Changes in antidromic latencies of medullary respiratory neurons in hypercapnia and hypoxia

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.

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.


1987 ◽  
Vol 57 (4) ◽  
pp. 1101-1117 ◽  
Author(s):  
B. G. Lindsey ◽  
L. S. Segers ◽  
R. Shannon

Arrays of extracellular electrodes were used to monitor simultaneously several (2-8) respiratory neurons in the lateral medulla of anesthetized, paralyzed, bilaterally vagotomized, artificially ventilated cats. Efferent phrenic nerve activity was also recorded. The average discharge rate as a function of time in the respiratory cycle was determined for each neuron. Most cells were tested for spinal or vagal axonal projections using antidromic stimulation methods. Cross-correlational methods were used to analyze spike trains of 480 cell pairs. Each pair included at least one neuron most active during the expiratory phase. All simultaneously recorded neurons were located in the same side of the brain stem. Twenty-six percent (33/129) of the expiratory (E) neuron pairs exhibited short time scale correlations indicative of paucisynaptic interactions or shared inputs, whereas 8% (27/351) of the pairs consisting of an E neuron and an inspiratory (I) cell were similarly correlated. Evidence for several inhibitory actions of E neurons was found: 1) inhibition of I neurons by E neurons with both decrementing (DEC) and augmenting (AUG) firing patterns; 2) inhibition of E-DEC and E-AUG neurons by E-DEC cells; 3) inhibition of E-DEC and E-AUG neurons by E-AUG neurons; and 4) inhibition of E-DEC neurons by tonic I-E phase-spanning cells. Because several cells were recorded simultaneously, direct evidence for concurrent parallel and serial inhibitory processes was also obtained. The results suggest and support several hypotheses for mechanisms that may help to generate and control the pattern and coordination of respiratory motoneuron activities.


1981 ◽  
Vol 45 (2) ◽  
pp. 167-183 ◽  
Author(s):  
Armand L. Bianchi ◽  
Walter M. St. John

2009 ◽  
Vol 21 (6) ◽  
pp. 1683-1713 ◽  
Author(s):  
Osamu Hoshino

There has been compelling evidence that the GABA transporter is crucial not only for removing gamma-aminobutyric acid (GABA) from but also releasing it into extracellular space, thereby clamping ambient GABA (GABA in extracellular space) at a certain level. The ambient GABA is known to activate extrasynaptic GABA receptors and provide tonic inhibitory current into neurons. We investigated how the transporter regulates the level of ambient GABA, mediates tonic neuronal inhibition, and influences ongoing spontaneous neuronal activity. A cortical neural network model is proposed in which GABA transporters on lateral (L) and feedback (F) inhibitory (GABAergic) interneurons are functionally made. Principal (P) cell assemblies participate in expressing information about elemental sensory features. At membrane potentials below the reversal potential, there is net influx of GABA, whereas at membrane potentials above the reversal potential, there is net efflux of GABA. Through this transport mechanism, ambient GABA concentration is kept within a submicromolar range during an ongoing spontaneous neuronal activity time period. Here we show that the GABA transporter on L cells regulates the overall level of ambient GABA across cell assemblies, and that on F cells it does so within individual cell assemblies. This combinatorial regulation of ambient GABA allows P cells to oscillate near firing threshold during the ongoing time period, thereby reducing their reaction time to externally applied stimuli. We suggest that the GABA transporter, with its forward and reverse transport mechanism, could regulate the ambient GABA. This transporter-mediated ambient GABA regulation may contribute to establishing an ongoing subthreshold neuronal state by which the network can respond rapidly to subsequent sensory input.


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.


1989 ◽  
Vol 61 (5) ◽  
pp. 918-926 ◽  
Author(s):  
D. C. Bolser ◽  
J. E. Remmers

1. Stimulation of intercostal muscle tendon organs or their afferent fibers reduces medullary inspiratory neuron activity, decreases motor output to inspiratory muscles, and increases the activity of expiratory laryngeal motoneurons. The present study examines the synaptic mechanisms underlying these changes to obtain information about medullary neurons that participate in the afferent limb of this reflex pathway. 2. Membrane potentials of medullary respiratory neurons were recorded in decerebrate paralyzed cats. Postsynaptic potentials (PSPs) elicited in these neurons by intercostal nerve stimulation (INS) were compared before and after intracellular iontophoresis of chloride ions. After chloride injection, the normal hyperpolarization caused by inhibitory (I) PSPs is "reversed" to depolarization. 3. In inspiratory neurons, reversal of IPSPs by chloride injection also reversed hyperpolarization produced by INS when applied during any portion of the respiratory cycle. This observation suggests that increased chloride conductance of the postsynaptic membrane mediated the inhibition. Further, it is very likely that the last-order interneuron in the afferent pathway must be excited by INS and alter inspiratory neuron activity via an inhibitory synapse. The linear relationship between the amplitude of the INS induced PSP and membrane potential of inspiratory neurons provided evidence that neurons in the afferent pathway are not respiratory modulated. 4. The membranes of expiratory vagal motoneurons and post-inspiratory neurons were depolarized by INS during all portions of the respiratory cycle before IPSP reversal. Reversal of IPSPs affected neither this depolarization of expiratory vagal motoneurons during stage I and II expiration nor that of post-inspiratory neurons during stage I expiration. Thus this depolarization probably resulted from synaptic excitation.(ABSTRACT TRUNCATED AT 250 WORDS)


1985 ◽  
Vol 53 (6) ◽  
pp. 1590-1603 ◽  
Author(s):  
T. E. Dick ◽  
A. J. Berger

Activity was recorded extracellularly from 26 inspiratory bulbospinal neurons in anesthetized, paralyzed, artificially ventilated cats. All but one were located in the ventral respiratory group. A neuron was classified as either I alpha or I beta by comparing its firing pattern during inspiratory cycles with lung inflation to its pattern when lung inflation was withheld during the central inspiratory phase (2, 14, 15). In this study, the projection and conduction velocity of these axons were determined using two methods: antidromic activation (AA) of the bulbospinal neurons and spike-triggered averaging (STA) of the extracellular field potentials. These methods have been compared directly because the same electrode was used both for stimulating the axon of the bulbospinal neuron and recording its axonal potential in the same location. Axonal projections from these neurons were mapped in the contralateral spinal cord with a mobile electrode by determining where the lowest stimulus threshold occurs for AA and greatest axonal potential can be recorded with STA. The locations of these axons were in the ventral and lateral funiculi. Each method determined a similar location for an axon. Positions of 10 axons were determined at both the third (C3) and fourth (C4) cervical segments. Single axons maintained their positions in either descending tract from rostral C3 to mid-C4. In five of six cases where two “neighboring” medullary units were characterized, the axons of each pair projected together within 350 micron of each other in the cervical spinal cord. Estimates of mean axonal conduction velocity (CV) from antidromic activation from a single stimulus site, “single-point AA,” were as much as 42% less than corresponding estimates from STA extracellular field potentials at that point (P less than 0.001). Such single-point estimates were less than determinations that were calculated from the difference in conduction time and the difference in conduction distance from two points in the spinal cord. These two-point determinations averaged 55.4 +/- 13.1 m/s (using AA) and 53.3 +/- 13.1 (using STA) for 10 neurons. These values were not significantly (P greater than 0.2) different from each other and are greater than most earlier reports, which used the single-point AA method. Either method, AA or STA, can be used to determine axonal position and CV. The advantages and disadvantages of each method are discussed.(ABSTRACT TRUNCATED AT 400 WORDS)


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