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Aging is associated with deterioration in the structure and function of the pulmonary circulation. We characterized the lung diffusing capacity for carbon monoxide (DL CO ), alveolar-capillary membrane conductance (Dm CO ), and pulmonary-capillary blood volume (Vc) response to discontinuous incremental exercise at 25, 50, 75, and 90% of peak work (W peak ) in four groups: 1 ) Young [27 ± 3 yr, maximal oxygen consumption (V̇o 2max ): 110 ± 18% age predicted]; 2) Young Highly Fit (27 ± 3 yr, V̇o 2max : 147 ± 8% age predicted); 3 ) Old (69 ± 5 yr, V̇o 2max : 116 ± 13% age predicted); and 4 ) Old Highly Fit (65 ± 5 yr, V̇o 2max : 162 ± 18% age predicted). At rest and at 90% W peak , DL CO , Dm CO , and Vc were decreased with age. At 90% W peak , DL CO , Dm CO , and Vc were greater in Old Highly Fit vs. Old adults. The slope of the DL CO -cardiac output (Q̇) relationship from rest to end exercise at 90% W peak was not different between Young, Young Highly Fit, Old, and Old Highly Fit (1.35 vs. 1.44 vs. 1.10 vs. 1.35 ml CO ·mmHg -1 ·liter blood -1 , P = 0.388), with no evidence of a plateau in this relationship during exercise; this was also true for Dm CO -Q̇ and Vc-Q̇. V̇o 2max was positively correlated with 1 ) DL CO , Dm CO , and Vc at rest; and 2 ) the rest to end exercise change in DL CO , Dm CO , and Vc. In conclusion, these data suggest that despite the age-associated deterioration in the structure and function of the pulmonary circulation, expansion of the pulmonary capillary network does not become limited during exercise in healthy individuals regardless of age or cardiorespiratory fitness level. NEW & NOTEWORTHY Healthy aging is a crucial area of research. This article details how differences in age and cardiorespiratory fitness level affect lung diffusing capacity, particularly during high-intensity exercise. We conclude that highly fit older adults do not experience a limit in lung diffusing capacity during high-intensity exercise. Interestingly, however, we found that highly fit older individuals demonstrate greater values of lung diffusing capacity during high-intensity exercise than their less fit age-matched counterparts., (Copyright © 2017 the American Physiological Society.)

Intestinal intussusception (ISS) commonly causes intestinal obstruction in children. One mechanism that has been proposed to cause ISS is inflammation-induced alteration of intestinal motility. We investigated whether innate inflammatory factors or altered motility is required for induction of ISS by LPS. We compared rates of ISS among BALB/c and C57BL/6 mice, mice lacking lymphocytes or depleted of phagocytes, or mice with defects in the Toll-like receptor 4 (TLR4) signaling pathway following administration of LPS or the Ca(2+) analog MnCl2. At 6 or 2 h after administration of LPS or MnCl2, respectively, mice underwent image analysis to assess intestinal contraction rate or laparotomy to identify ISS. LPS-induced ISS (LPS-ISS) was observed in BALB/c mice, but not in C57BL/6 mice or any BALB/c mice with disruptions of TLR4 signaling. LPS-induced serum TNF-α, IL-6, and nitric oxide (NO) and intestinal NO levels were similar in BALB/c and C57BL/6 mice. The rate of LPS-ISS was significantly reduced in phagocyte-depleted, but not lymphocyte-deficient, mice. Intestinal contraction rates were reduced in LPS-ISS-susceptible BALB/c mice, but not in LPS-ISS-resistant C57BL/6 or TLR4 mutant mice, suggesting a role for reduced intestinal contraction rate in LPS-ISS susceptibility. This was tested with MnCl2, a Ca(2+) antagonist that reduced intestinal contraction rates and induced ISS, irrespective of mouse strain. Therefore, LPS-ISS is initiated by innate immune signaling that requires TLR4 and phagocytes but may be independent of TNF-α, IL-6, and NO levels. Furthermore, alteration of intestinal motility, specifically, reduced intestinal contraction rate, is a key factor in the development of ISS.

Adeno-associated virus (AAV) vectors might offer solutions for restenosis and angiogenesis by transducing nondividing cells and providing long-term gene expression. We investigated the feasibility of vascular cell transduction by AAV vectors in an in vivo rabbit carotid artery model. Time course of gene expression, inflammatory reaction to the vector, and effects of varying viral titer, exposure time, and intraluminal pressures on gene expression were examined. Recombinant AAV vectors with an Rous sarcoma virus promoter and alkaline phosphatase reporter gene were injected intraluminally into transiently isolated carotid segments. Following transduction, gene expression increased significantly over 14 days and then remained stable to 28 days, the last time point examined. Medial vascular smooth muscle cells were the main cell type transduced even with an intact endothelial layer. Increasing the viral titer and intraluminal pressure both enhanced transduction efficiency to achieve a mean of 34 +/- 7% of the subintimal layer of smooth muscle cells expressing gene product. A mild inflammatory reaction, composed of T cells with only rare macrophages, with minimal intimal thickening was demonstrated in 40% of transduced vessels; inflammatory cells were not detected in sham-operated control arteries. These findings demonstrate that AAV is a promising vector for intravascular applications in coronary and peripheral vascular diseases.

Reflex responses of hypoglossal motoneurons innervating the geniohyoid (GH) and thyrohyoid (TH) muscles from the superior laryngeal (SLN) and vestibular nerves and their behaviors during fictive swallowing and vomiting were examined by recording both the extracellular activities of 11 single cells in the hypoglossal nucleus and GH and TH muscle nerve activity in eight decerebrate, paralyzed, and artificially ventilated cats. The majority of TH motoneurons were either active and/or exhibited shortened antidromic latencies during early expiration. In contrast, GH motoneurons did not exhibit any respiratory-related activity. Electrical single-shock stimulation of the SLN never evoked an excitatory reflex response on GH or TH motoneurons but rather evoked inhibitory responses on the THs. Unlike other hypoglossal motoneurons, GH and TH motoneurons do not appear to receive vestibular inputs. However, they can exhibit robust activities during fictive swallowing and vomiting, particularly during expulsion. Thus these motoneurons may play an important role in airway protection during swallowing and vomiting but not in controlling upper airway patency regulated by vestibular afferents.

1. Activation of the vestibular system produces reflex modulation of expiratory muscle activity. The purpose of the present study was to investigate the possible role of bulbospinal expiratory (E) neurons located in the caudal ventral respiratory group (VRG) in mediating vestibulo-respiratory reflexes. Experiments were carried out in decerebrated, paralyzed, and artificially ventilated cats. 2. Electrical stimulation of the vestibular nerve (VN), using short trains of current pulses, elicited bilateral reflex responses on abdominal muscle nerves (ABDNs). This response was not affected by lesions of the cochlear nuclei made by kainic acid injections. The ABDN response typically consisted of a combination of short-latency excitation and long-latency inhibition on the ipsilateral side and, in contrast, a combination of short-latency inhibition and long-latency excitation on the contralateral side. 3. Extracellular recordings were made from 43 caudal VRG bulbospinal E neurons that were activated antidromically from the contralateral upper lumbar spinal cord. More than 80% of these neurons responded to either ipsi- and/or contralateral VN stimulation. The neuronal response consisted of either a combination of excitation and inhibition or only inhibition. The majority of neurons had response patterns appropriate to contribute to the response observed on the contralateral ABDN; however, the latency of the VRG E neuron response was too long to initiate the ABDN response. 4. To further evaluate the contribution of caudal VRG E neurons to the vestibulo-abdominal reflex, ABDN responses were compared before and after sectioning the axons of caudal VRG bulbospinal E neurons where they cross the midline between the obex and first cervical spinal segment. These midsagittal lesions abolished expiratory modulation of ABDN discharge. The lesions also decreased the amplitude of the vestibular-evoked ABDN response but could not abolish the response. The postlesion amplitude was decreased on average to approximately 70% of prelesion values. 5. In conclusion, although the present results indicate that the majority of caudal VRG bulbospinal E neurons respond appropriately to contribute to the vestibulo-abdominal reflex, the reflex largely is unaffected by the removal of caudal VRG E input. The additional descending inputs that are important for mediating the reflex remain to be investigated and may include vestibulospinal and/or reticulospinal tracts.

The objective of this study was to determine which brain stem regions that have projections to sympathetic preganglionic neurons or phrenic motoneurons ae necessary for vestibulosympathetic or vestibulorespiratory responses in decerebrate cats. Bilateral kainic acid injections into the rostral ventrolateral medulla abolished splanchnic nerve responses to electrical stimulation of the vestibular nerve, suggesting that this region is critical for the production of vestibulosympathetic responses. In contrast, injections into the caudal medullary raphe nuclei had no apparent effect on the responses. Neither the dorsal nor the ventral respiratory group appears to be necessary for mediating vestibular influences on the phrenic nerve, suggesting that nonrespiratory neurons (such as vestibulospinal neurons) may be important for producing vestibulorespiratory responses.

1. The vestibular system responds to accelerations of the head and produces reflex responses that serve a variety of compensatory functions. The neuronal circuitry that mediates vestibulo-respiratory reflexes is largely unknown. The purpose of the present study was to investigate the possible role of bulbospinal inspiratory neurons located in the para-ambigual region of the ventral respiratory group (VRG) in mediating these reflexes. Experiments were carried out in cats that were decerebrated, paralyzed, and artificially ventilated. 2. Activation of the vestibular nerve by electrical stimulation produced prominent bilateral reflex responses recorded from the phrenic nerve, which supplies the diaphragm. The responses could be complex and consisted of a decrease and/or increase in nerve discharge. 3. Extracellular recordings were made from 35 VRG inspiratory neurons that were antidromically activated from the upper cervical spinal cord. Almost one-half of these neurons (15/35, 43%) responded to vestibular stimulation. The neuronal response patterns were consistent with VRG inspiratory neurons contributing to the vestibular reflex response simultaneously recorded from the phrenic nerve. 4. The present results indicate that approximately one-half of VRG bulbospinal inspiratory neurons contribute to vestibulo-respiratory reflexes. These findings are in contrast to our recent neuroanatomic and electrophysiological studies which revealed a paucity of vestibular inputs to the dorsal respiratory group (DRG) located in the ventrolateral nucleus of the solitary tract. Thus there appears to be a difference between inspiratory neurons in the DRG and VRG in regard to participating in vestibulo-respiratory reflexes.

The vestibular system is involved in maintaining stable blood pressure and respiration during changes in posture and is essential for eliciting motion sickness-related vomiting. Because the nucleus tractus solitarius (NTS) participates in the regulation of sympathetic and inspiratory outflow and the triggering of emesis, we tested the hypothesis that this region receives vestibular inputs in cats. In one set of experiments, microinjections of the tracer Phaseolus vulgaris leucoagglutinin into the medial and inferior vestibular nuclei labeled projections to the middle and lateral regions of the NTS. In electrophysiological experiments, electrical stimulation of the vestibular nerve modified the firing rates of neurons located in the same regions. Some neurons with vestibular inputs received convergent signals from the abdominal vagus nerve and could potentially mediate motion sickness-related vomiting. Others received convergent baroreceptor inputs and could act as a substrate for some components of vestibulosympathetic reflexes. In contrast, inspiratory neurons in the dorsal respiratory group received little vestibular input, suggesting that vestibulorespiratory reflexes are mediated by cells located elsewhere.

1. To study the properties of vestibulosympathetic reflexes we recorded outflow from the splanchnic nerve during natural vestibular stimulation in multiple vertical planes in decerebrate cats. Most of the animals were cerebellectomized, although some responses were recorded in cerebellum-intact preparations. Vestibular stimulation was produced by rotating the head in animals whose upper cervical dorsal roots were transected to remove inputs from neck receptors; a baroreceptor denervation and vagotomy were also performed to remove visceral inputs. 2. The plane of head rotation that produced maximal modulation of splanchnic nerve activity (response vector orientation) was measured at 0.2-0.5 Hz. The dynamics of the response were then studied with sinusoidal (0.05- to 1-Hz) stimuli aligned with this orientation. 3. Typically, maximal modulation of splanchnic nerve outflow was elicited by head rotations in a plane near pitch; nose-up rotations produced increased outflow and nose-down rotations reduced nerve discharges. The gains of the responses remained relatively constant across stimulus frequencies and the phases were consistently near stimulus position, like regularly firing otolith afferents. Similar response dynamics were recorded in cerebellectomized and cerebellum-intact animals. 4. The splanchnic nerve responses to head rotation could be abolished by microinjections of the excitotoxin kainic acid into the medial and inferior vestibular nuclei, which is concordant with the responses resulting from activation of vestibular receptors. 5. The properties fo vestibulosympathetic reflexes recorded from the splanchnic nerve support the hypothesis that the vestibular system participates in compensating for posturally related changes in blood pressure.

1. The patterns of membrane potential changes of phrenic motoneurons were compared during fictive vomiting, fictive coughing, and fictive swallowing in decerebrate, paralyzed cats. These fictive behaviors were identified by motor nerve discharge patterns similar to those recorded from the muscles of nonparalyzed animals. Phrenic motoneurons (n = 54) were identified by antidromic activation from the thoracic phrenic nerve. Intracellular recordings were obtained from 27 motoneurons during fictive vomiting, 40 during fictive coughing, and 27 during fictive swallowing. Sixteen motoneurons were recorded during both fictive coughing and fictive swallowing, eight during both fictive coughing and fictive vomiting, and two during both fictive vomiting and fictive swallowing. Seven motoneurons were studied during all three behaviors. 2. Fictive vomiting, typically evoked by electrical stimulation of abdominal vagal afferents, was characterized by a series of bursts of coactivation of phrenic and abdominal motor nerves, culminating in an expulsion phase in which abdominal discharge was prolonged both with respect to phrenic discharge and to abdominal discharge during the preceding retching phase. During fictive vomiting, phrenic motoneurons depolarized abruptly, and the amplitude of depolarization was significantly greater than during control inspirations. They then repolarized slowly throughout the phrenic burst, rapidly repolarizing at the end of each phrenic burst during retching and reaching a level similar to that observed during expiration. During the expulsion phase, the pattern was initially the same. However, after the cessation of phrenic discharge, the membrane potential repolarized slowly until the end of the abdominal burst, exhibiting greater synaptic noise than during expiration. One phrenic motoneuron, presumably innervating the periesophageal region of the diaphragm, received a strong hyperpolarization just before the onset of the emetic episode and fired for shorter periods during fictive vomiting than did other phrenic motoneurons.(ABSTRACT TRUNCATED AT 250 WORDS)

In decerebrate, paralyzed cats, phrenic (PHR) and lumbar abdominal (ABD) nerve discharges during both neural respiration and fictive vomiting (FV) were subjected to spectral and coherence analyses. During respiration, PHR discharge exhibited high-frequency oscillation (HFO), manifested as a narrow spectral peak (range 57-90 Hz) in autospectra and left-right coherence spectra. During FV, the following occurred: 1) the HFO peak disappeared and was replaced by a broad peak with higher modal frequency (range 84-120 Hz), indicating elimination of inputs from the medullary inspiratory pattern generator. 2) Left-right PHR coherence spectra had no distinct peaks, indicating that correlations between opposite PHR discharges were now not frequency specific. 3) Although ABD and PHR autospectra were similar, PHR-ABD coherences were near zero, indicating lack of common inputs on a short time scale. 4) Nonzero coherences between ABD nerves were confined to ipsilateral pairs. Thus coherence analysis indicates that the outputs of the vomiting pattern generator are temporally dispersed on a short time scale and are not necessarily common to different motoneuron populations.

1. The role of upper cervical inspiratory (UCI)-modulated neurons in respiratory muscle control during vomiting was examined by recording the impulse activity of these neurons during fictive vomiting in decerebrate, paralyzed cats. Fictive vomiting was identified by a characteristic series of bursts of coactivation of phrenic and abdominal muscle nerves, elicited either by electrical stimulation of supradiaphragmatic vagal nerve afferents or by emetic drugs, which would be expected to produce expulsion of gastric contents in nonparalyzed animals. 2. Data were recorded from 43 propriospinal UCI neurons, located in the C1-C3 spinal segments near the border of the intermediate gray matter and lateral funiculus, which were antidromically activated with floating pin electrodes placed in the ipsilateral lateral funiculus, usually at T1-T3. Some cells (9/21 tested) were also activated from the upper lumbar cord (L1). During respiration, most neurons (n = 40) had an augmenting discharge pattern during inspiration. In addition, more than one-half (55%) fired tonically during the remainder of the respiratory cycle. About 40% of UCI neurons showed variations in their firing pattern during the noninspiratory portion of respiration. These latter two properties of UCI neurons were not observed in dorsal and ventral respiratory group (DRG and VRG-, respectively) bulbospinal inspiratory (I) neurons previously recorded under similar conditions. 3. During fictive vomiting, the firing pattern of most UCI neurons fell into one of three main categories. More than one-half (53%) were active in phase with bursts of phrenic discharge and were thus classified as Active-type cells.(ABSTRACT TRUNCATED AT 250 WORDS)

The possible contribution of spinal reflexes to abdominal muscle activation during vomiting was assessed in decerebrate cats. The activity of these muscles is partly controlled by bulbospinal expiratory neurons in the caudal ventral respiratory group (VRG). In a previous study it was found that the abdominal muscles are still active during vomiting after midsagittal lesion of the axons of these neurons between C1 and the obex (A.D. Miller, L.K. Tan, and I. Suzuki. J. Neurophysiol. 57: 1854-1866, 1987). The present experiments indicate that this postlesion activity was due to spinal stretch reflexes because 1) such midsagittal lesions eliminate abdominal muscle nerve activity during fictive vomiting in paralyzed cats in which there are no abdominal stretch reflexes, 2) the abdominal muscles are activated during vomiting by spinal reflexes after upper thoracic cord transections, and 3) the normal 100-ms delay between diaphragmatic and abdominal activation during vomiting is reduced to approximately 20-25 ms after both types of lesions, which is consistent with postlesion abdominal reflex activation. Our results also suggest that, during normal vomiting, abdominal stretch and tension reflexes have only a minor role if any and abdominal muscle activation is probably mediated primarily or exclusively by expiratory neurons in the caudal ventral respiratory group. However, our finding that phrenic activity is reduced both during vomiting after thoracic transections and during fictive vomiting after paralysis is consistent with a contribution of reflex activity from abdominal and/or intercostal muscles to phrenic discharge during normal vomiting.

1. The role of dorsal and ventral respiratory group (DRG and VRG) bulbospinal inspiratory (I) neurons in the control of diaphragmatic and external intercostal (inspiratory) muscle activity during vomiting was examined by recording from these neurons during fictive vomiting in decerebrate, paralyzed cats. Fictive vomiting was defined by a characteristic series of bursts of coactivation of phrenic and abdominal muscle nerves, elicited either by electrical stimulation of abdominal vagal afferents or by emetic drugs, which would be expected to produce vomiting if the animals were not paralyzed. 2. Data were recorded from 22 DRG and 29 VRG I neurons that were antidromically activated from the fourth cervical spinal segment (C4). Only 10% (5/51) of these neurons started to fire near the beginning of phrenic discharge during fictive vomiting and thus had the appropriate discharge pattern to contribute to the initial activation of the diaphragm and coactive external intercostal muscles during vomiting. The frequency of occurrence of these Active neurons was not significantly different in the DRG (3/22) and VRG (2/29) (chi 2 test). Most remaining neurons were either totally silent (n = 7) or had only sporadic, infrequent firing (n = 16) (Silent neurons, 23/51 = 45%), or else fired near the end of phrenic discharge during fictive vomiting (End neurons, 21/51 = 41%). Two neurons were categorized as having miscellaneous (Misc) behavior. 3. No differences were found among neurons having different response patterns during fictive vomiting in regard to the following: the manner in which fictive vomiting was elicited: cell location: conduction velocity; and neuronal firing onset, rate, and pattern during respiration.(ABSTRACT TRUNCATED AT 250 WORDS)

The responses of central vestibular neurons in the decerebrate cat subjected to whole-body tilt were examined as a function both of stimulus orientation (with respect to the cat's head) and frequency, with the aim of understanding the neural processing responsible for producing the observed response patterns. Responses to whole-body tilt were recorded from vestibular neurons in and around the lateral vestibular nucleus (LVN). By plugging all six semicircular canals, the otolith contribution was studied in isolation. For each neuron, a response vector was defined as having three components: orientation, gain, and phase. These components were examined using sinusoidal stimulus frequencies of 0.01 to 2 Hz. The orientation component of the neural response vector does not vary as a function of stimulus frequency. Thus response dynamics previously described with a fixed (roll) axis cannot be explained by changes in the angle between the response vector orientation and a fixed stimulus axis. Two major classes of neural responses were observed. One class had a phase lead at low frequencies and gain that showed a modest increase with frequency. It could be described by a model that included a fractional s exponent operator. These response dynamics resemble that of otolith afferents, suggesting that these neurons may be acting as simple relays. The other major response class was characterized by a large gain increase and a phase lag of as much as 180 degrees as frequency increased; such response dynamics have been previously observed in otolith-evoked neck and forelimb reflexes. A more complex model, consisting of a parallel excitatory and high-pass-filtered inhibitory limb, was necessary to describe these responses. The orientation component of the response vector of most of the neurons whose dynamics were best described by the parallel pathway model pointed toward the contralateral side, implying they would be excited by side-up tilt (at low frequencies). Most other neurons had ipsilateral vectors.

Control of abdominal musculature by brain stem respiratory neurons was studied in decerebrate unanesthetized cats by determining 1) which brain stem respiratory neurons could be antidromically activated from the lumbar cord, from which the abdominal muscles receive part of their innervation, and 2) if lumbar-projecting respiratory neurons make monosynaptic connections with abdominal motoneurons. A total of 462 respiratory neurons, located between caudal C2 and the retrofacial nucleus (Bötzinger complex), were tested for antidromic activation from the upper lumbar cord. Fifty-eight percent of expiratory (E) neurons (70/121) in the caudal ventral respiratory group (VRG) between the obex and rostral C1 were antidromically activated from contralateral L1. Eight of these neurons were activated at low thresholds from lamina VIII and IX in the L1-2 gray matter. One-third (14/41) of the E neurons that projected to L1 could also be activated from L4-5. Almost all antidromic E neurons had an augmenting firing pattern. Ten scattered inspiratory (I) neurons projected to L1 but could not be activated from L4-5. No neurons that fired during both E and I phases (phase-spanning neurons) were antidromically activated from the lumbar cord. In order to test for possible monosynaptic connections between descending E neurons and abdominal motoneurons, cross-correlations were obtained between 27 VRG E neurons, which were antidromically activated from caudal L2 and contralateral L1 and L2 abdominal nerve activity (47 neuron-nerve combinations). Only two neurons showed a correlation with one of the two nerves tested. Although there is a large projection to the lumbar cord from expiratory neurons in the ventral respiratory group caudal to the obex, cross-correlation analyses suggest that strong monosynaptic connections between these neurons and abdominal motoneurons are scarce.

Responses to head tilt were recorded from vestibular neurons in and around the lateral vestibular nucleus (LVN) of the decerebrate cat. Each animal had all six semicircular canals rendered nonfunctional by a plugging procedure. Each cell was studied by slowly tilting the cat, using one or both of two paradigms. In the first method, sinusoidal tilts (0.05 or 0.1 Hz) were used to produce bidirectional stimuli in up to 12 pairs of directions, including left/right (roll tilt) and fore/aft (pitch). The second method imposed a constant 10 degree tilt; the direction of the tilt was rotated around the animal by an appropriate combination of roll and pitch motions. Neurons responded by maximally increasing their discharge frequency in a particular direction of head tilt from the horizontal. Each cell's response could be described by a vector in the animal's horizontal plane whose orientation is given by the direction of the most effective stimulus and whose length represents the neuron's maximal sensitivity to tilt. The two methods of stimulation yielded equivalent response vectors. Response vectors were obtained for 100 neurons. The distribution of vector directions for these vestibular neurons was not uniform; there was a conspicuous absence of neurons with fore/aft-directed vectors. The sensitivity of these cells (length of the response vector) ranged from 10 to 230 impulses X s-1 X g-1 (median 50). Neurons whose vectors lay in the ipsilateral half-plane (which would be excited by ear-down tilt) tended to be less sensitive than those with contralateral vectors. Neurons excited by ear-up tilt tended to be located ventrally in the LVN, while those excited by ear-down tilt were more evenly distributed. There was no other obvious correlation of vector orientation with the anatomical locus of the cell in the LVN. The directional selectivity of the responses of these neurons to head tilts are similar to those previously reported tin utricular afferents. The broad distribution of response vector orientations provides an appropriate substrate for vestibulospinal reflexes to a wide variety of head tilts.

The role of ventral respiratory group (VRG) expiratory (E) neurons in the control of abdominal and internal intercostal (expiratory) muscle activity during vomiting was examined in decerebrate cats by recording from these neurons during fictive vomiting in paralyzed animals and comparing abdominal muscle activity during vomiting before and after sectioning the axons of these descending neurons. Fictive vomiting was defined by a series of bursts of coactivation of abdominal and phrenic nerves elicited by either subdiaphragmatic vagus nerve stimulation or emetic drugs. Such coordinated activity would be expected to produce vomiting if the animals were not paralyzed. Data were recorded from 27 VRG E neurons that were antidromically activated from the lower thoracic (T13) or lumbar spinal cord. During fictive vomiting, almost two-thirds of these neurons (17/27) were mainly active in between periods of abdominal and phrenic nerve coactivation, when the internal intercostal motoneurons are known to be active. This group of neurons was termed INT neurons. INT neurons were subdivided according to whether they were active between every burst of phrenic and abdominal nerve coactivation (INTa neurons, n = 10) or only between some bursts (INTb neurons, n = 7). Another one-third of the VRG E neurons had normal or increased levels of activity when the abdominal nerves were active during fictive vomiting (ABD neurons). The one remaining neuron was mainly silent throughout fictive vomiting. ABD neurons were indistinguishable from INT neurons on the basis of their location in the VRG, type of firing pattern (ramp versus step ramp), conduction velocity, or extent of projection in the lumbar cord. However, INTa neurons had a significantly higher discharge rate during respiration than either ABD or INTb neurons. Abdominal muscle EMG and nerve activity were recorded from six unparalyzed cats before and after cutting the axons of VRG E neurons as they cross the midline between C1 and the obex. The lesions abolished or almost eliminated expiratory modulation of abdominal muscle activity. In contrast, the abdominal muscles were always active during vomiting; however, the amplitude of postlesion abdominal activity varied from approximately 70-100% of prelesion values in three cats to 60-70% of normal in a fourth animal to only approximately 20% of prelesion values in two other cats.(ABSTRACT TRUNCATED AT 400 WORDS)