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Melatonin-treated Animals (melatonin-treated + animals)
Selected AbstractsMelatonin ameliorates hippocampal nitric oxide production and large conductance calcium-activated potassium channel activity in chronic intermittent hypoxiaJOURNAL OF PINEAL RESEARCH, Issue 3 2008Y. W. Tjong Abstract:, Melatonin protects against hippocampal injury induced by intermittent hypoxia (IH). IH-induced oxidative stress is associated with decreases in constitutive production of nitric oxide (NO) and in the activity of large conductance calcium-activated potassium (BK) channels in hippocampal neurons. We tested the hypothesis that administration of melatonin alleviates the NO deficit and impaired BK channel activity in the hippocampus of IH rats. Sprague,Dawley rats were injected with melatonin (10 mg/kg, i.p.) or vehicle before daily IH exposure for 8 hr for 7 days. The NO and intracellular calcium ([Ca2+]i) levels in the CA1 region of hippocampal slices were measured by electrochemical microsenor and spectrofluorometry, respectively. The activity of BK channels was recorded by patch-clamping electrophysiology in dissociated CA1 neurons. Malondialdehyde levels were increased in the hippocampus of hypoxic rats and were lowered by the melatonin treatment. Levels of NO under resting and hypoxic conditions, and the protein expression of neuronal NO synthase (nNOS) were significantly reduced in the CA1 neurons of hypoxic animals compared with the normoxic controls. These deficits were mitigated in the melatonin-treated hypoxic rats with an improved [Ca2+]i response to acute hypoxia. The open probability of BK channels was decreased in the hypoxic rats and was partially restored in the melatonin-treated animals, without alterations in the expression of channel subunits and unitary conductance. Acute treatment of melatonin had no significant effects on the BK channel activity or on the [Ca2+]i response to hypoxia. Collectively, these results suggest that melatonin ameliorates the constitutive NO production and BK channel activity via an antioxidant mechanism against an IH-induced down-regulation of nNOS expression in hippocampal neurons. [source] Intravenous administration of melatonin reduces the intracerebral cellular inflammatory response following transient focal cerebral ischemia in ratsJOURNAL OF PINEAL RESEARCH, Issue 3 2007Ming-Yang Lee Abstract:, We have previously shown that exogenous melatonin improves the preservation of the blood,brain barrier (BBB) and neurovascular unit following cerebral ischemia,reperfusion. Recent evidence indicates that postischemic microglial activation exaggerates the damage to the BBB. Herein, we explored whether melatonin mitigates the cellular inflammatory response after transient focal cerebral ischemia for 90 min in rats. Melatonin (5 mg/kg) or vehicle was given intravenously at reperfusion onset. Immunohistochemistry and flow cytometric analysis were used to evaluate the cellular inflammatory response at 48 hr after reperfusion. Relative to controls, melatonin-treated animals did not have significantly changed systemic cellular inflammatory responses in the bloodstream (P > 0.05). Melatonin, however, significantly decreased the cellular inflammatory response by 41% (P < 0.001) in the ischemic hemisphere. Specifically, melatonin effectively decreased the extent of neutrophil emigration (Ly6G-positive/CD45-positive) and macrophage/activated microglial infiltration (CD11b-positive/CD45-positive) by 51% (P < 0.01) and 66% (P < 0.01), respectively, but did not significantly alter the population composition of T lymphocyte (CD3-positive/CD45-positive; P > 0.05). This melatonin-mediated decrease in the cellular inflammatory response was accompanied by both reduced brain infarction and improved neurobehavioral outcome by 43% (P < 0.001) and 50% (P < 0.001), respectively. Thus, intravenous administration of melatonin upon reperfusion effectively decreased the emigration of circulatory neutrophils and macrophages/monocytes into the injured brain and inhibited focal microglial activation following cerebral ischemia,reperfusion. The finding demonstrates melatonin's inhibitory ability against the cellular inflammatory response after cerebral ischemia,reperfusion, and further supports its pleuripotent neuroprotective actions suited either as a monotherapy or an add-on to the thrombolytic therapy for ischemic stroke patients. [source] Melatonin decreases neurovascular oxidative/nitrosative damage and protects against early increases in the blood,brain barrier permeability after transient focal cerebral ischemia in miceJOURNAL OF PINEAL RESEARCH, Issue 2 2006Hung-Yi Chen Abstract:, We have recently shown that melatonin decreases the late (24 hr) increase in blood,brain barrier (BBB) permeability and the risk of tissue plasminogen activator-induced hemorrhagic transformation following ischemic stroke in mice. In the study, we further explored whether melatonin would reduce postischemic neurovascular oxidative/nitrosative damage and, therefore, improve preservation of the early increase in the BBB permeability at 4 hr after transient focal cerebral ischemia for 60 min in mice. Melatonin (5 mg/kg) or vehicle was given intraperitoneally at the beginning of reperfusion. Hydroethidine (HEt) in situ detection and immunohistochemistry for nitrotyrosine were used to evaluate postischemic accumulation in reactive oxygen and nitrogen species, respectively, in the ischemic neurovascular unit. BBB permeability was evaluated by spectrophotometric and microscopic quantitation of Evans Blue leakage. Relative to controls, melatonin-treated animals not only had a significantly reduced superoxide accumulation in neurovascular units in boundary zones of infarction, by reducing 35% and 54% cytosolic oxidized HEt in intensity and cell-expressing percentage, respectively (P < 0.001), but also exhibited a reduction in nitrotyrosine by 52% (P < 0.01). Additionally, melatonin-treated animals had significantly reduced early postischemic disruption in the BBB permeability by 53% (P < 0.001). Thus, melatonin reduced postischemic oxidative/nitrosative damage to the ischemic neurovascular units and improved the preservation of BBB permeability at an early phase following transient focal cerebral ischemia in mice. The findings further highlight the ability of melatonin in anatomical and functional preservation for the ischemic neurovascular units and its relevant potential in the treatment of ischemic stroke. [source] Morphological and Morphometric Changes of Pituitary Lactotrophs of Viscacha (Lagostomus maximus maximus) in Relation to Reproductive Cycle, Age, and SexTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2010Verónica Filippa Abstract Lactotrophs in pituitary pars distalis (PD) of viscacha were studied by immunohistochemistry and morphometric analysis in the following groups: 1) adult males throughout the reproductive cycle (reproductive, gonadal regression, and recovery periods), 2) melatonin-treated adults, 3) castrated adults, 4) prepubertal, 5) non-pregnant females, and 6) pregnant females (early, mid, and late pregnancy). Immunopositive percentage area (%IA), cell percentage in PD (% PDC), number of cells per reference area (no.cell/RA), major cellular and nuclear diameters were analyzed. Lactotrophs were mainly localized in the ventro,medial region and the caudal extreme of PD. In the male viscachas, they were isolated in small and big groups, close to blood vessels and near follicles. These cells were pleomorphic and with a heterogeneous cytoplasmic immunolabeling pattern. In the adult males of the gonadal regression period the morphometric parameters were the lowest. Most parameters of lactotrophs in the prepubertal were significantly lower than in the adult males in the reproductive period. In the melatonin-treated animals and in castrated animals there was a decrease in %IA, %PDC, and no.cell/RA. In the females, the morphometric parameters increased at the end of pregnancy. Non-pregnant females exhibited a higher immunopositive area and number, but a smaller size of cells than males. Our results showed that in the adult male viscacha, lactotrophs vary seasonally, probably due to the photoperiod effect through melatonin. Besides the changes observed after castration, in prepubertal animals, in adults of different sex, and during pregnancy suggest that the gonadal steroid hormones might modify the lactotrophs activity. Anat Rec, 293:150,161, 2010. © 2010 Wiley-Liss, Inc. [source] | ||||||||||