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1.
PLoS One ; 8(2): e57115, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23437327

RESUMO

Seasonal Affective Disorder (SAD) is one of the most common mood disorders with depressive symptoms recurring in winter when there is less sunlight. The fact that light is the most salient factor entraining circadian rhythms leads to the phase-shifting hypothesis, which suggests that the depressive episodes of SAD are caused by misalignments between the circadian rhythms and the habitual sleep times. However, how changes in environmental lighting conditions lead to the fluctuations in mood is largely unknown. The objective of this study is to develop an animal model for some of the features/symptoms of SAD using the diurnal grass rats Arvichantis niloticus and to explore the neural mechanisms underlying the light associated mood changes. Animals were housed in either a 12∶12 hr bright light∶dark (1000lux, BLD) or dim light∶dark (50lux, DLD) condition. The depression-like behaviors were assessed by sweet-taste Saccharin solution preference (SSP) and forced swimming test (FST). Animals in the DLD group showed higher levels of depression-like behaviors compared to those in BLD. The anxiety-like behaviors were assessed in open field and light/dark box test, however no significant differences were observed between the two groups. The involvement of the circadian system on depression-like behaviors was investigated as well. Analysis of locomotor activity revealed no major differences in daily rhythms that could possibly contribute to the depression-like behaviors. To explore the neural substrates associated with the depression-like behaviors, the brain tissues from these animals were analyzed using immunocytochemistry. Attenuated indices of 5-HT signaling were observed in DLD compared to the BLD group. The results lay the groundwork for establishing a novel animal model and a novel experimental paradigm for SAD. The results also provide insights into the neural mechanisms underlying light-dependent mood changes.


Assuntos
Depressão/etiologia , Luz , Transtorno Afetivo Sazonal/etiologia , Animais , Ansiedade/etiologia , Comportamento Animal , Ritmo Circadiano , Modelos Animais de Doenças , Neurônios Dopaminérgicos/metabolismo , Masculino , Camundongos , Atividade Motora , Transtorno Afetivo Sazonal/metabolismo , Serotonina/metabolismo
2.
Neurosci Lett ; 515(2): 177-80, 2012 May 02.
Artigo em Inglês | MEDLINE | ID: mdl-22465247

RESUMO

Disruptions in circadian rhythms, as seen in human shift workers, are often associated with many health consequences including impairments in cognitive functions. However, the mechanisms underlying these affects are not well understood. The objective of the present study is to explore the effects of circadian disruption on hippocampal neurogenesis, which has been implicated in learning and memory and could serve as a potential pathway mediating the cognitive consequences associated with rhythm disruption. Circadian rhythm disruptions were introduced using a weekly 6 h phase shifting paradigm, in which male Wistar rats were subjected to either 6 h phase advances (i.e. traveling eastbound from New York to Paris) or 6 h phase delays (i.e. traveling westbound from Paris to New York) in their light/dark schedule every week. The effects of chronic phase shifts on hippocampal neurogenesis were assessed using doublecortin (DCX), a microtubule binding protein expressed in immature neurons. The results revealed that chronic disruption in circadian rhythms inhibits hippocampal neurogenesis, and the degree of reduction in neurogenesis depends upon the direction and duration of the shifts. In two cohorts of animals that experienced phase shifts for either 4 or 8 weeks, a greater decrease in neurogenesis was observed when the phase was advanced versus delayed in both groups. The direction-dependent effect mirrors the findings on clock gene expression in the SCN, suggesting a causal link between the reduction in hippocampal neurogenesis and a disrupted SCN circadian clock.


Assuntos
Ritmo Circadiano/fisiologia , Hipocampo/fisiopatologia , Síndrome do Jet Lag/fisiopatologia , Neurogênese/fisiologia , Animais , Proteína Duplacortina , Masculino , Atividade Motora/fisiologia , Ratos , Ratos Wistar , Núcleo Supraquiasmático/fisiopatologia
3.
J Ethnopharmacol ; 85(1): 25-32, 2003 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-12576199

RESUMO

In this study, in vitro inhibitory effects of 33 ethanol extracts obtained from 24 plant species (representing 11 different families) on cyclooxygenase-1 (COX-1) were evaluated. The plant materials selected for this study have been used in aboriginal medicine in Australia and traditional medicine in China for the treatment of various diseases that are considered as inflammation in nature, e.g. asthma, arthritis, rheumatism, fever, edema, infections, snakebite and related inflammatory diseases. All of the selected plants, with one exception, showed inhibitory activity against COX-1, which supports their traditional uses. The most potent COX-1 inhibition were observed from the extracts of Acacia ancistrocarpa leaves (IC(50)=23 microg/ml). Ficus racemosa bark, Clematis pickeringii stem, Acacia adsurgens leaves, Tinospora smilacina stem and Morinda citrifolia fruit powder exhibited inhibition of COX-1 with the IC(50) of 100, 141, 144, 158 and 163 microg/ml, respectively. Aspirin and indomethacin used as the reference COX-1 inhibitors in this study inhibited COX-1 with IC(50) of 241 and 1.2 microg/ml, respectively. The findings of this study may explain at least in part why these plants have been traditionally used for the treatment of inflammatory conditions in Australian aboriginal medicine and traditional Chinese medicine.


Assuntos
Anti-Inflamatórios/química , Inibidores de Ciclo-Oxigenase/química , Extratos Vegetais/química , Austrália , China , Ciclo-Oxigenase 1 , Medicamentos de Ervas Chinesas/química , Etanol , Isoenzimas/química , Plantas Medicinais , Prostaglandina-Endoperóxido Sintases/química
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