Axonal trajectory and terminal distribution of inspiratory neurons of the dorsal respiratory group in the cat's medulla

1989 ◽  
Vol 286 (2) ◽  
pp. 218-230 ◽  
Author(s):  
Kazuyoshi Otake ◽  
Hiroshi Sasaki ◽  
Kazuhisa Ezure ◽  
Motomu Manabe
Keyword(s):  
Inspiratory Neurons ◽  
Dorsal Respiratory Group

Activity of respiratory neurons during hypoxia in the chemodenervated cat

1995 ◽  
Vol 78 (3) ◽  
pp. 856-861 ◽  
Author(s):  
S. J. England ◽  
J. E. Melton ◽  
M. A. Douse ◽  
J. Duffin
Keyword(s):  
Respiratory Depression ◽  
Late Onset ◽  
Respiratory Neurons ◽  
Ventral Respiratory Group ◽  
Inspiratory Neurons ◽  
Dorsal Respiratory Group ◽  
Premotor Neurons ◽  
Acute Hypoxic Hypoxia ◽  
Subsequent Loss ◽  
Initial Depression

Exposure of anesthetized paralyzed vagotomized peripherally chemodenervated cats to hypoxia results in initial depression and subsequent loss of the phrenic neurogram. To determine whether hypoxic respiratory depression results from the inhibition of respiratory premotor neurons by bulbospinal neurons of the Botzinger complex (Bot-E neurons), extracellular recordings were made of dorsal and ventral respiratory group bulbospinal inspiratory neurons and Bot-E neurons during acute hypoxic hypoxia. All neurons recorded decreased firing rate during hypoxia. Bot-E neurons became silent before the loss of phasic phrenic activity during hypoxia and commenced firing before or coincident with the return of the phrenic neurogram during reoxygenation. Inspiratory neurons ceased firing coincident with phrenic silence. Dorsal respiratory group and ventral respiratory group neurons that had a late onset of firing with respect to the phrenic neurogram during normoxia fired progressively earlier in inspiration during hypoxia, an effect that was reversed during reoxygenation. These data are consistent with inhibition and/or disfacilitation as the mechanism of hypoxic respiratory depression but suggest that Bot-E neurons are not the source of this inhibition.

GABA-immunoreactive boutons make synapses with inspiratory neurons of the dorsal respiratory group

1990 ◽  
Vol 529 (1-2) ◽  
pp. 309-314 ◽  
Author(s):  
J. Lipski ◽  
H.J. Waldvogel ◽  
P. Pilowsky ◽  
C. Jiang
Keyword(s):  
Inspiratory Neurons ◽  
Dorsal Respiratory Group

Physiological Properties of Late Inspiratory Neurons and Their Possible Involvement in Inspiratory Off-Switching in Cats

2002 ◽  
Vol 87 (2) ◽  
pp. 1057-1067 ◽  
Author(s):  
Akira Haji ◽  
Mari Okazaki ◽  
Hiromi Yamazaki ◽  
Ryuji Takeda
Keyword(s):  
Nmda Receptors ◽  
Gaba Release ◽  
Membrane Depolarization ◽  
Inhibitory Neurons ◽  
Acid Decarboxylase ◽  
Postsynaptic Potentials ◽  
Inspiratory Neurons ◽  
Small Constant ◽  
Physiological Properties ◽  
Decerebrate Cats

To assess the functional significance of late inspiratory (late-I) neurons in inspiratory off-switching (IOS), membrane potential and discharge properties were examined in vagotomized, decerebrate cats. During spontaneous IOS, late-I neurons displayed large membrane depolarization and associated discharge of action potentials that started in late inspiration, peaked at the end of inspiration, and ended during postinspiration. Depolarization was decreased by iontophoresis of dizocilpine and eliminated by tetrodotoxin. Stimulation of the vagus nerve or the nucleus parabrachialis medialis (NPBM) also evoked depolarization of late-I neurons and IOS. Waves of spontaneous chloride-dependent inhibitory postsynaptic potentials (IPSPs) preceded membrane depolarization during early inspiration and followed during postinspiration and stage 2 expiration of the respiratory cycle. Iontophoresed bicuculline depressed the IPSPs. Intravenous dizocilpine caused a greatly prolonged inspiratory discharge of the phrenic nerve (apneusis) and suppressed late-inspiratory depolarization as well as early-inspiratory IPSPs, resulting in a small constant depolarization throughout the apneusis. NPBM or vagal stimulation after dizocilpine produced small, stimulus-locked excitatory postsynaptic potentials (EPSPs) in late-I neurons. Neurobiotin-labeled late-I neurons revealed immunoreactivity for glutamic acid decarboxylase as well as N-methyl-d-aspartate (NMDA) receptors. These results suggest that late-I neurons are GABAergic inhibitory neurons, while the effects of bicuculline and dizocilpine indicate that they receive periodic waves of GABAergic IPSPs and glutamatergic EPSPs. The data lead to the conclusion that late-I neurons play an important inhibitory role in IOS. NMDA receptors are assumed to augment and/or synchronize late-inspiratory depolarization and discharge of late-I neurons, leading to GABA release and consequently off-switching of bulbar inspiratory neurons and phrenic motoneurons.

Effects of contralateral superior laryngeal nerve stimulation on dorsal medullary inspiratory neurons

1989 ◽  
Vol 505 (1) ◽  
pp. 149-152 ◽  
Author(s):  
David F. Donnelly ◽  
Anthony L. Sica ◽  
Morton I. Cohen ◽  
Heng Zhang
Keyword(s):  
Nerve Stimulation ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Inspiratory Neurons

Interaction between chemoreceptor and stretch receptor inputs at medullary respiratory neurons

1994 ◽  
Vol 266 (6) ◽  
pp. R1951-R1961 ◽  
Author(s):  
J. Bajic ◽  
E. J. Zuperku ◽  
M. Tonkovic-Capin ◽  
F. A. Hopp
Keyword(s):  
Time Course ◽  
Afferent Input ◽  
Respiratory Neurons ◽  
Neuronal Responses ◽  
Additive Interaction ◽  
Dorsal Respiratory Group ◽  
Afferent Inputs ◽  
Discharge Patterns ◽  
Carotid Body Chemoreceptors ◽  
Common Carotid Arteries

The interaction between afferent inputs from carotid body chemoreceptors (CCRs) and from slowly adapting pulmonary stretch receptors (PSRs) on the discharge patterns of medullary inspiratory (I) and expiratory (E) neurons was characterized in thiopental sodium-anesthetized, paralyzed, ventilated dogs. A cycle-triggered ventilator was used to produce control and test pulmonary afferent input patterns. The CCRs were stimulated by phase-synchronized bolus injections of CO2-saturated saline into the common carotid arteries. Only those neurons whose discharge time course was altered by both inflation and CCR activation were studied. The dorsal respiratory group (DRG) I inflation-insensitive neurons were also included. Cycle-triggered histograms of unit activity were obtained for the neuronal responses to inflation, CO2 bolus, and their combination, as well as for the spontaneous control condition. Linearity of the interaction was tested by comparing the sum of the net individual responses to the net response of the combined afferent inputs. The results suggest that a linear (additive) interaction between CCR and PSR inputs exists for the DRG I inflation-sensitive neurons, the ventral respiratory group (VRG) I decrementing, and caudal VRG E augmenting neurons, while a nonadditive interaction exists for caudal VRG E decrementing bulbospinal neurons. The implications of these findings are discussed.

scholarly journals Mechanisms Underlying Regulation of Respiratory Pattern by Nicotine in PreBötzinger Complex

2001 ◽  
Vol 85 (6) ◽  
pp. 2461-2467 ◽  
Author(s):  
Xuesi M. Shao ◽  
Jack L. Feldman
Keyword(s):  
Respiratory Frequency ◽  
Neonatal Rat ◽  
Respiratory Pattern ◽  
Dependent Manner ◽  
Baseline Noise ◽  
Arterial Blood ◽  
Inspiratory Neurons ◽  
Excitatory Neurotransmission ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

Cholinergic neurotransmission plays a role in regulation of respiratory pattern. Nicotine from cigarette smoke affects respiration and is a risk factor for sudden infant death syndrome (SIDS) and sleep-disordered breathing. The cellular and synaptic mechanisms underlying this regulation are not understood. Using a medullary slice preparation from neonatal rat that contains the preBötzinger Complex (preBötC), the hypothesized site for respiratory rhythm generation, and generates respiratory-related rhythm in vitro, we examined the effects of nicotine on excitatory neurotransmission affecting inspiratory neurons in preBötC and on the respiratory-related motor activity from hypoglossal nerve (XIIn). Microinjection of nicotine into preBötC increased respiratory frequency and decreased the amplitude of inspiratory bursts, whereas when injected into XII nucleus induced a tonic activity and an increase in amplitude but not in frequency of inspiratory bursts from XIIn. Bath application of nicotine (0.2–0.5 μM, approximately the arterial blood nicotine concentration immediately after smoking a cigarette) increased respiratory frequency up to 280% of control in a concentration-dependent manner. Nicotine decreased the amplitude to 82% and increased the duration to 124% of XIIn inspiratory bursts. In voltage-clamped preBötC inspiratory neurons (including neurons with pacemaker properties), nicotine induced a tonic inward current of −19.4 ± 13.4 pA associated with an increase in baseline noise. Spontaneous excitatory postsynaptic currents (sEPSCs) present during the expiratory period increased in frequency to 176% and in amplitude to 117% of control values; the phasic inspiratory drive inward currents decreased in amplitude to 66% and in duration to 89% of control values. The effects of nicotine were blocked by mecamylamine (Meca). The inspiratory drive current and sEPSCs were completely eliminated by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) in the presence or absence of nicotine. In the presence of tetrodotoxin (TTX), low concentrations of nicotine did not induce any tonic current or any increase in baseline noise, nor affect the input resistance in inspiratory neurons. In this study, we demonstrated that nicotine increased respiratory frequency and regulated respiratory pattern by modulating the excitatory neurotransmission in preBötC. Activation of nicotinic acetylcholine receptors (nAChRs) enhanced the tonic excitatory synaptic input to inspiratory neurons including pacemaker neurons and at the same time, inhibited the phasic excitatory coupling between these neurons. These mechanisms may account for the cholinergic regulation of respiratory frequency and pattern.

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