Accommodative reactions of medullary respiratory neurons of the cat

1975 ◽  
Vol 38 (5) ◽  
pp. 1172-1180 ◽  
Author(s):  
D. W. Richter ◽  
F. Heyde

In most of the bulbospinal respiratory neurons, threshold depolarization increased during the early period of their spontaneous burst discharge but decreased again at the end of a burst. In some vagal respiratory neurons, however, threshold depolarization increased steadily until the very end of their discharge period. These changes generally were accompanied by changes in the rate of depol1rization of the spikes, the amplitude of their overshoot, and their discharge frequency. For a given synaptic input, as indicated by the constancy of the interspike membrane potential trajectories, threshold depolarization of bulbospinal neurons remained constant or even decreased. Only in some vagal neurons was an increase in threshold deplarization observed under these conditions. With the exception of some vagal neurons, most of the respiratory neurons did not show a pronounced accommodative behavior when stimulated with linear rising currents. When stimulating with current pulses, all neurons discharged repetitively with only slight adaptation, which was already complete by the first few spike intervals. The current-frequency relationship was linear and revealed a primary and secondary range. The results support neither accommodation nor adaptation as important mechanisms in the genesis of the rhythmic activity of respiratory neurons.

1987 ◽  
Vol 57 (6) ◽  
pp. 1837-1853 ◽  
Author(s):  
E. G. Merrill ◽  
J. Lipski

The investigation examined the synaptic input from medullary respiratory neurons in the nucleus retroambigualis (NRA) to external (EIM) and internal (IIM) intercostal motoneurons. Antidromic mapping revealed that 112/117 (96%) tested NRA units had axons descending into thoracic spinal cord with extensive arborizations at many thoracic segments, mainly contralaterally. The conduction velocities ranged from 10 to 105 m X s-1. The descending projections did not appear to be somatotopically arranged. Cross-correlation of the spike trains of NRA inspiratory units with the discharge of external intercostal nerves (performed usually with 4 contralateral nerves) showed significant narrow peaks only in 5 out of 40 averages. Of the 25 trigger units tested for the thoracic projection in this series of experiments, 24 were antidromically activated. Intracellular recordings were made from 52 IIMs [mean membrane potential 65.3 mV, central respiratory drive potentials (CRDPs) greater than 1 mV present in 23/52] and 53 EIM (mean membrane potential 54.3 mV, CRDPs in 31/53). During the depolarizing phase of the CRDPs, synaptic noise with frequent and apparently unitary EPSPs with amplitudes in excess of 1 mV was observed. Spike-triggered averages of synaptic noise were computed for 153 pairings between 137 NRA neurons and 105 contralateral intercostal motoneurons. Only four PSPs were revealed: two monosynaptic EPSPs between expiratory NRA units and IIMs and two probably disynaptic EPSPs between inspiratory NRA units and EIMs. When advancing the microelectrode down to the motoneuron pools, frequent recordings were made from interneurons with spontaneous respiratory discharge (inspiratory or expiratory) located dorsal and medial to the motor nuclei. The interneurons could be excited following stimulation of segmental afferents. It is concluded that monosynaptic connections between respiratory NRA neurons and intercostal motoneurons are rare (connectivity no more than approximately 4%). Segmental interneurons, interposed between the majority of descending respiratory axons and intercostal motoneurons, are likely to produce large unitary EPSPs and, thus, short-term synchronization in the discharge of intercostal motoneurons as observed by others.


2016 ◽  
Vol 116 (4) ◽  
pp. 1554-1563 ◽  
Author(s):  
Yinbo Chen ◽  
Xinping Li ◽  
Horacio G. Rotstein ◽  
Farzan Nadim

Oscillatory networks often include neurons with membrane potential resonance, exhibiting a peak in the voltage amplitude as a function of current input at a nonzero (resonance) frequency ( f res). Although f res has been correlated to the network frequency ( f net) in a variety of systems, a causal relationship between the two has not been established. We examine the hypothesis that combinations of biophysical parameters that shift f res, without changing other attributes of the impedance profile, also shift f net in the same direction. We test this hypothesis, computationally and experimentally, in an electrically coupled network consisting of intrinsic oscillator (O) and resonator (R) neurons. We use a two-cell model of such a network to show that increasing f res of R directly increases f net and that this effect becomes more prominent if the amplitude of resonance is increased. Notably, the effect of f res on f net is independent of the parameters that define the oscillator or the combination of parameters in R that produce the shift in f res, as long as this combination produces the same impedance vs. frequency relationship. We use the dynamic clamp technique to experimentally verify the model predictions by connecting a model resonator to the pacemaker pyloric dilator neurons of the crab Cancer borealis pyloric network using electrical synapses and show that the pyloric network frequency can be shifted by changing f res in the resonator. Our results provide compelling evidence that f res and resonance amplitude strongly influence fnet, and therefore, modulators may target these attributes to modify rhythmic activity.


2009 ◽  
Vol 102 (3) ◽  
pp. 1976-1983 ◽  
Author(s):  
Bjoern Ch. Ludwar ◽  
Colin G. Evans ◽  
Jian Jing ◽  
Elizabeth C. Cropper

Two distinct mechanisms mediate potentiating effects of depolarization on synaptic transmission. Recently there has been renewed interest in a type of plasticity in which a neuron's somatic membrane potential influences synaptic transmission. We study mechanisms that mediate this type of control at a synapse between a mechanoafferent, B21, and B8, a motor neuron that receives chemical synaptic input. Previously we demonstrated that the somatic membrane potential determines spike propagation within B21. Namely, B21 must be centrally depolarized if spikes are to propagate to an output process. We now demonstrate that this will occur with central depolarizations that are only a few millivolts. Depolarizations of this magnitude are not, however, sufficient to induce synaptic transmission to B8. B21-induced postsynaptic potentials (PSPs) are only observed if B21 is centrally depolarized by ≥10 mV. Larger depolarizations have a second impact on B21. They induce graded changes in the baseline intracellular calcium concentration that are virtually essential for the induction of chemical synaptic transmission. During motor programs, subthreshold depolarizations that increase calcium concentrations are observed during one of the two antagonistic phases of rhythmic activity. Chemical synaptic transmission from B21 to B8 is, therefore, likely to occur in a phase-dependent manner. Other neurons that receive mechanoafferent input are electrically coupled to B21. Differential control of spike propagation and chemical synaptic transmission may, therefore, represent a mechanism that permits selective control of afferent transmission to different types of neurons contacted by B21. Afferent transmission to neurons receiving chemical synaptic input will be phase specific, whereas transmission to electrically coupled followers will be phase independent.


1985 ◽  
Vol 59 (4) ◽  
pp. 1208-1213 ◽  
Author(s):  
A. L. Bianchi ◽  
W. M. St John

We evaluated mechanisms underlying changes in discharge frequencies of medullary respiratory neurons. This evaluation was made by determining variations in antidromic latencies; these variations reflect changes in membrane potentials. In decerebrate, vagotomized, paralyzed, and ventilated cats, activities of the phrenic nerve and single respiratory neurons were monitored in hyperoxic normocapnia, hyperoxic hypercapnia, and/or normocapnic hypoxia. Axonal projections were defined as bulbospinal or laryngeal by antidromic activation. At normocapnic hyperoxia, antidromic latencies fell to minima during periods of spontaneous neuronal activity, with maxima occurring between neuronal bursts. In hypercapnia or hypoxia, these minima were not altered, whereas maximum latencies typically rose for neurons whose discharge frequencies increased. However, the increased frequencies most strongly correlated with increases in the difference between maximum and minimum latencies. No such correlation was evident for neurons whose discharge frequencies declined. We conclude that the overall change of membrane potential primarily defines neuronal discharge frequencies. Changes in membrane potentials induced by peripheral and central chemoreceptor afferents and by direct actions of hypercapnia and hypoxia are discussed.


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