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1.
Neuropeptides ; 48(5): 313-8, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25130282

RESUMO

Both common eating disorders anorexia nervosa and bulimia nervosa are characteristically diseases of women. To characterize the role of the 5-HT1A receptor (5-HT1A-R) in these eating disorders in females, we investigated the effect of saline or 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) treatment on feeding behavior and body weight in adult WT female mice and in adult 5-HT1A-R knockout (KO) female mice. Our results showed that KO female mice have lower food intake and body weight than WT female mice. Administration of 8-OH-DPAT decreased food intake but not body weight in WT female mice. Furthermore, qRT-PCR was employed to analyze the expression levels of neuropeptides, γ-aminobutyric acid A receptor subunit ß (GABAA ß subunits) and glutamic acid decarboxylase in the hypothalamic area. The results showed the difference in food intake between WT and KO mice was accompanied by differential expression of POMC, CART and GABAA ß2, and the difference in body weight between WT and KO mice was associated with significantly different expression levels of CART and GABAA ß2. As such, our data provide new insight into the role of 5-HT1A-R in both feeding behavior and the associated expression of neuropeptides and the GABAA receptor.


Assuntos
Anorexia Nervosa/metabolismo , Bulimia Nervosa/metabolismo , Comportamento Alimentar/fisiologia , Hipotálamo/metabolismo , Neuropeptídeos/genética , Receptor 5-HT1A de Serotonina/metabolismo , 8-Hidroxi-2-(di-n-propilamino)tetralina/farmacologia , Animais , Peso Corporal/fisiologia , Feminino , Expressão Gênica , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , RNA Mensageiro/metabolismo , Receptor 5-HT1A de Serotonina/genética , Receptores de GABA-A/metabolismo , Agonistas do Receptor de Serotonina/farmacologia
2.
Adv Exp Med Biol ; 775: 187-94, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23392935

RESUMO

We have previously shown that chronic supplementation of taurine to mice significantly ameliorated the age-dependent decline in memory acquisition and retention. We also showed that concomitant with the amelioration in cognitive function, taurine caused significant alterations in the GABAergic and somatonergic system. These changes include increased levels of the neurotransmitters GABA and glutamate, increased expression of both isoforms of GAD and the neuropeptide somatostatin, decreased hippocampal expression of the beta (ß) 2/3 subunits of the GABA(A) receptor, an increase in the number of somatostatin-positive neurons, and an increase in the amplitude and duration of population spikes recorded from CA1 in response to Schaefer collateral stimulation and enhanced paired pulse facilitation in the hippocampus. These specific alterations of the inhibitory system caused by taurine treatment oppose those naturally induced by aging, suggesting a protective role of taurine in this process. In this study, we further investigated the effects of taurine on gene expression of relevant proteins of the inhibitory synapses using qRT-PCR method and found that taurine affects gene expression of various subunits of the GABA(A) receptors and GAD. Increased understanding the effects of taurine on gene expression will increase our understanding of age-related taurine-mediated neurochemical changes in the GABAergic system and will be important in elucidating the underpinnings of the functional changes of aging. Taurine might help forestall the age-related decline in cognitive functions through interaction with the GABAergic system.


Assuntos
Regulação da Expressão Gênica/efeitos dos fármacos , Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos , Potenciais Pós-Sinápticos Inibidores/genética , Taurina/administração & dosagem , Taurina/farmacologia , Animais , Suplementos Nutricionais , Glutamato Descarboxilase/genética , Glutamato Descarboxilase/metabolismo , Camundongos , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Receptores de GABA-A/genética , Receptores de GABA-A/metabolismo , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/genética
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