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Prolonged TRPV1 activation increases frequency and amplitudes of glutamatergic events in NTS neurons
Author(s) -
Hofmann Mackenzie E,
Fawley Jessica A,
Andresen Michael C
Publication year - 2012
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.26.1_supplement.701.6
Subject(s) - trpv1 , capsaicin , desensitization (medicine) , chemistry , solitary tract , ampa receptor , postsynaptic potential , biophysics , neuroscience , glutamate receptor , medicine , endocrinology , receptor , biology , transient receptor potential channel , biochemistry
TRPV1 is located presynaptically at some 2 nd order neurons in the solitary tract nucleus (NTS) and its activation causes release of glutamate from vesicles independent of action potentials. Here we investigated whether prolonged activation of TRPV1 causes fast receptor desensitization similar to spinal afferents (~30 sec). In patch recordings, capsaicin (100 nM), a TRPV1 agonist, triggered increases in frequency (1385.1 ± 454.6%) and, surprisingly, amplitudes (149.0 ± 18.4%) of spontaneous or miniature EPSCs (n=6). Capsaicin responses rapidly (1 min) peaked with a slow decay of 19.9 ± 3.3 min (n=4) before returning to baseline. To guard against errors from compound events, we reduced release frequency by lowering external calcium from 2 to 1 mM or by reducing capsaicin to 50 nM. Both maneuvers reduced the peak frequencies but capsaicin increased mEPSC amplitudes nonetheless. Finally, increases in temperature activate TRPV1 independent of capsaicin. Increases in temperature resulted in increases to event frequency and amplitudes (184.5 ± 2.0% and 116 ± 2.8%, respectively, n=2). Potentially, presynaptic calcium stores might contribute to the amplitude changes but postsynaptic trafficking of AMPA receptors cannot yet be ruled out. Lastly, TRPV1 desensitization occurs slowly in ST afferents in NTS and TRPV1 might provide uniquely sustained TRPV1 signaling at NTS neurons.