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Acute effects of nerve growth factor (NGF) on membrane properties of mouse lower airway parasympathetic ganglionic neurons
Author(s) -
Myers Allen C,
Rohde Holly K
Publication year - 2008
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.22.1_supplement.764.13
Subject(s) - nerve growth factor , excitatory postsynaptic potential , medicine , endocrinology , chemistry , membrane potential , biology , neuroscience , inhibitory postsynaptic potential , receptor
The neurotrophin, NGF, is located in lower airway smooth muscle and glands, tissue innervated by local parasympathetic ganglionic neurons, and NGF is increased by inflammation in this tissue. However, the acute effect of NGF release on parasympathetic nerves is unknown. Using single cell current clamp recording of tracheal and bronchial ganglionic neurons, NGF (30 ng/ml) decreased the action potential afterhyperpolarization amplitude and duration from 17±2mV and 52±8ms, respectively, in control neurons to 11±3 mV and 34±14ms after treatment (n=7); NGF (1–30 ng/ml) had no effect on accommodation in phasic (n=4) or tonic (n=3) neurons. NGF (1–30 ng/ml) had no effect on the resting membrane potential or input resistance (n=7). Using intracellular QX314, vagus nerve stimulation evoked 16±2mV (range of 13–19 mV; n=6) nicotinic fast excitatory postsynaptic potentials (fEPSPs) in control neurons which were increased to 21±3mV in the presence of 30ng/ml NGF. Using whole cell patch clamp recording, DMPP (1μM, 30s) evoked a 213pA inward current in a control neuron and 258pA in the presence of NGF (10ng/ml). In this study, we determined that NGF affects action potential and synaptic membrane properties of mouse ganglionic neurons; the effect on fEPSPs is possibly postsynaptic as NGF increased the nicotinic current. This study provides additional support that NGF has short‐term, as well as long‐term, effects on adult mammalian neurons. This work was supported by NIH‐NHLBI (ACM).