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Hyperosmotic stimulation elicits a purinergic‐glutamatergic coupling in PVN presympathetic neurons (1130.8)
Author(s) -
Candido Ferreira Neto Hildebrando,
Antunes Vagner,
Stern Javier
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1130.8
Subject(s) - ppads , ampa receptor , glutamate receptor , chemistry , nmda receptor , glutamatergic , stimulation , purinergic receptor , cnqx , osmotic concentration , medicine , receptor , neuroscience , endocrinology , biophysics , biology , biochemistry
We have previously shown that ATP applied in the PVN induces an increase in sympathetic activity, an effect attenuated by the antagonism of P2 and/or glutamatergic receptors. Here, we evaluated precise mechanisms underlying the ATP‐glutamate interaction in the PVN, and assessed whether this interaction contributed to osmotically‐driven PVN presympathetic neuronal activity. Whole‐cell patch clamp recordings obtained from PVN‐RVLM neurons showed that ATP (100 µM, 1 min, bath applied) induced an increase in firing rate (62±26%, 14/20), an effect blocked by kynurenic acid (1 mM) or PPADS (10 µM). While ATP did not evoke changes in synaptic activity, glutamate currents evoked by focal application of L‐glu (1 mM, 100 ms, n=9) were increased in amplitude (194±73%) and area (241±116%) by ATP. Glutamate potentiation did not involve NMDA receptors, since focal application of NMDA (50 µM, 100 ms, n=13) was not changed by ATP. However, AMPA receptor‐evoked currents (50 µM, 50 ms, n=15) were potentiated by ATP (amplitude: 100% vs 132±7%; area: 100% vs 149±8%), an effect blocked by PPADS (n=12) and intracellular BAPTA (n=14). Finally, a hyperosmotic stimulus (mannitol 1%, 355 mOsm, 1 min, n=9) potentiated AMPA responses (amplitude: 136±12%; area: 155±23%), an effect blunted by PPADS (n=6). Our data suggest that P2 and AMPA receptors in PVN‐RVLM presympathetic neurons participate in the responses evoked by hyperosmotic stimulation. Grant Funding Source : Supported by FAPESP (#2010/17997‐0; 2010/05037‐1; 2012/12444‐8) and NIH