Classification of the medullary respiratory neurons of the rat by their projections and transmitters

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.

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Excitation of Medullary Respiratory Neurons in REM Sleep

SLEEP ◽

10.1093/sleep/28.7.801 ◽

2005 ◽

Vol 28 (7) ◽

pp. 801-807 ◽

Cited By ~ 32

Author(s):

John M. Orem ◽

Andrew T. Lovering ◽

Edward H. Vidruk

Keyword(s):

Rem Sleep ◽

Respiratory Neurons ◽

Medullary Respiratory Neurons

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Functional associations among simultaneously monitored lateral medullary respiratory neurons in the cat. II. Evidence for inhibitory actions of expiratory neurons

Journal of Neurophysiology ◽

10.1152/jn.1987.57.4.1101 ◽

1987 ◽

Vol 57 (4) ◽

pp. 1101-1117 ◽

Cited By ~ 60

Author(s):

B. G. Lindsey ◽

L. S. Segers ◽

R. Shannon

Keyword(s):

Discharge Rate ◽

Respiratory Neurons ◽

Short Time Scale ◽

Axonal Projections ◽

Medullary Respiratory Neurons ◽

Antidromic Stimulation ◽

Expiratory Neurons ◽

Short Time ◽

And Control ◽

The Brain

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.

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Responses of bulbospinal and laryngeal respiratory neurons to hypercapnia and hypoxia

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.4.1201 ◽

1985 ◽

Vol 59 (4) ◽

pp. 1201-1207 ◽

Cited By ~ 26

Author(s):

W. M. St John ◽

A. L. Bianchi

Keyword(s):

Spinal Cord ◽

Recurrent Laryngeal Nerve ◽

Phrenic Nerve ◽

Action Potentials ◽

Respiratory Muscles ◽

Laryngeal Nerve ◽

Respiratory Neurons ◽

Peripheral Chemoreceptor ◽

Medullary Respiratory Neurons ◽

Neuronal Groups

The purpose was to evaluate activities of medullary respiratory neurons during equivalent changes in phrenic discharge resulting from hypercapnia and hypoxia. Decerebrate, cerebellectomized, paralyzed, and ventilated cats were used. Vagi were sectioned at left midcervical and right intrathoracic levels caudal to the origin of right recurrent laryngeal nerve. Activities of phrenic nerve and single respiratory neurons were monitored. Neurons exhibiting antidromic action potentials following stimulations of the spinal cord and recurrent laryngeal nerve were designated, respectively, bulbospinal or laryngeal. The remaining neurons were not antidromically activated. Hypercapnia caused significant augmentations of discharge frequencies for all neuronal groups. Many of these neurons had no change or declines of activity in hypoxia. We conclude that central chemoreceptor afferent influences are ubiquitous, but excitatory influences from carotid chemoreceptors are more limited in distribution among medullary respiratory neurons. Hypoxia will increase activities of neurons that receive sufficient excitatory peripheral chemoreceptor afferents to overcome direct depression by brain stem hypoxia. The possibility that responses of respiratory muscles to hypoxia are programmed within the medulla is discussed.

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Differing activities of medullary respiratory neurons in eupnea and gasping

Journal of Applied Physiology ◽

10.1152/jappl.1991.70.3.1265 ◽

1991 ◽

Vol 70 (3) ◽

pp. 1265-1270 ◽

Cited By ~ 16

Author(s):

D. Zhou ◽

M. J. Wasicko ◽

J. M. Hu ◽

W. M. St John

Keyword(s):

Carbon Monoxide ◽

Brain Stem ◽

Phrenic Nerve ◽

Peak Discharge ◽

Discharge Frequency ◽

Respiratory Neurons ◽

Ventilatory Pattern ◽

Medullary Respiratory Neurons ◽

Inspiratory Neurons ◽

Expiratory Neurons

Our purpose was to compare further eupneic ventilatory activity with that of gasping. Decerebrate, paralyzed, and ventilated cats were used; the vagi were sectioned within the thorax caudal to the laryngeal branches. Activities of the phrenic nerve and medullary respiratory neurons were recorded. Antidromic invasion was used to define bulbospinal, laryngeal, or not antidromically activated units. The ventilatory pattern was reversibly altered to gasping by exposure to 1% carbon monoxide in air. In eupnea, activities of inspiratory neurons commenced at various times during inspiration, and for most the discharge frequency gradually increased. In gasping, the peak discharge frequency of inspiratory neurons was unaltered. However, all commenced activities at the start of the phrenic burst and reached peak discharge almost immediately. The discharge frequencies of all groups of expiratory neurons fell in gasping, with many neurons ceasing activity entirely. These data are consistent with the hypothesis that brain stem mechanisms controlling eupnea and gasping differ fundamentally.

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