| Abstract No.: | C-B3037 |
| Country: | Canada |
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| Title: | STRESS HORMONES GATE SHORT-TERM SYNAPTIC PLASTICITY IN NEUROENDOCRINE CELLS. |
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| Authors/Affiliations: | 1 Vincent Marty*; 1 Jaideep Bains;
1 Hotchkiss Brain Institute, Calgary, AB, Canada
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| Content: | Objectives: The corticotropin-releasing factor (CRF) has been identified as a key neuropeptide regulating the endocrine, autonomic and behavioral adaptative responses to stressful events or immune challenge (Vale et al., 1981; Smagin et al., 2001). CRF is synthesized in the parvocellular neurons of the hypothalamic paraventricular nucleus (PVN) and is responsible of the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the subsequent release of glucocorticoids. Administration of CRF receptor antagonists is very effective in reversing stress-induced HPA activation and anxiety-like behavior (McElroy et al., 2002). Despite its pivotal role in the regulation of the homeostatic response generated through the HPA axis, little is known about the modulatory effects of CRH on the synaptic transmission in the PVN. The goal of this study was to characterize the effects of CRF on excitatory glutamatergic postsynaptic currents (EPSC) on rat PVN putative parvocellular neurons using whole cell patch-clamp recordings.
Materials and methods: We obtained whole-cell recordings from parvocellular neurons in brain slices containing the PVN of postnatal day 21-44 rats. Excitatory postsynaptic currents (EPSCs) were evoked by extracellular stimulation with a glass microelectrode.
Results: Bath application of CRF (1 μM) had no effect on spontaneous and evoked EPSCs. High-frequency train of electrical stimulation (HFS) induced a short-term potentiation (STP) of evoked EPSC amplitude which is not modified by CRH. In contrast, when HFS is paired with membrane depolarization at 0 mV we did not observe any variation of evoked EPSC amplitude in control condition. However, after five minutes application of CRF the same pairing HFS protocol induced a STP of evoked EPSC amplitude. The decrease in the paired-pulse ratio during the CRF-induced STP after the pairing HFS protocol suggests a presynaptic mechanism by which the release probability of glutamate is increased.
Conclusion: Taken together these results suggest that CRF allows for the maintenance of high synaptic efficacy transmission when high presynaptic activity occurs with postsynaptic depolarization. Therefore, CRF could act as a high-pass filter converting irrelevant into relevant information which may be critical for the homeostatic response during stress events.
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