scholarly journals Tracheal occlusion-evoked respiratory load compensation and inhibitory neurotransmitter expression in rats

2014 ◽  
Vol 116 (8) ◽  
pp. 1006-1016 ◽  
Author(s):  
Hsiu-Wen Tsai ◽  
Paul W. Davenport
Keyword(s):  
Neural Network ◽  
Brain Stem ◽  
Breathing Pattern ◽  
Respiratory Rhythm ◽  
Inhibitory Neurotransmitter ◽  
Load Compensation ◽  
Efferent Projections ◽  
Motor Reflex ◽  
Sensory Pathway ◽  
The Brain

Respiratory load compensation is a sensory-motor reflex generated in the brain stem respiratory neural network. The nucleus of the solitary tract (NTS) is thought to be the primary structure to process the respiratory load-related afferent activity and contribute to the modification of the breathing pattern by sending efferent projections to other structures in the brain stem respiratory neural network. The sensory pathway and motor responses of respiratory load compensation have been studied extensively; however, the mechanism of neurogenesis of load compensation is still unknown. A variety of studies has shown that inhibitory interconnections among the brain stem respiratory groups play critical roles for the genesis of respiratory rhythm and pattern. The purpose of this study was to examine whether inhibitory glycinergic neurons in the NTS were activated by external and transient tracheal occlusions (ETTO) in anesthetized animals. The results showed that ETTO produced load compensation responses with increased inspiratory, expiratory, and total breath time, as well as elevated activation of inhibitory glycinergic neurons in the caudal NTS (cNTS) and intermediate NTS (iNTS). Vagotomized animals receiving transient respiratory loads did not exhibit these load compensation responses. In addition, vagotomy significantly reduced the activation of inhibitory glycinergic neurons in the cNTS and iNTS. The results suggest that these activated inhibitory glycinergic neurons in the NTS might be essential for the neurogenesis of load compensation responses in anesthetized animals.

Genesis of rhythmic respiratory activity in pons independent of medulla

1985 ◽  
Vol 59 (3) ◽  
pp. 684-690 ◽  
Author(s):  
W. M. St John ◽  
T. A. Bledsoe
Keyword(s):  
Brain Stem ◽  
Phrenic Nerve ◽  
Respiratory Activity ◽  
Respiratory Rhythm ◽  
Related Activity ◽  
Pharmacological Agents ◽  
Pneumotaxic Center ◽  
Trigeminal Nerves ◽  
The Brain ◽  
Pontomedullary Junction

We hypothesized that rhythmic respiratory-related activity could be generated in pons independent of medullary mechanisms. In decerebrate, cerebellectomized, vagotomized, paralyzed, and ventilated cats, we recorded efferent activities of the phrenic nerve and mylohyoid branch of the trigeminal nerve. Following transections of the brain stem at the pontomedullary junction, the phrenic and trigeminal nerves discharged with independent rhythms. Spontaneous trigeminal discharges eventually ceased but were reestablished after strychnine, doxapram, and/or protriptyline were administered. In some animals having no spontaneous trigeminal discharges after transection, these discharges appeared, with a rhythm different from the phrenic, following administration of these agents. In other cats having no transections between pons and medulla, these pharmacological agents induced trigeminal and phrenic discharges after kainic acid had been injected into the entire dorsal and ventral medullary respiratory nuclei. Phrenic and trigeminal discharges were linked, indicating survival of bulbospinal neurons or presence of pontospinal units. We conclude that rhythms, similar to respiratory rhythm, can occur by mechanisms in isolated pons. Such mechanisms are hypothesized to be within the pneumotaxic center and may underlie the neurogenesis of eupnea.

EFFECTS OF PRENATAL PASSIVE SMOKING ON CHOLINERGIC MECHANISMS SIMULATION RESPIRATORY RHYTHM IN NEONATAL RATS (IN VITRO)

2020 ◽  
Vol 6(72) (2) ◽  
pp. 3-12
Author(s):  
S. E. Bolychevsky ◽  
E. A. Zinchenko ◽  
I. V. Miroshnichenko
Keyword(s):  
Neural Network ◽  
Tobacco Smoke ◽  
Passive Smoking ◽  
Respiratory Rhythm ◽  
Control Group ◽  
Newborn Rats ◽  
Pregnant Rats ◽  
Nicotinic Cholinergic Receptors ◽  
The Brain ◽  
Experimental Group

Both active and passive smoking increases the risk of sudden death of the newborn. Researchers are actively studying the effect of chronic nicotine infusion, as one of the leading neurogenic factors of tobacco smoke on cholinergic mechanisms of respiratory control. In this paper, using a fumigation model of passive smoking, tested the assumption that second-hand smoke that is transferred in the prenatal period, changes the expression mediated by nicotinic receptors activating influence of the cholinergic system of the brain stem to the processes of the respiratory activity of the neural network generation. It is found that the fumigation of tobacco smoke pregnant rats decreases their progeny respiratory sensitivity to the action of a neural network and exogenous nicotine increases cholinergic part tonic effect mediated by nicotinic cholinergic receptors in the modulation of respiratory rhythm. The study uses data obtained from 40 brain stem-spinal cord preparations (BSP) of the newborn rats. The experimental group was 22, and the control group was 18 newborn rats. In the processing of neurograms, the duration of the cycle of respiratory activity, duration, and the amplitude of inspiratory discharges were measured. To describe the peaks of the respiratory discharge spectrum, the following parameters were used: the peak frequency and the peak power spectral density of the peak. Analysis of the statistical differences was made using Student’s t-test for mean values. Differences were considered significant at p<0.05. Our results confirm the presence for exogenous nicotine of powerful activating effect on the generation frequency, amplitude and duration of inspiratory discharges of the BSP of newborn rats in the control group. It is established that an increase in the amplitude of the inspiratory discharges is accompanied by an increase in the spectral power density in the mid-frequency range of their spectrograms. In the BSP of the brain of newborn rats with prenatal exposure to tobacco smoke, exogenous nicotine increased only the frequency of inspiratory discharge generation. The amplitude of the inspiratory discharges and the power of the mid-frequency oscillations under the influence of exogenous nicotine in the BSP of the experimental group was significantly reduced. Mecamylamine, a selective blocker of nAChR, added to the perfusate of the BSP of the control group, caused a significant increase in the amplitude and duration of the inspiratory discharges, without significantly changing the duration of the respiratory cycle. At the same time, in BSP of newborn rats subjected to prenatal exposure to tobacco smoke, nAChR blockade resulted in an increase in the duration of the respiratory cycle. Thus, our study showed that fumigation of pregnant rats with tobacco smoke reduces the sensitivity of the respiratory neural network to the action of exogenous nicotine in early postnatal period and increases the involvement of tonic cholinergic effect mediated by nicotinic cholinergic receptors in modulating the respiratory rhythm.

Influence of halothane on control of breathing in intact and decerebrated cats

1987 ◽  
Vol 63 (2) ◽  
pp. 546-553 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora ◽  
D. Zaoui
Keyword(s):  
Brain Stem ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Control Of Breathing ◽  
Halothane Anesthesia ◽  
Peripheral Chemoreceptor ◽  
Duration Relationship ◽  
The Brain ◽  
Ventilatory Response To Co2

The effects of halothane anesthesia have been investigated in intact and in decerebrated cats. Pulmonary ventilation and breathing pattern were studied during room-air breathing, hypercapnia, and O2 inhalation. The following results have been demonstrated. First, halothane anesthesia does not modify pulmonary ventilation, but a tachypnea much more intense in intact than in decerebrated cats is observed. This indicates that halothane-induced tachypnea originates mainly in structures rostral to the brain stem. Second, decerebrated animals exhibit a breathing pattern and a ventilatory response to CO2 similar to those of intact conscious cats, suggesting that forebrain facilitatory and inhibitory influences on brain stem are cancelled out by decerebration. However, the tidal volume vs. inspiratory duration relationship observed in decerebrated cats differs from that in conscious cats. Finally, during halothane anesthesia, ventilatory response to CO2 is markedly depressed. Third, during O2 inhalation, except in decerebrated, anesthetized animals, ventilation is only slightly depressed. This suggests that central stimulatory effect of O2 is enhanced and/or that peripheral chemoreceptor drive is reduced.

How Is the Respiratory Rhythm Generated? A Model

Physiology ◽  
1986 ◽  
Vol 1 (3) ◽  
pp. 109-112 ◽  
Author(s):  
DW Richter ◽  
D Ballantyne ◽  
JE Remmers
Keyword(s):  
Brain Stem ◽  
Neuronal Network ◽  
Respiratory Rhythm ◽  
Synaptic Activity ◽  
Membrane Properties ◽  
Respiratory Neurons ◽  
Control Sequence ◽  
Intrinsic Membrane Properties ◽  
The Brain ◽  
Respiratory Movements

This article presents a model of the neuronal network that generates the rhythm for respiratory movements. It incorporates new data on the synaptic activity and discharge properties of respiratory neurons in the brain stem and on the modulation of their excitability by nonsynaptic intrinsic membrane properties. The model allows a description of the control sequence that generates the rhythm.

scholarly journals Computational Model for Biological Neural Network for Localisation of Sound in the Vertical Plane

2020 ◽  
Author(s):  
Anandita De ◽  
Daniel Cox
Keyword(s):  
Neural Network ◽  
Brain Stem ◽  
Neural Circuit ◽  
Broad Band ◽  
Vertical Plane ◽  
Rate Model ◽  
Biological Neural Network ◽  
Band Noise ◽  
Pure Tones ◽  
The Brain

AbstractWe build a computational rate model for a biological neural network found in mammals that is thought to be important in the localisation of the sound in the vertical plane. We find the response of neurons in the brain stem that participate in the localisation neural circuit to pure tones, broad band noise and notched noise and compare them to experimentally obtained response of these neurons. Our model is able to reproduce the sensitivity of these neurons in the brain stem to spectral properties of sounds that are important in localisation. This is the first rate based population model that elucidates all the response properties of the neurons in the vertical localisation pathway to our knowledge.

Connections of midbrain periaqueductal gray in the monkey. II. Descending efferent projections

1983 ◽  
Vol 49 (3) ◽  
pp. 582-594 ◽  
Author(s):  
P. W. Mantyh
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Reticular Formation ◽  
Cervical Spinal Cord ◽  
Great Majority ◽  
Periaqueductal Gray ◽  
Locus Ceruleus ◽  
Contralateral Projection ◽  
Efferent Projections ◽  
The Brain

1. We have defined the descending efferent projections of the midbrain periaqueductal gray (PAG) by injecting small amounts of [3H]leucine into the various regions of the squirrel monkey PAG. 2. Despite the fact that different regions of the PAG were injected in separate animals, the majority of the brain stem areas labeled remained constant. 3. The PAG exhibited a dense projection to the superior colliculus, the nucleus cuneiformis, and the locus ceruleus. Parts of the reticular formation (nucleus reticularis: pontis oralis, pontis caudalis, gigantocellularis, magnocellularis, and ventralis) received a projection from the PAG, as did the nucleus parabrachial pars lateralis, ambiguous, the nucleus raphe magnus, and raphe pallidus. 4. In contrast to the brain stem, the deep laminae of the nucleus caudalis and the deep laminae of the cervical spinal cord were labeled only after injections of the lateral aspect of the PAG. 5. The main route for the PAG leads to brain stem projections is through the lateral edge of the paramedian reticular formation. The great majority of the anterograde labeling was ipsilateral to the injection although a small contralateral projection was present. 6. These results indicate that the PAG projects to the brain stem and spinal cord in the monkey. Many of the brain stem areas that the PAG projects to are known to project to the spinal cord. These secondary spinal projections coupled with the direct PAG leads to spinal projection provide a wide variety of routes through which the PAG may influence spinal cord activity.

Catecholaminergic modulation of respiratory rhythm in an in vitro turtle brain stem preparation

1998 ◽  
Vol 85 (1) ◽  
pp. 105-114 ◽  
Author(s):  
Rebecca A. Johnson ◽  
Stephen M. Johnson ◽  
Gordon S. Mitchell
Keyword(s):  
Brain Stem ◽  
Sch 23390 ◽  
Respiratory Rhythm ◽  
Peak Frequency ◽  
Receptor Activation ◽  
Adrenergic Agonist ◽  
Nerve Roots ◽  
Adrenergic Antagonist ◽  
The Brain

An in vitro brain stem preparation from adult turtles was used to determine effects of dopamine (DA) and norepinephrine (NE) on the pattern of respiratory motor output recorded from hypoglossal nerve roots (XII). Bath-applied DA (10–200 μM) increased the frequency of respiratory bursts (peaks) from 0.9 ± 0.2 to 2.4 ± 0.3 (SE) peaks/min, resulting in a 99 ± 9% increase in neural minute activity. R[+]-SCH-23390 (10 μM, D1 antagonist) and eticlopride (20 μM, D2 antagonist) attenuated the DA-mediated increase in peak frequency by 52 and 59%, respectively. On the other hand, the DA-receptor agonists apomorphine (D1, D2), quinelorane (D2), and SKF-38393 (D1) had no effect on peak frequency. Prazosin, an α1-adrenergic antagonist (250 nM) abolished the DA-mediated frequency increase. Although NE (10–200 μM) and phenylephrine (10–200 μM, α1-adrenergic agonist) increased peak frequency from 0.5 ± 0.1 to 1.2 ± 0.3 peaks/min and from 0.6 ± 0.1 to 1.0 ± 0.2 peaks/min, respectively, these effects were not as large as that with DA alone. The data suggest that both dopaminergic and adrenergic receptor activation in the brain stem increase respiratory frequency in turtles, but the DA receptor-mediated increase is dependent on coactivation of α1-adrenergic receptors.

scholarly journals Oscillation patterns are enhanced and firing threshold is lowered in medullary respiratory neuron discharges by threshold doses of a μ-opioid receptor agonist

2017 ◽  
Vol 312 (5) ◽  
pp. R727-R738 ◽  
Author(s):  
Peter M. Lalley ◽  
Steve W. Mifflin
Keyword(s):  
Spike Train ◽  
Brain Stem ◽  
Opioid Receptor ◽  
Respiratory Rhythm ◽  
Opioid Receptor Agonist ◽  
Respiratory Network ◽  
Three Phase ◽  
Μ Opioid Receptor ◽  
Effective Doses ◽  
The Brain

μ-Opioid receptors are distributed widely in the brain stem respiratory network, and opioids with selectivity for μ-type receptors slow in vivo respiratory rhythm in lowest effective doses. Several studies have reported μ-opioid receptor effects on the three-phase rhythm of respiratory neurons, but there are until now no reports of opioid effects on oscillatory activity within respiratory discharges. In this study, effects of the μ-opioid receptor agonist fentanyl on spike train discharge properties of several different types of rhythm-modulating medullary respiratory neuron discharges were analyzed. Doses of fentanyl that were just sufficient for prolongation of discharges and slowing of the three-phase respiratory rhythm also produced pronounced enhancement of spike train properties. Oscillation and burst patterns detected by autocorrelation measurements were greatly enhanced, and interspike intervals were prolonged. Spike train properties under control conditions and after fentanyl were uniform within each experiment, but varied considerably between experiments, which might be related to variability in acid-base balance in the brain stem extracellular fluid. Discharge threshold was shifted to more negative levels of membrane potential. The effects on threshold are postulated to result from opioid-mediated disinhibition and postsynaptic enhancement of N-methyl-d- aspartate receptor current. Lowering of firing threshold, enhancement of spike train oscillations and bursts and prolongation of discharges by lowest effective doses of fentanyl could represent compensatory adjustments in the brain stem respiratory network to override opioid blunting of CO2/pH chemosensitivity.

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