[PMID]: | 22578217 |
[Au] Autor: | Yu G; Sharp BM |
[Ad] Endereço: | Department of Pharmacology, University of Tennessee Health Science Center, Memphis, Tennessee, USA. |
[Ti] Título: | Nicotine modulates multiple regions in the limbic stress network regulating activation of hypophysiotrophic neurons in hypothalamic paraventricular nucleus. |
[So] Source: | J Neurochem;122(3):628-40, 2012 Aug. |
[Is] ISSN: | 1471-4159 |
[Cp] País de publicação: | England |
[La] Idioma: | eng |
[Ab] Resumo: | Nicotine intake affects CNS responses to stressors. We reported that nicotine self-administration (SA) augmented the hypothalamo-pituitary-adrenal (HPA) stress response, in part because of the altered neurotransmission and neuropeptide expression within hypothalamic paraventricular nucleus (PVN). Limbic-PVN interactions involving medial prefrontal cortex, amygdala, and bed nucleus of the stria terminalis (BST) greatly impact the HPA stress response. Therefore, we investigated the effects of nicotine SA on stress-induced neuronal activation in limbic-PVN network, using c-Fos protein immunohistochemistry and retrograde tracing. Nicotine decreased stress-induced c-Fos in prelimbic cortex (PrL), anteroventral BST (avBST), and peri-PVN, but increased c-Fos induction in medial amygdala (MeA), locus coeruleus, and PVN. Fluoro-gold (FG) was injected into avBST or PVN, as GABAergic neurons in avBST projecting to PVN corticotrophin-releasing factor neurons relay information from both PrL glutamatergic and MeA GABAergic neurons. The stress-induced c-Fos expression in retrograde-labeled FG+ neurons was decreased in PrL by nicotine, but increased in MeA, and also reduced in avBST. Therefore, within limbic-PVN network, nicotine SA exerts selective regional effects on neuronal activation by stress. These findings expand the mechanistic framework by demonstrating altered limbic-BST-PVN interactions underlying the disinhibition of PVN corticotrophin-releasing factor neurons, an essential component of the amplified HPA response to stress by nicotine. |
[Mh] Termos MeSH primário: |
Neurônios/efeitos dos fármacos Nicotina/administração & dosagem Agonistas Nicotínicos/administração & dosagem Núcleo Hipotalâmico Paraventricular/patologia Hormônios Liberadores de Hormônios Hipofisários/metabolismo Estresse Psicológico/patologia
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[Mh] Termos MeSH secundário: |
Animais Encéfalo/efeitos dos fármacos Encéfalo/metabolismo Condicionamento Operante/efeitos dos fármacos Eletrochoque/efeitos adversos Regulação da Expressão Gênica/efeitos dos fármacos Masculino Proteínas Proto-Oncogênicas c-fos/metabolismo Ratos Ratos Sprague-Dawley Autoadministração Estilbamidinas/metabolismo Estresse Psicológico/etiologia Fatores de Tempo
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[Pt] Tipo de publicação: | JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL |
[Nm] Nome de substância:
| 0 (2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt); 0 (Nicotinic Agonists); 0 (Pituitary Hormone-Releasing Hormones); 0 (Proto-Oncogene Proteins c-fos); 0 (Stilbamidines); 6M3C89ZY6R (Nicotine) |
[Em] Mês de entrada: | 1209 |
[Cu] Atualização por classe: | 161019 |
[Lr] Data última revisão:
| 161019 |
[Sb] Subgrupo de revista: | IM |
[Da] Data de entrada para processamento: | 120515 |
[St] Status: | MEDLINE |
[do] DOI: | 10.1111/j.1471-4159.2012.07785.x |
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