Activity Of Medullary Neurons Research Articles

Parabrachial tachykinin1-expressing neurons involved in state-dependent breathing control

Breathing is regulated automatically by neural circuits in the medulla to maintain homeostasis, but breathing is also modified by behavior and emotion. Mice have rapid breathing patterns that are unique to the awake state and distinct from those driven by automatic reflexes. Activation of medullary neurons that control automatic breathing does not reproduce these rapid breathing patterns. By manipulating transcriptionally defined neurons in the parabrachial nucleus, we identify a subset of neurons that express the Tac1, but not Calca, gene that exerts potent and precise conditional control of breathing in the awake, but not anesthetized, state via projections to the ventral intermediate reticular zone of the medulla. Activating these neurons drives breathing to frequencies that match the physiological maximum through mechanisms that differ from those that underlie the automatic control of breathing. We postulate that this circuit is important for the integration of breathing with state-dependent behaviors and emotions.

Essential role of RVL medullary neuronal activity in the long term maintenance of hypertension in conscious SHR.

It is well established that sympathetic nervous system is responsible for the onset, development and maintenance of neurogenic hypertension. The rostroventrolateral medulla (RVLM) and medullo-cervical pressor area (MCPA) are important central sympathoexcitatory regions whose role on neurogenic hypertension remains unknown. To establish RVLM and MCPA roles in the long-term regulation of blood pressure by depressing their neuron activity through the over-expression of hKir2.1-potassium channel in conscious spontaneously hypertensive rats (SHR). In SHR, a lentiviral vector LVV-hKir2.1 was microinjected into RVLM or MCPA areas. A sham group was injected with LVV-eGFP. Blood pressure (BP) and heart rate (HR) were continuously monitored for 75 days. Baroreflex and chemoreflex functions were evaluated. Baroreflex gain, chemoreflex sensitivity, BP and HR variability were calculated. LVV-hKir2.1 expression in RVLM, but not in MCPA, produced a significant time-dependent decrease in systolic, diastolic, mean-BP and LF of systolic BP at 60-days post-injection. No significant changes were seen in LVV-eGFP RVLM injected SHR. Data show that chronic expression of Kir2.1 in the RVLM of conscious SHR caused a marked and sustained decrease in BP without changes in the baro- and peripheral chemoreceptor reflex evoked responses. This decrease was mostly due to a reduction in sympathetic output revealed indirectly by a decrease in the power density of the SBP-LF band. Our data are amongst the firsts to demonstrate the role of the RVLM in maintaining BP levels in hypertension in conscious SHR. We suggest that a decrease in RVLM neuronal activity is an effective anti-hypertensive treatment strategy.

Impact of Swimming Exercise Training on the Effects of Modulation of Mitochondrial Permeability Transition and NOS-1 Activation in Medullary Cardiovascular Neurons of Rats

Physical inactivity can be considered one of the major risk factors related to cardiovascular diseases. There are reasons to believe that the positive effect of exercise training is, to a large extent, mediated by modulation of the nervous control of the circulation system. In our previous studies, we showed that modulation of mitochondrial permeability transition in medullary cardiovascular neurons significantly contributes to the hemodynamic reactions in both the norm and a number of pathological states. In this study, we examined in acute experiments on urethane-anesthetized rats the hemodynamic effects mediated by either modulation of mitochondrial permeability transition in medullary neurons, or activation of neuronal NO synthase (NOS-1) in these neuronal populations after preliminary moderate exercise training (everyday swimming sessions of increased duration carried out for four weeks). It was shown that, after exercise training had been completed, the effects of injections of an inductor of mitochondrial permeability transition pore (MPTP) opening, phenylarsine oxide (PAO, 0.5 to 1.5 nmol), into populations of cardiovascular neurons in the medullary autonomic nuclei (nucl. tractus solitarius and paramedian and lateral reticular nuclei) were less expressed, as compared with those in control (untrained) animals. The data obtained suggest that exercise training can exert a protective action on functional activity of medullary neurons due to the decreased sensitivity of MPTPs to their opening. Injections of an inhibitor of MPTP opening, melatonin (0.7 to 2.1 nmol), into populations of medullary neurons under study in trained rats induced a decrease in the systemic arterial pressure (SAP), in contrast to untrained animals demonstrating mostly hypertensive responses following injections of melatonin into the above nuclei. Injections of an activator of neuronal NO synthase (NOS-1), L-arginine, into the medullary nuclei of swimming-trained rats resulted in more expressed hemodynamic shifts than in control animals, which suggests an increase in the activity of neuronal NO synthase in medullary neurons of such animals.

Commentaries on Viewpoint: Initiating inspiration outside the medulla does produce eupneic breathing

Commentaries on Viewpoint: Initiating inspiration outside the medulla does produce eupneic breathing

Point:Counterpoint: Medullary pacemaker neurons are essential for both eupnea and gasping in mammals vs. medullary pacemaker neurons are essential for gasping, but not eupnea, in mammals

to the editor: Implicit in the commentaries concerning the possible role of medullary pacemakers in the neurogenesis of eupnea and gasping is one critical and recurring question: How are in vitro rhythms related to these classical patterns of automatic ventilatory activity? Suzue ([5][1]) considered

Sustained activation of the central baroreceptor pathway in obesity hypertension.

The major goal of this study was to determine whether there is increased activation of medullary neurons that participate in the central baroreceptor reflex pathway in dogs with obesity-induced hypertension, a model of hypertension that is associated with increased sympathetic activity. We used Fos-like (Fos-Li) protein immunohistochemical methods to determine activation of neurons in the nucleus tractus solitarius (NTS), caudal ventrolateral medulla (CVLM), and rostral ventrolateral medulla (RVLM). Dogs were fed either a regular diet or an identical diet with the addition of 0.5 to 0.9 kg of cooked beef fat. After approximately 6 weeks of the high fat diet, body weight (36.3+/-0.4 vs 21.5+/-0.5 kg), mean arterial pressure (105+/-4 vs 91+/-3 mm Hg), and heart rate (97+/-4 vs 70+/-3 bpm) were significantly greater in obese than in control dogs, respectively. There was little Fos-Li immunoreactivity in medullary neurons of control dogs but marked reactivity in obese dogs. Specifically, the number of Fos-Li-positive cells in the NTS and CVLM was 3 to 5 times greater in obese than in control dogs. Furthermore, despite sustained activation of these baroreceptor-sensitive neurons, there was a significantly greater number of Fos-Li positive cells in the RVLM of dogs fed the high fat diet. As baroreceptor suppression of sympathoexcitatory cells in the RVLM is mediated by activation of neurons in the NTS and CVLM, these results support recent findings indicating that baroreflex suppression of sympathetic activity is a long-term compensatory response in hypertension. However, sympathoexcitatory inputs onto RVLM neurons would appear to predominate over the inhibitory effects of the baroreflex in obesity hypertension.

Respiratory-modulated neuronal activities of the rostral medulla which may generate gasping.

Different neurophysiological mechanisms have been proposed to generate eupnea and gasping. Gasping is generated by neuronal mechanisms intrinsic to the medulla whereas a ponto-medullary neuronal circuit has been hypothesized to generate eupnea. Hence, neurons in the rostral medullary region which are critical for the neurogenesis of gasping are hypothesized to discharge differently in eupnea and gasping. In a perfused in situ preparation of the juvenile rat, these rostral medullary neuronal activities had inspiratory, expiratory and phase-spanning patterns in eupnea. In gasping, most expiratory and phase-spanning activities ceased, whereas many inspiratory neuronal activities changed to a decrementing pattern as that of the phrenic nerve. A limited proportion of neuronal activities acquired a 'pre-inspiratory' discharge in gasping. These neuronal activities, which were inspiratory or phase-spanning in eupnea, commenced discharge in neural expiration. This discharge peaked at the onset of the gasp and then decremented during neural inspiration. We hypothesize that these 'pre-inspiratory' neuronal activities generate the gasp by intrinsic pacemaker mechanisms.

Muscle tone facilitation and inhibition after orexin-a (hypocretin-1) microinjections into the medial medulla.

Orexins/hypocretins are synthesized in neurons of the perifornical, dorsomedial, lateral, and posterior hypothalamus. A loss of hypocretin neurons has been found in human narcolepsy, which is characterized by sudden loss of muscle tone, called cataplexy, and sleepiness. The normal functional role of these neurons, however, is unclear. The medioventral medullary region, including gigantocellular reticular nucleus, alpha (GiA) and ventral (GiV) parts, participates in the induction of locomotion and muscle tone facilitation in decerebrate animals and receives moderate orexinergic innervation. In the present study, we have examined the role of orexin-A (OX-A) in muscle tone control using microinjections (50 microM, 0.3 microl) into the GiA and GiV sites in decerebrate rats. OX-A microinjections into GiA sites, previously identified by electrical stimulation as facilitating hindlimb muscle tone bilaterally, produced a bilateral increase of muscle tone in the same muscles. Bilateral lidocaine microinjections (4%, 0.3 microl) into the dorsolateral mesopontine reticular formation decreased muscle rigidity and blocked muscle tone facilitation produced by OX-A microinjections into the GiA sites. The activity of cells related to muscle rigidity, located in the pedunculopontine tegmental nucleus and adjacent reticular formation, was correlated positively with the extent of hindlimb muscle tone facilitation after medullary OX-A microinjections. OX-A microinjections into GiV sites were less effective in muscle tone facilitation, although these sites produced a muscle tone increase during electrical stimulation. In contrast, OX-A microinjections into the gigantocellular nucleus (Gi) sites and dorsal paragigantocellular nucleus (DPGi) sites, previously identified by electrical stimulation as inhibitory points, produced bilateral hindlimb muscle atonia. We propose that the medioventral medullary region is one of the brain stem target for OX-A modulation of muscle tone. Facilitation of muscle tone after OX-A microinjections into this region is linked to activation of intrinsic reticular cells, causing excitation of midbrain and pontine neurons participating in muscle tone facilitation through an ascending pathway. Moreover, our results suggest that OX-A may also regulate the activity of medullary neurons participating in muscle tone suppression. Loss of OX function may, therefore, disturb both muscle tone facilitatory and inhibitory processes at the medullary level.

Sustained activation of the central baroreceptor pathway in angiotensin hypertension.

Recent studies indicate that renal sympathetic nerve activity is chronically suppressed in angiotensin (Ang II) hypertension and that baroreflexes play a critical role in mediating this response. To support these findings, we determined whether the hypertension associated with chronic infusion of Ang II at 4.8 pmol/kg per minute (5ng/kg per minute) produces sustained activation of medullary neurons that participate in the central baroreceptor reflex pathway. We used Fos-like (Fos-Li) protein immunohistochemical methods to determine activation of neurons in the nucleus tractus solitarius (NTS), caudal ventrolateral medulla (CVLM), and rostral ventrolateral medulla (RVLM). Results were compared in three groups of chronically instrumented dogs subjected to infusion of: 1) saline (control); 2) Ang II-2 hours (acute); and 3) Ang II-5 days (chronic). Mean arterial pressure increased 22 +/- 3 and 35 +/- 3 mm Hg during acute and chronic Ang II infusion, respectively. There was little Fos-Li immunoreactivity in medullary neurons in control dogs. In contrast, during acute Ang II infusion there was a 2- to 3-fold increase in Fos-Li staining in the NTS and CVLM, but no increase in staining in RVLM neurons. As baroreceptor suppression of sympathoexcitatory cells in the RVLM is mediated by activation of neurons in the NTS and CVLM, these results were expected. More importantly, this same pattern of central neuronal activation was observed during chronic Ang II hypertension. Therefore, these results support recent findings indicating that baroreflex suppression of renal sympathetic nerve activity is a long-term compensatory response in Ang II hypertension.

Lower esophageal sphincter relaxation and activation of medullary neurons by subdiaphragmatic vagal stimulation in the mouse

Background & Aims: Isolated lower esophageal sphincter (LES) relaxation associated with belching and vomiting and the transient LES relaxation associated with gastroesophageal reflux are gastric afferent-mediated vagovagal reflexes. We aimed to identify the brain stem vagal subnuclei involved in these reflexes. Methods: In anesthetized mice, LES pressures were recorded using a manometric technique and response to electrical stimulation of the ventral trunk of subdiaphragmatic vagus was investigated. Anatomy of the vagal subnuclei was defined, and activated subnuclei with ventral subdiaphragmatic vagus stimulation were detected by c-fos immunohistochemical staining. Results: Ventral subdiaphragmatic vagal stimulation elicited frequency-dependent LES relaxation without evoking esophageal contractions and induced c-fos expression in interneurons in medial, dorsomedial, and commissural subnuclei along with outer shell of area postrema and motoneurons in the caudal dorsal motor nucleus of vagus. Brain stem subnuclei including interstitial, intermediate, and central subnuclei, and nucleus ambiguus, which have been reported to be involved in the response to swallowing, were not activated. Conclusions: Stimulation of the ventral subdiaphragmatic vagus causes isolated LES relaxation and activates neurons in select vagal subnuclei that may represent the brain stem circuit involved in the abdominal vagal-afferent–evoked isolated LES relaxation. These observations suggest that different brain stem circuits are involved in swallow-induced and gastric afferent-mediated isolated LES relaxations.GASTROENTEROLOGY 2000;119:1600-1609

Evidence for ascending visceral nociceptive information in the dorsal midline and lateral spinal cord

The effect of acute, mid-cervical spinal cord lesions on neuronal and reflex activity evoked by the noxious visceral stimulus, colorectal distension (CRD; 80 mmHg, 20 s), was determined in halothane-anesthetized rats. Extracellular recordings were performed of neurons stereotaxically located within the ventrobasal group of the thalamus and in the region of the medullary lateral reticular nucleus. CRD-evoked activity of thalamic neurons was attenuated by lesions of the dorsal midline, but minimally affected by lateral lesions of the spinal cord. In contrast, CRD-evoked activity of medullary neurons was attenuated by lateral lesions ipsilateral to the recording site, but minimally affected by contralateral lateral lesions or dorsal midline lesions. Pseudaffective visceromotor/cardiovascular responses were vigorous in rats with dorsal midline lesions and absent/attenuated in rats with bilateral lateral spinal lesions. This study presents evidence that visceral nociceptive information ascends in the spinal cord by both dorsal midline and lateral spinal pathways.

Lower esophageal sphincter relaxation and activation of medullary neurons by diaphragmatic vagal nerve stimulation in the mouse

Lower esophageal sphincter relaxation and activation of medullary neurons by diaphragmatic vagal nerve stimulation in the mouse

Rostral medullary respiratory neuronal activities of decerebrate cats in eupnea, apneusis and gasping

Eupnea is generated by mechanisms within the pons and medulla. Following removal of pons or exposure to anoxia, gasping is elicited. Eupnea and gasping are markedly different ventilatory patterns. The genesis of gasping is dependent upon rostral medullary neuronal activities. To generate the gasp, these activities should commence before the phrenic burst. In decerebrate, vagotomized, paralyzed and ventilated cats, eupnea was altered to gasping in anoxia. Rostral medullary neuronal activities had inspiratory, expiratory and phase-spanning patterns in eupnea. During gasping, some inspiratory neuronal activities commenced before the phrenic gasp; these same neurons had commenced activities after the onset of the eupneic phrenic burst. Expiratory and phase-spanning neurons did not discharge. Neuronal activities which are consonant with a role in the neurogenesis of gasping had very different discharge patterns in eupnea. Results support the concept that medullary mechanisms for gasping are incorporated in the ponto–medullary circuit responsible for the neurogenesis and expression of eupnea.

Effects of extracellular calcium and magnesium on central respiratory control in the brainstem–spinal cord of neonatal rat

The influence of extracellular Ca 2+ and Mg 2+ concentrations ([Ca 2+] ECF and [Mg 2+] ECF, respectively) on central respiratory control was analyzed using the isolated brainstem–spinal cord of the neonatal rat. Central respiratory activity was recorded from the C4 ventral roots. The depth profile of [Ca 2+] ECF below the ventral medullary surface was measured with ion-sensitive electrodes. The gradient in [Ca 2+] ECF disappeared about 1 h after changing superfusate Ca 2+ ([Ca 2+] CSF) from 2 to 0.5 mM, but not even in 2 h after switching to Ca 2+-free superfusate. High [Ca 2+] CSF (4 mM) or high [Mg 2+] CSF (4, 8 mM) decreased respiratory frequency ( f R), whereas low [Ca 2+] CSF (0.5 mM) increased f R and augmented the respiratory CO 2 responsiveness. High [Ca 2+] CSF as well as low [Mg 2+] CSF (0.5 mM) disturbed respiratory rhythm and pattern, which were markedly restored by high CO 2. The depressing effect of high [Ca 2+] ECF and the stimulating effect of low [Ca 2+] ECF on the medullary neuronal activity were confirmed by perforated patch recordings. These results suggest that [Ca 2+] ECF and [Mg 2+] ECF determine the excitability of the respiratory neuron network by modulating the neuronal surface potential, transmembrane Ca 2+ influx, Ca 2+-sensitive cation channel gating, and synaptic transmission. Furthermore, some of these actions appear to be antagonized by CO 2/H +.

Neurons of the rostral para-ambiguual field have activity correlated to the 10-Hz rhythm in sympathetic nerve discharge of urethane-anesthetized cat

Using the techniques of time domain correlation (mid-signal spike-triggered averaging) and frequency domain correlation (neuron-to-nerve coherence), 24% (54) of a sample of 229 neurons of the rostral para-ambiguual field have shown to have activity correlated to the 8- to 13-Hz rhythm in the inferior cardiac sympathetic nerve discharge (SND) of urethane-anesthetized cat. This correlation existed in both baroreceptor-innervated and -denervated animals. Of the correlated neurons, 37% (20) were non-rhythmically firing and displayed flat autospectra, while 63% (34) fired rhythmically and contained well-defined peaks in their autospectra. The group firing rate of these neurons was 4.3±0.4 spikes/s, indicating that they are not pacemaker neurons for the 10-Hz SND rhythm. The group time of firing of these neurons to the next peak of the SND slow wave was 52±4 ms. Correlation of the activity of medullary neurons with the 8–13-Hz rhythm of the SND was previously claimed only for rostral ventrolateral medulla, caudal raphe, and rostral caudal ventrolateral medulla. This present finding suggests that this behavior may be more widely spread throughout the medulla.

Medullary regions for neurogenesis of gasping: noeud vital or noeuds vitals?

Gasping is a critical mechanism for survival in that it serves as a mechanism for autoresuscitation when eupnea fails. Eupnea and gasping are separable patterns of automatic ventilatory activity in all mammalian species from the day of birth. The neurogenesis of the gasp is dependent on the discharge of neurons in the rostroventral medulla. This gasping center overlaps a region termed "the pre-Bötzinger complex." Neuronal activities of this complex, characterized in an in vitro brain stem spinal cord preparation of the neonatal rat, have been hypothesized to underlie respiratory rhythm generation. Yet, the rhythmic activity of this in vitro preparation is markedly different from eupnea but identical with gasping in vivo. In eupnea, medullary neuronal activities generating the gasp and the identical rhythm of the in vitro preparation are incorporated into a portion of the pontomedullary circuit defining eupneic ventilatory activity. However, these medullary neuronal activities do not appear critical for the neurogenesis of eupnea, per se.

Corticotropin-Releasing Factor Enhances Locomotion and Medullary Neuronal Firing in an Amphibian

Corticotropin-releasing factor (CRF) administration has been shown to act centrally to enhance locomotion in rats and amphibians. In the present study we used an amphibian, the roughskin newt (Taricha granulosa), to characterize changes in medullary neuronal activity associated with CRF-induced walking and swimming in animals chronically implanted with fine-wire microelectrodes. Neuronal activity was recorded from the raphe and adjacent reticular region of the rostral medulla. Under baseline conditions most of the recorded neurons showed low to moderate amounts of neuronal activity during periods of immobility and pronounced increases in firing that were time-locked with episodes of walking. These neurons sometimes showed further increases in discharge during swimming. Injections of CRF but not saline into the lateral ventricle produced a rapidly appearing increase in walking and pronounced changes (mostly increases) in firing rates of the medullary neurons. CRF produced diverse changes in patterns of firing in different neurons, but for these neurons as a group, the effects of CRF showed a close temporal association with the onset and expression of the peptide's effect on locomotion. In neurons that were active exclusively during movement prior to CRF treatment, the post-CRF increase in firing was evident during episodes of walking; in other neurons that also were spontaneously active during immobility prior to CRF infusion, post-CRF activity changes were evident during immobility as well as during episodes of locomotion. Thus, a principal effect of CRF was to potentiate the level of neuronal firing in a population of medullary neurons with locomotor-related properties. Due to the route of administration CRF may have acted on multiple central nervous system sites to enhance locomotion, but the results are consistent with neurophysiological effects involving medullary locomotion-regulating neurons.

Medullary respiratory neuronal activity modulated by stimulation of the fastigial nucleus of the cerebellum

The ability of the rostral fastigial nucleus (FNr) of the cerebellum to modulate medullary respiratory neuronal activity was examined in 17 anesthetized, paralyzed and ventilated cats. A bipolar stimulating electrode was positioned into the FNr and tungsten microelectrodes used to record units within the nucleus tractus solitarius (NTS), nucleus ambiguus (NA) and nucleus retroambigualis (NRA). Transient stimuli (< 150 μA, 5–200 Hz) were delivered during inspiration or expiration, and the effects noted on medullary neuronal activity and the phrenic neurogram. The results showed that FNr stimulation: (1) modulated inspiratory and expiratory neuronal (ramp-, early- and late- inspiratory and stage I and II expiratory) discharges recorded from the NTS, NA and NRA ( n = 67, 14 and 28) when stimuli (⩾ 20–50 Hz) were delivered during either the inspiratory or expiratory phases; (2) terminated the burst durations of inspiratory (77%) and expiratory (94%) neurons with stimulus-response latencies of 28.2 ± 3.1 ms (inspiratory) and 29.4 ± 3.6 ms (expiratory); (3) elicited changes in phrenic neurogram concomitant with the effects noted on medullary neuronal activities; (4) failed to change heart rate and arterial blood pressure; and (5) did not affect medullary neuronal and phrenic nerve activity following kainic acid injection into the FNr. We conclude that activation of the FNr (likely its cell bodies) can modulate the respiratory output via influences on medullary respiratory-related neurons. The primary cerebellar effect across all sub-types of respiratory neurons was early termination.

Preferential correlations of a medullary neuron's activity to different sympathetic outflows as revealed by partial coherence analysis.

1. In vagotomized, paralyzed, decerebrate cats, simultaneous recordings were taken from one or more sympathetic nerves [cervical sympathetic (CS), inferior cardiac (IC), splanchnic (SP)] and from medullary neurons in vasomotor-related regions. Coherence analyses were used to ascertain the presence of sympathetic rhythms (2-6 Hz or "3-Hz rhythm," 7-13 Hz or "10-Hz rhythm") that were correlated between different signals. The occurrence of a significant peak at such a frequency in a unit-nerve coherence spectrum allowed the identification of a medullary neuron as sympathetic related. 2. A serendipitous example is given of a rostral ventrolateral medullary neuron that had significant unit-nerve 10-Hz coherence peaks for three sympathetic nerves (CS, IC, SP); but, as revealed by partial coherence analysis, the unit activity's correlation with one nerve's activity could be partially or completely dependent on its correlation with other nerve activities. Thus in this case the unit-CS and unit-IC coherences at 10 Hz were completely dependent on the SP rhythm, whereas the unit-SP coherence was not significantly affected by the CS and IC rhythms. This asymmetry suggests that the neuron was preferentially connected to SP-generating medullary circuits. 3. This example indicates the strength of partial coherence analysis as a means of studying differential connectivity between medullary sympathetic-related neurons and sympathetic output neuron populations.

Medullary neuronal activities in gasping induced by pharyngeal stimulation and hypoxia

We examined the hypothesis that medullary respiratory-related and non-respiratory-related neuronal activities are similarly altered with the “aspiration reflex”, induced by mechanical stimulation of the epipharyngeal mucosa, and gasping, induced by severe hypoxia. Extracellular neuronal activities were recorded in decerebrate, paralyzed and ventilated cats. Phrenic activity and neuronal activities were monitored in eupnea and gasping. Seventy-one unit activities were recorded in the lateral medulla including the nucleus tractus solitorii (NTS), lateral tegmental field (LTF) and the nucleus ambiguus (NA). The respiratory modulation of a neuronal activity was quantified by a η 2 statistic (Orem, J. and Dick, T., 1983, J. Neurophysiol. 50: 1098–1107). The η 2 values of the units ranged from 0.02 to 0.93. Inspiratory-related activities with relative high η 2 values ( n = 16) were recorded in the region closed to the NTS. Phase-spanning ( n = 7) and expiratory-related activities ( n = 10) were recorded in the ventral medullary region. Units with low η 2 values ( n = 29) and with no spontaneous activity ( n = 9) in eupnea were recorded in the region of the LTF. In both “aspiration reflex” and gasping, inspiratory-related activities were augmented and expiratory-related activities were suppressed. Tonic units were activated and additional activities were recruited. The modulation of the neuronal activities to gasping induced by anoxia was identical to that induced by pharyngeal stimulation in either hyperoxia or severe hypoxia. We concluded that medullary gasping mechanism is recruited by pharyngeal stimulation. In addition, the present findings are compatible with the idea that different brainstem mechanisms are responsible for the control of eupnea and gasping.