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At least 883 records · Page 49Linked to original sources
PubMed2001

Pituitary adenylate cyclase-activating polypeptide induces period1 and period2 gene expression in the rat suprachiasmatic nucleus during late night.

The suprachiasmatic nucleus generates circadian rhythms which are synchronized to the environmental light-dark cycle via the retinohypothalamic tract. Pituitary adenylate cyclase-activating polypeptide and glutamate, two neurotransmitters co-stored in the retinohypothalamic tract of the rat, are able to phase shift the endogenous rhythm similar to light. The "clock genes" period1 (per1) and per2, which show circadian oscillation within the suprachiasmatic nucleus, have been attributed a role in light-induced resetting of the mammalian circadian clock due to rapid induction of the period (per) genes after light stimulation at night. Using a rat in vitro brain slice model, we demonstrate by quantitative in situ hybridization histochemistry that the diurnal alteration in expression of both per genes in the suprachiasmatic nucleus was retained in vitro. In the model, we examined the effects of pituitary adenylate cyclase-activating polypeptide and glutamate alone and in combination on per1 and per2 gene expression at late subjective night (circadian time 19). Glutamate administration (10(-3)M) induced both per1 and per2 gene expression in the suprachiasmatic nucleus of the brain slice within 1h. The per gene responses were similar to the induction of gene expression observed after light stimulation in vivo at late night. Pituitary adenylate cyclase-activating polypeptide (10(-6)M) administered alone had no effect on the per gene expression, but when pituitary adenylate cyclase-activating polypeptide in micromolar concentration was applied before glutamate, the neuropeptide blocked the glutamate-induced per1 and per2 gene expression in the suprachiasmatic nucleus. In contrast to the lack of effect of pituitary adenylate cyclase-activating polypeptide itself in micromolar concentration, pituitary adenylate cyclase-activating polypeptide (10(-9)M) induced both per1 and per2 gene expression, an effect which was not augmented by co-application of glutamate. Our results provide the molecular substrate for the previous electrophysiological findings that pituitary adenylate cyclase-activating polypeptide in high concentration is able to block glutamate-induced phase advance at late night, and that the peptide in low concentration can induce a phase advance similar to light and glutamate.

Animals↗
PubMed1981

Mechanism for strand-break induction in DNA-proflavine complexes exposed to visible light.

Proflavine bound-superhelical phi XRFI DNA Molecules undergo single-strand scission upon irradiation with visible light at high fluence rate. As shown by agarose gel electrophoresis analyses, the nicking reaction is (i) oxygen-dependent, (ii) strongly inhibited by catalase and an electron scavenger such as cystamine, and (iii) totally suppressed by ceruloplasmin and radical scavengers such as t-butanol sodium benzoate. This indicates that H2O2, e-, O2 and OH, respectively, are involved in the cleavage process. NaN3, a singlet-oxygen quencher, has very little effect on strand-breakage but it prevents almost completely the alteration of guanine residues (a lesion already observed after irradiation at low fluence rate). Since, in the presence of NaN3, strand scission can occur and guanine (as the other bases) recovered intact, it follows that the radical intermediates produced during breakages are probably not involved in any permanent modification of the DNA bases.

Acridines↗
PubMed1973

Antagonistic components of the late receptor potential in the barnacle photoreceptor arising from different stages of the pigment process.

The late receptor potential (LRP) recorded in barnacle photoreceptor cells exhibits, at high light levels, a strong dependence on the color of the stimulus and of the preceding adaptation. Most strikingly, red illumination of a cell previously adapted to blue light results in a depolarization which may last for up to 30 min after the light goes off, while blue illumination of a cell previously adapted to red light cuts short this extended depolarization or prevents its induction by a closely following red light. Comparison of the action spectra for the stimulus-coincident LRP and for the extended depolarization and its curtailment with those previously measured for the early receptor potential (ERP) confirms that these phenomena derive from the same bi-stable pigment as the ERP. The stimulus-coincident response and the extended depolarization appear to arise from substantial activation of the stable 532 nm state of the pigment, while activation of the stable 495 state depresses or prevents the extended depolarization and probably also depresses the stimulus-coincident response. Since either process can precede the other, with mutually antagonistic effects, one is not simply the reversal of the other; they must be based on separate mechanisms. Furthermore, comparison with ERP kinetics shows that both processes involve mechanisms additional to the pigment changes, as seen in the ERP. A model is proposed and discussed for the LRP phenomena and their dependences on wavelength, intensity, and duration of illumination based on excitor-inhibitor interactions.

Adaptation, Ocular↗
PubMed1997

Ultraviolet light-induced keratinocyte apoptosis: a potential mechanism for the induction of skin lesions and autoantibody production in LE.

Systemic lupus erythematosus (SLE) is a prototype systemic autoimmune disease which is characterized clinically by pleiotropy and periodicity. The immune features which accompany the characteristic flares of the disease have strongly suggested that the autoimmune response is driven by self antigen, and is T cell-dependent. These features have prompted the search for potential initiating process(es) which induce the release of self-antigens in a form which causes T cell tolerance to those self molecules to be broken. We review here several recent observations which implicate apoptotic cells as an important potential source of clustered and concentrated autoantigens in SLE, and present our current model whereby the novel autoantigen fragments generated in apoptotic surface blebs initiate and drive the autoimmune response in this disease.

Apoptosis↗
PubMed2006

Phenotypic plasticity in Passiflora suberosa L.(Passifloraceae): induction and reversion of two morphs by variation in light intensity.

Leaf morphology may vary considerably even within a branch of Passiflora suberosa plants. Leaves are of a typical green type in shaded areas, but in open fields turn into violet, and apparently have greater thickness and trichome density. The proximate causes and the adaptive meaning, if any, for the existence of the violet morph are still unknown. By cultivating P. suberosa clones under two light regimes (total and partial exposure to sunlight), we consecutively induced (first year) and then reversed (second year) the appearance of the violet morph. We evaluated the corresponding changes in morpho-anatomic and chemical leaf characteristics. Plants that were grown under partial sunlight had a greater size and did not alter their green color, but those grown under total sunlight changed into violet, were smaller in size and their leaves were tougher, thicker, and had a greater number of trichomes. The violet morph had increased anthocyanins and phenolic derivatives. It also showed cellular hypertrophy, a greater number of cell layers in the mesophyll, and a lignified pericycle. Since these morphs are interchangeable by changing light conditions, we inferred that they are not determined by genotypic diversity, but are mainly a result of a physiological response to light stress, and thus part of P. suberosa phenotypic plasticity.

Anthocyanins↗