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This review article summarizes the potential role of circadian rhythmicity and melatonin in psychiatric disorders. The melatonin rhythm, with high blood levels at night and low values during the day, is a reflection of the biological clock, i.e., the suprachiasmatic nucleus (SCN). The SCN receive information about the prevailing light: dark conditions from specialized ganglion cells (only 1-2% of the total ganglion cells) in the retina. These unique cells contain a newly-discovered photopigment, melanopsin, which responds to a rather narrow band width of light that peaks at roughly 480 nm. The axons of these ganglion cells project via the retinohypothalamic tract through the optic nerve to the SCN, located just above the optic chiasm in the anterior hypothalamus. Via this pathway, light detected by the retina synchronizes the circadian clock to precisely 24 hours. In the absence of light, i.e., darkness, the SCN signals the pineal gland to produce melatonin via a complex neural pathway that involves fibers that project from the hypothalamus to the preganglionic sympathetic neurons in the intermediolateral cell column of the upper thoracic cord. Axons of these neurons exit the spinal cord to eventually synapse on neurons in the superior cervical ganglia. Then, postganglionic fibers convey the information to the pineal gland mediating the nighttime rise in melatonin synthesis. Because melatonin is only elevated at night, it is referred to as the <
La melatonina (N-acetil-5-metoxitriptamina) es una indolamina que produce la glándula pineal durante la noche. Se libera directamente en la circulación general con un ritmo circadiano. En las enfermedades psiquiátricas se presentan alteraciones en los ritmos biológicos. La melatonina es un cronobiótico ya que sincroniza los ritmos biológicos como el ciclo sueño-vigilia, el de la temperatura corporal y el ciclo de liberación de cortisol, con el fotoperiodo. Esta indolamina no actúa como un hipnótico clásico. Los efectos que ejerce sobre el sueño son acortar su latencia, prolongar el periodo de sueño natural y reducir los despertares nocturnos. Por lo anterior, se ha descrito como un compuesto que <
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Uncontrolled hydrochloric acid secretion and ulceration in the stomach due to various factors are serious global problems today. Although the mechanism of acid secretion from the parietal cell is now fairly known, the mechanism of gastric ulceration is still not clear today. Among various causes of gastric ulceration, lesions caused by stress, alcohol consumption, Helicobacter pylori infection and use of nonsteroidal antiinflammatory drugs have been shown to be mediated largely through the generation of reactive oxygen species especially hydroxyl radical (*OH). A number of excellent drugs have been proved useful in controlling hyperacidity and ulceration but their long term uses are not devoid of disturbing side-effects. Hence, the search is still on to find out a compound possessing antisecretory, antiulcer and antioxidant properties which will serve as a powerful therapeutic agent to cure gastric hyperacidity and ulcer. This article describes the role of reactive oxygen species in gastric ulceration, drugs controlling them with their merits and demerits and, the role of melatonin, a pineal hormone in protecting the gastric lesions with a final commentary on how melatonin research with respect to gastric pathophysiology can be taken forward with a view to projecting this indole as a promising therapeutic agent to control gastric ulceration in humans.
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Animales , Antiulcerosos/farmacología , Depuradores de Radicales Libres/farmacología , Mucosa Gástrica/efectos de los fármacos , Humanos , Melatonina/farmacología , Especies Reactivas de Oxígeno/efectos adversos , Úlcera Gástrica/inducido químicamenteRESUMEN
Background. The noncompetitive NMDA antagonists phencyclidine (PCP) and dizocilpine (MK-801) have been considered for use as neuroprotective therapeutic agents, although both produce injury in neurons of cingulate and retrosplenial cortices in rodents. The low-affinity, noncompetitive NMDA antagonist dextrorphan has been considered for use as a neuroprotective therapeutic drug. The aim of the present work was to evaluate the neurotoxicity of dextrorphan. Methods. Sprague-Dawley male rats were used and injected with either saline or dextorphan (30 mg/kg i.p.). The animals were sacrificed 30 min later, and the brain was examined for histopathological changes. Results. After. systemic administration of the drug, hyperchromatic and shrunken nuclei with chromatin condensation and disruption were observed. Also. granular and vacuolated cytoplasm was apparent in pyramidal neurons in the retrosplenial (posterior cingulate) cortex. Status spongious (spongy degeneration) of the neuropil was also detected. Conclusions. Morphological changes are similar to those described previously, which are induced by high-affinity, noncompetitive NMDA antagonists, such as MK-801
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Animales , Masculino , Ratas , Dextrorfano/efectos adversos , Neuronas/efectos de los fármacos , Fármacos Neuroprotectores/efectos adversos , Cerebro/efectos de los fármacos , Ratas Sprague-DawleyRESUMEN
La glándula de Harder es una glándula túbulo-alveolar localizada en la parte posterior de la órbita ocular de animales que poseen membrana nictitante. En estos mamiferos la glándula contiene una gran cantidad de lípidos. La glándula de Harder de roedores contiene un pigmento café rojizo, el cual ha sido identificado como porfirina. Las funciones de la glándula de Harder son; síntesis y liberación de ferhormonas, fotoprotección y termorregulación, osmoprotección y se le ha propuesto además un papel inmunoendocrino