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5‐Hydroxytrptamine 7 receptors (5‐HT7R) in the nucleus tractus solitarii (nTS) modulate synaptic transmission.
Author(s) -
Matott Michael P,
Kline David D
Publication year - 2013
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.27.1_supplement.697.22
Subject(s) - excitatory postsynaptic potential , chemistry , solitary tract , neurotransmission , postsynaptic current , postsynaptic potential , neuroscience , depolarization , solitary nucleus , biophysics , inhibitory postsynaptic potential , nucleus , receptor , biology , biochemistry
5‐HT is a potent cardiorespiratory neuromodulator. 5‐HT7Rs are functionally located in the nTS, the central termination site of sensory afferents, where they modulate chemo and autonomic reflexes. Here we examined the mechanism of 5‐HT7Rs action in nTS by examining their influence on synaptic and membrane properties. Spontaneous (s) and solitary tract (TS)‐evoked excitatory post‐synaptic currents (EPSCs), and membrane potential, were examined in rat nTS slices following 5‐HT7R activation (LP‐44; 2–100 μM). Regardless of concentration, 5‐ HT7R activation decreased TS‐EPSC amplitude in the majority of cells (21/34); the remaining cells increased (11/34) or did not change TS‐EPSC amplitude. The magnitude of decrease was concentration‐related; with 100 μM producing complete synaptic failure in 40% of cells. 5‐HT7R‐induced synaptic depression was of presynaptic origin as indicated by an increased paired pulse ratio (PPR) of consecutive TS‐EPSCs. Conversely, 5‐HT7R‐induced synaptic augmentation did not change the PPR, suggesting a postsynaptic mechanism. 5‐HT7R did not alter sEPSCs or membrane potential, but did eliminate spiking to current‐depolarization in 24% of cells, with the remaining cells showing an increased spike half‐width. Altogether, these results suggest 5‐ HT7R's modulate cardiorespiratory reflexes by modulating nTS neurons via pre‐ and post‐synaptic mechanisms.