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Alternating-current light-emitting devices based on conjugated polymers (1996)

Wang, Y. Z. ; Gebler, D. D. ; Lin, L. B. ; [et al.]

Woodbury, NY : American Institute of Physics (AIP)

Applied Physics Letters 68 (1996), S. 894-896

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ISSN: 1077-3118

Source: AIP Digital Archive

Topics: Physics

Notes: Most polymer electroluminescent devices to date are represented as tunnel diodes and operate under direct-current (dc) driving field. Here we report the fabrication of symmetrically configured alternating-current (ac) light-emitting (SCALE) devices based on conjugated polymers. The new devices consist of an emissive polymer layer sandwiched between two redox polymer layers. This configuration enables the SCALE devices to work under both forward and reverse dc bias as well as in ac modes. The nearly ohmic electrode/redox polymer contacts improve the charge injection efficiency significantly and make the SCALE device operation insensitive to electrode work functions. Symmetric operation supports the key role of redox polymer/emissive polymer interface states. © 1996 American Institute of Physics.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1063/1.116222

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Interactive effects of nicotine and MPTP on striatal tetrahydrobiopterin in mice (1996)

Tsai, M. J. ; Wang, H. L. ; Lee, E. H. Y.

Springer

Journal of biomedical science 3 (1996), S. 47-53

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ISSN: 1423-0127

Keywords: Nicotine ; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Mecamylamine ; Biopterin ; Dopamine ; Striatum

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin known to cause dopamine (DA) neuron degeneration, while the psychoactive compound nicotine is known to excite DA neurons. Tetrahydrobiopterin is the cofactor for tyrosine hydroxylase (TOH) in the regulation of DA biosynthesis. The present study investigated the interactions between nicotine and MPTP on striatal biopterin, DA and TOH activity in BALB/c mice. The results indicated that both acute and chronic nicotine administrations at various concentrations significantly increased biopterin and DA levels in the striatum, while MPTP markedly decreased these measures. Pretreatment with nicotine at a dose having no significant effect alone, partially protected against MPTP's toxicity on biopterin and DA. Increasing the dose of nicotine did not have a further protective action. The toxicity of MPTP on TOH was also prevented by nicotine. Further, the above effects of nicotine were probably mediated through the cholinergic nicotinic receptors since mecamylamine reversed the effects of nicotine. These results suggest that nicotine interacts with the dopaminergic system probably at the level of DA biosynthesis through activating TOH and its coenzyme tetrahydrobiopterin.