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Noisy Timing Of Nicotinic Synaptic Activity Promotes Amplification In Sympathetic Ganglia
Author(s) -
Horn John P,
Kullmann Paul H.M.
Publication year - 2017
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.31.1_supplement.718.7
Subject(s) - neuroscience , superior cervical ganglion , sympathetic ganglion , stimulation , neurotransmission , excitatory postsynaptic potential , chemistry , biology , biophysics , medicine , anatomy , inhibitory postsynaptic potential , receptor
Hypertension and heart failure can be driven and exacerbated by sympathetic hyperactivity. We hypothesize that remodeling of synaptic integration in sympathetic ganglia may contribute to such hyperactivity. Here we describe normal physiological properties of cholinergic nicotinic synapses using high resolution patch‐clamp recordings from the isolated, intact rat superior cervical ganglion. Synaptic currents were recorded under voltage‐clamp from individual synapses using minimal presynaptic stimulation of the cervical sympathetic trunk. Using dynamic‐clamp, the excitability of each cell was then measured in terms of the threshold‐synaptic conductance required to stimulate an action potential. Synaptic strength was then calibrated by calculating the synaptic conductance (g syn ) and expressing it as fraction of thresh‐g syn . This revealed that synaptic strength ranges from 10 to 1000% thresh‐g syn . The effect of timing was analyzed by comparing EPSC amplitudes evoked by 1Hz stimulation at regular 1 second intervals with those evoked using exponentially distributed intervals. Interestingly, noisy 1 Hz stimulation increased the variability (sd) of EPSCs, but had no effect on their average amplitude. This effect was seen across the full range of synaptic strengths observed. To explore the consequences of this finding, we simulated how regular and noisy trains of synaptic events modeled on our data evoked spikes in a conductance‐based model neuron. The results showed that when noisy stimulation increased the variability of EPSCs, the spike output of the system increased. We conclude that noisy synaptic activity, like that seen in intracellular recordings from sympathetic neurons in living animals, creates a form of stochastic resonance. In other words, the noise introduced by timing in conjunction with quantal fluctuations observed with regular stimulation has the effect of increasing the output signal (spikes) from this system.