| Abstract No.: | A-E1164 |
| Country: | Canada |
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| Title: | RAPID PRESYNAPTIC HOMEOSTASIS IN AUTONOMIC NUCLEI FOLLOWING HEMORRHAGE |
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| Authors/Affiliations: | 1 Brent Kuzmiski*; 1 Quentin Pittman; 1 Jaideep Bains;
1 University of Calgary, AB, Canada
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| Content: | Neuroendocrine and autonomic adjustments necessary to maintain fluid balance are made by neurons in the hypothalamus which integrate local and synaptic information regarding blood volume1. Glutamate synapses onto these neurons exhibit long-term plasticity in vitro2-4, but a critical test of the relevance of synaptic plasticity during physiological perturbations is still required. Here, we report that noradrenaline (NA) which is released in the paraventricular nucleus of the hypothalamus (PVN) in response to hemorrhage causes a long-term depression (LTDNA) of glutamatergic synapses onto magnocellular neurosecretory cells (MNCs). LTDNA is mediated by the release of endocannabinoids, expressed presynaptically and is accompanied by a loss of function at presynaptic group III metabotropic glutamate receptors (mGluRs). Subsequent high frequency stimulation (HFS) of glutamatergic afferents results in a rapid dedepression of transmission to pre-NA levels and a gain of mGluR function, consistent with the hypothesis that mGluRs are critical molecular switches for the induction of metaplasticity. Following hemorrhage, synapses exhibit features consistent with LTDNA, including low release probability (Pr) and unresponsive group III mGluRs. HFS of these synapses induces a rapid potentiation of glutamate release indicating that inactivation of presynaptic mGluRs unmasks a state permissive for subsequent LTP generation. These findings provide evidence for a novel form of metaplasticity at glutamate synapses onto MNCs in the PVN in response to changes in blood volume. |
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