Repeated Stress Impairs Endocannabinoid Signaling in the Paraventricular Nucleus of the Hypothalamus
| العنوان: | Repeated Stress Impairs Endocannabinoid Signaling in the Paraventricular Nucleus of the Hypothalamus |
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| المؤلفون: | Jaideep S. Bains, J. Brent Kuzmiski, Jaclyn I. Wamsteeker |
| المصدر: | The Journal of Neuroscience. 30:11188-11196 |
| بيانات النشر: | Society for Neuroscience, 2010. |
| سنة النشر: | 2010 |
| مصطلحات موضوعية: | Male, Restraint, Physical, endocrine system, Cannabinoid receptor, Presynaptic Terminals, In Vitro Techniques, Biology, Hippocampus, Receptors, G-Protein-Coupled, Rats, Sprague-Dawley, Glucocorticoid receptor, Neuroendocrine Cells, Receptor, Cannabinoid, CB1, Postsynaptic potential, Cannabinoid Receptor Modulators, Animals, gamma-Aminobutyric Acid, Neurons, General Neuroscience, Glutamate receptor, Neural Inhibition, Articles, Endocannabinoid system, Rats, Inhibitory Postsynaptic Potentials, nervous system, Hypothalamus, Chronic Disease, Synapses, Retrograde signaling, Signal transduction, Neuroscience, Stress, Psychological, hormones, hormone substitutes, and hormone antagonists, Endocannabinoids, Paraventricular Hypothalamic Nucleus, Signal Transduction |
| الوصف: | Endocannabinoids (eCBs) are ubiquitous retrograde signaling molecules in the nervous system that are recruited in response to robust neuronal activity or the activation of postsynaptic G-protein-coupled receptors. Physiologically, eCBs have been implicated as important mediators of the stress axis and they may contribute to the rapid feedback inhibition of the hypothalamic–pituitary–adrenal axis (HPA) by circulating corticosteroids (CORTs). Understanding the relationship between stress and eCBs, however, is complicated by observations that eCB signaling is itself sensitive to stress. The mechanisms that link stress to changes in synaptic eCB signaling and the impact of these changes on CORT-mediated negative feedback have not been resolved. Here, we show that repetitive immobilization stress, in juvenile male rats, causes a functional downregulation of CB1receptors in the paraventricular nucleus of the hypothalamus (PVN). This loss of CB1receptor signaling, which requires the activation of genomic glucocorticoid receptors, impairs both activity and receptor-dependent eCB signaling at GABA and glutamate synapses on parvocellular neuroendocrine cells in PVN. Our results provide a plausible mechanism for how stress can lead to alterations in CORT-mediated negative feedback and may contribute to the development of plasticity of HPA responses. |
| تدمد: | 1529-2401 0270-6474 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8a9a38e733cbb8d726ae8929cf2ebc1eTest https://doi.org/10.1523/jneurosci.1046-10.2010Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....8a9a38e733cbb8d726ae8929cf2ebc1e |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15292401 02706474 |
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