PubMed Health⌕ Search

Biomedical subjects

D R McCrimmon

Publications and source records attributed to D R McCrimmon.

34 records · Page 2Linked to original sources
PubMed1993

Pulmonary stretch receptor afferents activate excitatory amino acid receptors in the nucleus tractus solitarii in rats.

1. The goal of the present study was to identify potential neurotransmitter candidates in the Breuer-Hering (BH) reflex pathway, specifically at synapses between the primary afferents and probable second-order neurones (pump cells) within the nucleus tractus solitarii (NTS). We hypothesized that if activation of specific receptors in the NTS is required for production of the BH reflex, then (1) injection of the receptor agonist(s) would mimic the reflex response (apnoea), (2) injection of appropriate antagonists would impair the apnoea produced by either lung inflation or agonist injection, and (3) second-order neurones in the pathway would be excited by either lung inflation or agonists while antagonists would prevent the response to either. 2. Studies were carried out either in spontaneously breathing or in paralysed, thoracotomized and ventilated rats in which either diaphragm EMG or phrenic nerve activity, expired CO2 concentration and arterial pressure were continuously monitored. The BH reflex was physiologically activated by inflating the lungs. 3. Pressure injections (0.03-15 pmol) of selective excitatory amino acid (EAA) receptor agonists, quisqualic acid (Quis) and N-methyl-D-aspartic acid (NMDA) into an area of the NTS shown previously to contain neurones required for production of the BH reflex produced dose-dependent apnoeas that mimicked the response to lung inflation. Injection of substance P (0.03-4 pmol) did not alter baseline respiratory pattern. 4. Injections of the EAA antagonists, kynurenic acid (Kyn; 0.6-240 pmol), 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX) or 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the BH region of the NTS reversibly impaired the apnoea produced by lung inflation. All three antagonists reduced or abolished the apnoeas resulting from injection of Quis or NMDA, and slowed baseline respiratory frequency. In contrast, injections of the highly selective NMDA receptor antagonist, D-2-amino-5-phosphonovaleric acids (AP5), in doses sufficient to block the apnoeic response to NMDA, neither altered the reflex apnoea evoked by lung inflation nor the baseline respiratory pattern. 5. Pump cells located within the BH region were excited by pressure injections of the broad spectrum EAA agonist, DL-homocysteic acid (DLH). Kyn reversibly blocked the excitation of pump cells in response to either lung inflation or DLH injection. 6. These findings suggest that EAAs mediate primary afferent excitation of second-order neurones in the Breuer-Hering reflex pathway, primarily through the activation of non-NMDA EAA receptor subtypes.

Amino Acids↗
PubMed1993

Time-dependent phrenic nerve responses to carotid afferent activation: intact vs. decerebellate rats.

The objectives were to determine 1) respiratory responses to carotid chemoreceptor inputs in anesthetized rats and 2) whether the cerebellar vermis plays a role in these responses. A carotid sinus nerve was stimulated (20 Hz) with five 2-min trains, each separated by approximately 3 min. During stimulation, respiratory frequency (f), peak amplitude of integrated phrenic nerve activity (integral of Phr), and their product (f x integral of Phr) immediately increased. As stimulation continued, integral of Phr progressively increased to a plateau [short-term potentiation (STP)], but f and f x integral of Phr decreased [short-term depression (STD)] to a value still above control. Upon stimulus termination, integral of Phr progressively decreased but remained above control; f and f x integral of Phr transiently decreased below baseline. After the final stimulation, integral of Phr remained above control for at least 30 min [long-term facilitation (LTF)]. Repeated 5-min episodes of isocapnic hypoxia also elicited STP, STD, and LTF. Vermalectomy lowered the CO2-apneic threshold and eliminated LTF. In conclusion, carotid chemoreceptor activation in rats elicits STP and LTF similar to that in cats; the vermis may play a role in LTF. A new response, STD, was observed.

Afferent Pathways↗
PubMed1990

Neurones in a discrete region of the nucleus tractus solitarius are required for the Breuer-Hering reflex in rat.

1. The Breuer-Hering reflex consists of a shortening of inspiration and lengthening of expiration in response to afferent input from slowly adapting pulmonary stretch receptors (SAR). We hypothesized that neurones in a discrete region of the nucleus tractus solitarius (NTS) are required for producing the reflex. Accordingly, the present studies were undertaken to: (1) identify sites in the NTS in which chemical excitation of neurones inhibited phrenic nerve discharge in a manner consistent with SAR activation, (2) determine whether localized interruption of synaptic transmission prevented the Breuer-Hering reflex, and (3) determine whether these regions contained pump cells and SAR terminal afferents. Studies were carried out in urethane-anaesthetized rats. 2. Injection of picomoles of an excitatory amino acid, DL-homocysteic acid (DLH), in the NTS, at the rostrocaudal level of the area postrema and immediately medial to the tractus solitarius, silenced phrenic nerve activity similarly to that expected from SAR activation. These apnoeas lasted from 3 to 43 s and were produced with little or no change in arterial pressure or heart rate. 3. The Breuer-Hering reflex, physiologically activated by maintaining lung inflation, was transiently impaired by interruption of synaptic transmission following injections of cobalt chloride in the DLH-responsive region. 4. Pump cell (SAR interneurone) and SAR afferent activity were recorded at the site in which DLH produced apnoea. 5. Taken together, the results of chemical excitation, interruption of synaptic transmission and extracellular recording, suggest that cells within a discrete region of the NTS, probably pump cells, are necessary for the production of the Breuer-Hering reflex.

Action Potentials↗
PubMed1990

Slow excitatory amino acid receptor-mediated synaptic transmission in turtle cerebellar Purkinje cells.

1. The excitatory synaptic responses of turtle Purkinje cells to climbing and parallel fiber (CF and PF) stimulation have been studied by the use of intrasomatic and intradendritic recordings in intact cerebellum and brain stem-cerebellum preparations in vitro. 2. Activation of CF inputs from the cerebellar peduncle or the region of the inferior olive evoked complex spikes followed by slow excitatory postsynaptic potentials (EPSPs), both of which were evoked in an all-or-none fashion. 3. Single stimuli applied to the cerebellar molecular layer activated fast PF-mediated EPSPs; brief trains of PF stimuli (2-5 stimuli, 50-100 Hz) evoked volleys of fast EPSPs followed by a slow, long-lasting EPSP. The amplitude of the fast and slow PF-mediated EPSPs were both graded with stimulus intensity. 4. Slow EPSPs evoked both by CF and PF stimulation were associated with an increase in membrane conductance and were increased in amplitude by hyperpolarization. 5. The CF-evoked slow EPSP was profoundly attenuated by repetitive activation at interstimulus intervals of less than 15-20 s, whereas the PF-evoked slow EPSP was not reduced by repetitive activation. 6. The PF-evoked slow EPSP readily triggered dendritic pacemaker discharges when activated at or near resting membrane potential. The activation of this potential by phasic PF volleys may, therefore, provide an appropriate synaptic drive to cerebellar Purkinje cells to entrain the intrinsic pacemaker properties of these cells to cycles of motor activity. 7. Both slow synaptic potentials were blocked by the excitatory amino acid antagonists kynurenate and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), but not by DL-2-amino-5-phosphonovalerate (DL-AP5) or L-serine-O-phosphate (L-SOP). The PF-evoked slow EPSP was selectively antagonized by L-2-amino-4-phosphonobutyrate (L-AP4; 20-100 microM). 8. It is suggested that the CF- and PF-evoked slow EPSPs observed in this study represent a novel class of excitatory amino acid receptor-mediated slow synaptic potentials activated by Purkinje cell afferents, which may play a role in synaptic integration and motor pattern generation in the cerebellum.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1989

Involvement of excitatory amino acids in neurotransmission of inspiratory drive to spinal respiratory motoneurons.

The role of excitatory amino acids in the transmission of bulbospinal respiratory drive to spinal motoneurons was investigated in the in vitro and in vivo spinal cord of the rat. In vitro studies were performed with a preparation of neonatal rat brain stem and spinal cord that spontaneously generates rhythmic respiratory drive to spinal respiratory motoneurons. This in vitro system allowed examination of the effects of pharmacological agents on spinal motoneuron activity, without perturbing the activity of bulbospinal neurons transmitting the respiratory drive. The amplitude of spontaneous motor discharge in spinal ventral roots containing phrenic and intercostal motor axons was reduced in a dose-dependent manner by antagonists to excitatory amino acids acting at NMDA receptors [D,L-2-amino-5-phosphonovaleric acid (D,L-AP5)] and non-NMDA receptors [kynurenic acid, gamma-D-glutamylglycine, gamma-D-glutamyltaurine, and L- and D,L-2-amino-4-phosphonobutyric acid (L-AP4,D,L-AP4)]. The order of potency of the antagonists for complete block of the motor output was L-AP4 greater than D,L-AP4 greater than kynurenic acid greater than gamma-D-glutamylglycine greater than D,L-AP5 greater than or equal to gamma-D-glutamyltaurine. Amino acid uptake inhibitors augmented the spontaneous motoneuron activity, further confirming the involvement of endogenous excitatory amino acids in transmission of respiratory drive. The results obtained in vitro with AP4, kynurenic acid, and amino acid uptake inhibitors were confirmed in vivo by bathing segments of the rat spinal cord in situ with solutions containing antagonists and uptake inhibitors. The present results suggest that an important component of the neurotransmission of bulbospinal respiratory drive involves endogenous excitatory amino acids acting at AP4-sensitive sites and other non-NMDA (quisqualate/kainate) receptors. The bulbospinal-spinal respiratory motoneuron synapse may provide a convenient model synapse in the spinal cord for detailed analysis of mechanisms underlying excitatory amino acid-mediated synaptic transmission of motor drive.

Amino Acids↗
PubMed1988

Cardiovascular function is altered by picomole injections of glutamate into rat medulla.

Local neural circuitry in the nucleus tractus solitarius (NTS) involved in cardiovascular control was studied by injecting nanoliter volumes of excitatory amino acids into the structure. Experiments were performed on urethane-anesthetized, artificially ventilated rats. Multibarrel micropipettes were used for pressure ejection of drugs or a dye for marking ejection sites. Ejected volumes, ranging from 200 pl to 25 nl, were directly monitored for every injection. Injections of as little as 200 fmol of L-glutamate in 200 pl into the medial and lateral NTS region rostral to the obex elicited marked, site-specific decreases in arterial pressure and heart rate. The majority of these responses were eliminated by blockade of parasympathetic and sympathetic neural outflow. At sites caudal to obex, in the commissural region of the NTS, L-glutamate injections produced marked elevations in heart rate and arterial pressure which were sympathetically mediated. Responses to L-glutamate were attenuated by concurrent injection of glutamic acid diethyl ester and DL-2-amino-4-phosphonobutyrate, or lidocaine. These results indicate a heterogeneity in the spatial organization of brain-stem circuitry underlying cardiovascular control that has not been previously described.

Animals↗
PubMed1987

Role of the ventrolateral region of the nucleus of the tractus solitarius in processing respiratory afferent input from vagus and superior laryngeal nerves.

The role of respiratory neurons located within and adjacent to the region of the ventrolateral nucleus of the tractus solitarius (vlNTS) in processing respiratory related afferent input from the vagus and superior laryngeal nerves was examined. Responses in phrenic neural discharge to electrical stimulation of the cervical vagus or superior laryngeal nerve afferents were determined before and after lesioning the vlNTS region. Studies were conducted on anesthetized, vagotomized, paralyzed and artificially ventilated cats. Arrays of 2 to 4 tungsten microelectrodes were used to record neuronal activity and for lesioning. Constant current lesions were made in the vlNTS region where respiratory neuronal discharges were recorded. The region of the vlNTS was probed with the microelectrodes and lesions made until no further respiratory related neuronal discharge could be recorded. The size and placement of lesions was determined in subsequent microscopic examination of 50 micron thick sections. Prior to making lesions, electrical stimulation of the superior laryngeal nerve (4-100 microA, 10 Hz, 0.1 ms pulse duration) elicited a short latency increase in discharge of phrenic motoneurons, primarily contralateral to the stimulated nerve. This was followed by a bilateral decrease in phrenic nerve discharge and, at higher currents, a longer latency increase in discharge. Stimulation of the vagus nerve at intensities chosen to selectively activate pulmonary stretch receptor afferent fibers produced a stimulus (current) dependent shortening of inspiratory duration. Responses were compared between measurements made immediately before and immediately after each lesion so that changes in response efficacy due to lesions per se could be distinguished from other factors, such as slight changes in the level of anesthesia over the several hours necessary in some cases to complete the lesions. Neither uni- nor bi-lateral lesions altered the efficacy with which stimulation of the vagus nerve shortened inspiratory duration. The short latency excitation of the phrenic motoneurons due to stimulation of the superior laryngeal nerve was severely attenuated by unilateral lesions of the vlNTS region ipsilateral to the stimulated nerve. Neither the bilateral inhibition nor the longer latency excitation due to superior laryngeal nerve stimulation was reduced by uni- or bi-lateral lesions of the vlNTS region.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1986

Respiratory motoneuronal activity is altered by injections of picomoles of glutamate into cat brain stem.

The local neural circuitry underlying the control of breathing was studied by injecting nanoliter volumes of excitatory amino acids into discrete regions of cat brain stem. Experiments were performed on chloralose-urethane anesthetized, vagotomized, paralyzed, and artificially ventilated cats. Phrenic, intercostal, and recurrent laryngeal nerve discharges were recorded. Multibarrel pipettes were used for recording and pressure ejection of drugs or a dye for marking recording and ejection sites. Ejected volumes were directly monitored for every injection. Injections, proximal to neurons discharging with a respiratory periodicity, of as little of 200 fmol of L-glutamate in 200 pl of saline elicited marked, site-specific increases or decreases in respiratory motoneuronal discharge. N-Methyl-D-aspartic acid and homocysteic acid elicited similar site-specific alterations in respiratory motor output, although some details of the response could differ qualitatively. Responses to all the excitatory agents used were attenuated by concurrent injection of kynurenic acid, DL-2-amino-4-phosphonobutyric acid, or glutamic acid diethyl ester. There was no change in spontaneous phrenic nerve discharge in response to injections of equivalent or larger volumes of saline or lidocaine. These results indicate a heterogeneity in the spatial organization of the brain-stem neural circuitry underlying respiratory control, which has not been described previously. This injection technique may provide a mechanism for probing the neural circuitry underlying other behaviors.

Animals↗
PubMed1984

Effect of synchronous activation of medullary inspiratory bulbo-spinal neurones on phrenic nerve discharge in cat.

The effects on phrenic nerve discharge elicited by intraspinal stimulation which produced synchronous activation of bulbo-spinal inspiratory neurones were investigated in chloralose-urethane anaesthetized, paralysed, vagotomized and artificially ventilated cats. Descending respiratory axons were activated in the ventrolateral spinal cord at the second cervical level using either monopolar or bipolar stimulation (25-200 microA, 100 microseconds, 1-300 Hz). Activation of bulbo-spinal axons was confirmed by recording both orthodromic phrenic nerve excitation and antidromic spike invasion of single, inspiratory modulated units in either the dorsal respiratory group (d.r.g.) or ventral respiratory group (v.r.g.). Antidromic activation of inspiratory bulbo-spinal neurones was confirmed by the criteria of high frequency following and collision tests. Spinal cord stimulation at intensities of 100 microA antidromically activated approximately half of the inspiratory bulbo-spinal neurones in the d.r.g. and v.r.g. Stimulation pulses delivered to the spinal cord elicited an orthodromic excitation of the ipsilateral phrenic nerve lasting 2-12 ms during inspiration. The onset latency of excitation was 2-4 ms, decreasing as inspiration progressed. Following the initial excitation there was a 4-30 ms period of reduced phrenic nerve discharge. Continuous trains of stimuli (less than 100 microA, 100 microseconds, 1-300 Hz) or phrenic gated trains delivered during every fourth inspiratory or expiratory cycle had little or no effect on the duration of inspiration or expiration. Brief trains (400 ms, 50 Hz, 100 microA) of bilateral spinal cord stimulation delivered at various delays from the onset of inspiration had only a transient effect on the pattern of phrenic nerve discharge, with no noticeable effect 60 ms after termination of stimulation. Based on the assumption that synchronous activation of a portion of the central pattern generator for respiration would phase shift or reset the rhythm, we conclude that the bulbo-spinal inspiratory neurones are not responsible for generation of respiratory timing signals and play, at most, a limited role in the generation of the augmenting central inspiratory activity.

Action Potentials↗
PubMed1983

Monoamine neurotransmitter metabolism during acclimatization to hypoxia in rats.

The levels and turnovers of NE, DA and 5HT were determined in whole brain, brain stem, cervical and thoracic spinal cord and carotid bodies (CB) of rats exposed to from 1 h to 7 days of hypobaric hypoxia (PB = 450 torr). Monoamine levels decreased only transiently upon acute exposure to hypoxia. Monoamine turnover in the CNS was estimated from the average of (a) monoamine buildup following inhibition of catabolism, and (b) monoamine breakdown following inhibition of synthesis. Hypoxic effects on CNS monoamine turnover showed that: (a) NE was not affected; (b) DA was not affected in acute hypoxia, but was reduced to about 40% of normoxia control after 1-7 days hypoxia; (c) 5HT fell 50-60% during acute hypoxia but returned to and was maintained at control over 1-7 days of hypoxia; (d) acute restoration of normoxia following acute hypoxia restored 5HT and DA to control or above and in the acclimatized animal acute normoxia increased DA and 5HT turnover to about 1.4 and 1.8 X control. In the CB, DA levels gradually increased to 4 X control after 7 days of hypoxia and further increased to 6 X control upon acute restoration of normoxia. Changes in the metabolism of both central 5HT and CB DA may be related to the mechanisms mediating ventilatory acclimatization to chronic hypoxia.

Adaptation, Physiological↗
PubMed1982

Inhibition of respiratory neural discharges by clonidine and 5-hydroxytryptophan.

Activation of receptors for norepinephrine or serotonin in the central nervous system by i.v. injection of clonidine (10-50 micrograms/kg) or 5-hydroxytryptophan (20-40 mg/kg) inhibits phrenic neural discharges in anesthetized, artificially ventilated cats. Clonidine induces a rapid and complete inhibition of phrenic nerve activity which lasts for 1 to 3.2 hr. The inhibition is prevented by prior administration of phenoxybenzamine (10 mg/kg) or tolazoline (3 mg/kg). 5-Hydroxytryptophan, injected after inhibition of peripheral amino acid decarboxylase (carbidopa, 30-50 mg/kg), elicits a gradual but complete inhibition of phrenic nerve discharges which persists for 1 to 10 hr and is unaltered by alpha or beta adrenoceptor blocking agents. The inhibitions produced by clonidine and 5-hydroxytryptophan are overcome transiently during hypercapnia. Stimulation of carotid body chemoreceptors by i.a. injections of lobeline, doxapram or 0.015 N HCl in saline also briefly reinstates phrenic nerve discharges after inhibition by clonidine. Inhibition is also overcome during electrical stimulation of the carotid sinus nerve.

5-Hydroxytryptophan↗
PubMed1979

Serotonin and the control of ventilation in awake rats.

In awake, unrestrained, intact rats, reserpine, para-chlorophenylalanine, 6-fluorotryptophan, and para-chloroamphetamine depleted whole brain serotonin and produced a substantial and sustained hyperventilation as evidenced by a 5--9 torr drop in PaCO2. Administration of 5-hydroxytryptophan to rats treated with para-chlorophenylalanine partially alleviated the hyperventilation. No change in ventilation was observed after alpha-methyltyrosine. 5,7-Dihydroxytryptamine produced contradictory results. On the basis of these pharmacological studies, we propose that some serotonin-mediated nerve transmissions might function under physiological conditions to inhibit the central nervous system output which controls normal breathing.

5,7-Dihydroxytryptamine↗
PubMed1976

Effect of training on plasma catecholamines in post myocardial infarction patients.

Exercise induced plasma catecholamine levels, of post myocardial infarct patients, were compared before and after a 27 week training program in two groups. Heavy Intensity Exercise (H.I.E.) and Light Intensity Exercise (L.I.E.). The men (age 38-54 years) were exercised on a bicycle ergometer at constant submaximal work loads (test load) and to a symptom limited maximum work load, both before and after the training program. Forearm venous samples were obtained after 30 minutes rest and within 3 minutes of completion of the test load. After training a significant increase in both maximum work load and heart rate (P less than 0.05) was observed in the H.I.E. group. At the test load these individuals had a small (6%) decrease in heart rate. No significant changes were observed in the L.I.E. group at submaximum or maximum exercise. Prior to training, exercise resulted in a significant increase in norepinephrine (NE) with no change in epinephrine (E). Training resulted in a significant reduction (P less than 0.05) in the NE response at the test load of the H.I.E. group while no change was found in the L.I.E. group. Endurance jogging reduced the sympathetic response to moderate exercise.

Adult↗
PubMedDate not supplied

Parvalbumin in respiratory neurons of the ventrolateral medulla of the adult rat.

A column of parvalbumin immunoreactive neurons is closely associated with the location of respiratory neurons in the ventrolateral medulla of the rat. The majority (66%) of bulbospinal neurons in the medullary ventral respiratory column (VRC) that were retrogradely labeled by tracer injections in the phrenic nucleus were also positive for parvalbumin. In contrast, only 18.8% of VRC neurons retrogradely labeled after a tracer injection in the VRC, also expressed parvalbumin. The average cross-sectional area of VRC neurons retrogradely labeled after VRC injections was 193.8 microm2 +/- 6.6 SE. These were significantly smaller than VRC parvalbumin neurons (271.9 microm2 +/- 12.3 SE). Parvalbumin neurons were found in the Bötzinger Complex, the rostral ventral respiratory group (VRG), and the caudal VRG, areas which all contribute to the bulbospinal projection. In contrast, parvalbumin neurons were sparse or absent in the preBötzinger Complex and in the vicinity of the retrotrapezoid nucleus, areas that have few bulbospinal projections. Parvalbumin was rarely colocalized within Neurokinin-1 receptor positive (NK1R) VRC neurons, which are found in the preBötzinger complex and in the anteroventral part of the rostral VRG. Parvalbumin neurons in the Bötzinger Complex and rostral VRG help define the rostrocaudal extent of these regions. The absence of parvalbumin neurons from the intervening preBötzinger complex also helps establish the boundaries of this region. Regional boundaries described in this manner are in good agreement with earlier physiological and anatomical studies. Taken together, the distributions of parvalbumin, NK1R and bulbospinal neurons suggest that the rostral VRG may be subdivided into distinct, anterodorsal, anteroventral, and posterior subdivisions.

Animals↗
PubMedDate not supplied

Pattern formation and rhythm generation in the ventral respiratory group.

1. There is increasing evidence that the kernel of the rhythm-generating circuitry for breathing is located within a discrete subregion of a column of respiratory neurons within the ventrolateral medulla referred to as the ventral respiratory group (VRG). It is less clear how this rhythm is transformed into the precise patterns appearing on the varied motor outflows. 2. Two different approaches were used to test whether subregions of the VRG have distinct roles in rhythm or pattern generation. In one, clusters of VRG neurons were activated or inactivated by pressure injection of small volumes of neuroactive agents to activate or inactivate groups of respiratory neurons and the resulting effects on respiratory rhythm and pattern were determined. The underlying assumption was that if rhythm and pattern are generated by neurons in different VRG subregions, then we should be able to identify regions where activation of neurons predominantly alters rhythm with little effect on pattern and other regions where pattern is altered with little effect on rhythm. 3. Based on the pattern of phrenic nerve responses to injection of an excitatory amino acid (DL-homocysteate), the VRG was divided into four subdivisions arranged along the rostrocaudal axis. Injections into the three rostral regions elicited changes in both respiratory rhythm and pattern. From rostral to caudal the regions included: (i) a rostral bradypnoea region, roughly associated with the Bötzinger complex; (ii) a dysrhythmia/tachypnoea area, roughly associated with the pre-Bötzinger complex (PBC); (iii) a second caudal bradypnoea area; and, most caudally, (iv) a region from which no detectable change in respiratory motor output was elicited. 4. In a second approach, the effect of unilateral lesions of one subregion, the PBC, on the Breuer-Hering reflex changes in rhythm were determined. Activation of this reflex by lung inflation shortens inspiration and lengthens expiration (TE). 5. Unilateral lesions in the PBC attenuated the reflex lengthening of TE, but did not change baseline respiratory rhythm. 6. These findings are consistent with the concept that the VRG is not functionally homogenous, but consists of rostrocaudally arranged subregions. Neurons within the so-called PBC appear to have a dominant role in rhythm generation. Nevertheless, neurons within other subregions contribute to both rhythm and pattern generation. Thus, at least at an anatomical level resolvable by pressure injection, there appears to be a significant overlap in the circuitry generating respiratory rhythm and pattern.

Animals↗