study investigated signaling mechanisms of the PACAP-induced prolonged nociceptive behaviors. Single i.t. injection of a selective PAC1-R agonist, maxadilan (Max), mimicked nociceptive behaviors in a dose-dependent manner similar to PACAP. Pre- or post-treatment of a selective PAC1-R antagonist, max.d.4, significantly inhibited the nociceptive behaviors by PACAP or Max. Coadministration of a protein kinase A inhibitor, Rp-8-Br-cAMPS, a mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase inhibitor, PD98059 or a c-Jun N-terminal kinase (JNK) inhibitor, SP600125, significantly inhibited the nociceptive behaviors by Max. Immunohistochemistry and immunoblotting analysis revealed that spinal administration of Max-induced ERK phosphorylation and JNK phosphorylation, and also augmented an astrocyte marker, glial fibrillary acidic protein in mouse spinal cord. Furthermore, an astroglial toxin, l-α-aminoadipate, significantly attenuated the development of the nociceptive behaviors and ERK phosphorylation by Max. These results suggest that the activation of spinal PAC1-R induces long-lasting nociception through the interaction of neurons and astrocytes.