Respiration-Related Rhythmic Activity in the Rostral Medulla of Newborn Rats

2006 ◽  
Vol 96 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Hiroshi Onimaru ◽  
Yuko Kumagawa ◽  
Ikuo Homma
Keyword(s):  
Facial Nerve ◽  
Rhythmic Activity ◽  
Motor Output ◽  
Ventrolateral Medulla ◽  
Neuron Activity ◽  
Nerve Activity ◽  
Bötzinger Complex ◽  
Old Rats ◽  
Parafacial Respiratory Group

There are at least two respiration-related rhythm generators in the medulla: the pre-Bötzinger complex, which produces inspiratory (Insp) neuron bursts, and the parafacial respiratory group (pFRG), which produces predominantly preinspiratory (Pre-I) neuron bursts. The pFRG Pre-I neuron activity has not been correlated with motor neuron activity in slice or block preparations of rostral medulla. In this study, we attempted to detect pFRG Pre-I activity as motor output in the rostral medulla. We recorded respiratory activity of the facial nerve in the brain stem–spinal cord preparation of 0- to 2-day-old rats. Facial nerve activity consisted of preinspiratory, Insp, and postinspiratory activity. Pre- and postinspiratory activity corresponded well with membrane potential trajectories of Pre-I neurons in the rostral ventrolateral medulla. In response to perfusion of 1 μM DAMGO (a μ-opiate agonist), fourth cervical ventral root (C4) Insp activity was depressed and facial nerve activity continued to synchronize with Pre-I neuron bursts. After transverse sectioning between the levels of the pre-Bötzinger complex and the pFRG, C4 Insp activity recovered within 15 min, but facial nerve activity was inhibited. When DAMGO was applied, C4 Insp activity was inhibited, and rhythmic facial nerve activity recovered. Subsequent elevation of K+ concentration reinduced C4 activity, but facial nerve activity was inhibited. Whole cell recordings in the rostral block revealed the presence of putative Pre-I neurons, the activity of which was synchronized with facial nerve activity. These results show that the rostral medulla, not including the pre-Bötzinger complex, produces Pre-I–like rhythmic activity that can be monitored as facial nerve motor output in newborn rat in vitro preparations.

scholarly journals Midline section of the medulla abolishes inspiratory activity and desynchronizes pre-inspiratory neuron rhythm on both sides of the medulla in newborn rats

2015 ◽  
Vol 113 (7) ◽  
pp. 2871-2878 ◽  
Author(s):  
Hiroshi Onimaru ◽  
Kayo Tsuzawa ◽  
Yoshimi Nakazono ◽  
Wiktor A. Janczewski
Keyword(s):  
Facial Nerve ◽  
Respiratory Rhythm ◽  
Root Activity ◽  
Respiratory Neurons ◽  
Neuron Activity ◽  
Newborn Rats ◽  
Inspiratory Neuron ◽  
Inspiratory Activity ◽  
Old Rats ◽  
Parafacial Respiratory Group

Each half of the medulla contains respiratory neurons that constitute two generators that control respiratory rhythm. One generator consists of the inspiratory neurons in the pre-Bötzinger complex (preBötC); the other, the pre-inspiratory (Pre-I) neurons in the parafacial respiratory group (pFRG), rostral to the preBötC. We investigated the contribution of the commissural fibers, connecting the respiratory rhythm generators located on the opposite side of the medulla to the generation of respiratory activity in brain stem-spinal cord preparation from 0- to 1-day-old rats. Pre-I neuron activity and the facial nerve and/or first lumbar (L1) root activity were recorded as indicators of the pFRG-driven rhythm. Fourth cervical ventral root (C4) root and/or hypoglossal (XII) nerve activity were recorded as indicators of preBötC-driven inspiratory activity. We found that a midline section that interrupted crossed fibers rostral to the obex irreversibly eliminated C4 and XII root activity, whereas the Pre-I neurons, facial nerve, and L1 roots remained rhythmically active. The facial and contralateral L1 nerve activities were synchronous, whereas right and left facial (and right and left L1) nerves lost synchrony. Optical recordings demonstrated that pFRG-driven burst activity was preserved after a midline section, whereas the preBötC neurons were no longer rhythmic. We conclude that in newborn rats, crossed excitatory interactions (via commissural fibers) are necessary for the generation of inspiratory bursts but not for the generation of rhythmic Pre-I neuron activity.

scholarly journals Genesis of gasping is independent of levels of serotonin in the Pet-1 knockout mouse

2009 ◽  
Vol 107 (3) ◽  
pp. 679-685 ◽  
Author(s):  
Walter M. St.-John ◽  
Aihua Li ◽  
J. C. Leiter
Keyword(s):  
Knockout Mice ◽  
Knockout Mouse ◽  
Critical Role ◽  
Genetic Defect ◽  
Rhythmic Activity ◽  
Ventrolateral Medulla ◽  
Sudden Infant ◽  
Slice Preparation ◽  
Serotonergic Neurons

Eupnea is normal breathing. If eupnea fails, as in severe hypoxia or ischemia, gasping is recruited. Gasping can serve as a powerful mechanism for autoresuscitation. A failure of autoresuscitation has been proposed as a basis of the sudden infant death syndrome. In an in vitro preparation, endogenous serotonin is reported to be essential for expression of gasping. Using an in situ preparation of the Pet-1 knockout mouse, we evaluated such a critical role for serotonin. In this mouse, the number of serotonergic neurons is reduced by 85–90% compared with animals without this homozygous genetic defect. Despite this reduction in the number of serotonergic neurons, phrenic discharge in eupnea and gasping of Pet-1 knockout mice was not different from that of wild-type mice. Indeed, gasping continued unabated, even after administration of methysergide, a blocker of many types of receptors for serotonin, to Pet-1 knockout mice. We conclude that serotonin is not critical for expression of gasping. The proposal for such a critical role, on the basis of observations in the in vitro slice preparation, may reflect the minimal functional neuronal tissue and neurotransmitters in this preparation, such that the role of any remaining neurotransmitters is magnified. Also, rhythmic activity of the in vitro slice preparation has been characterized as eupnea or gasping solely on the basis of activity of the hypoglossal nerve or massed neuronal activities of the ventrolateral medulla. The accuracy of this method of classification has not been established.

scholarly journals Hypothermia and recovery from respiratory arrest in a neonatal rat in vitro brain stem preparation

2002 ◽  
Vol 282 (2) ◽  
pp. R484-R491 ◽  
Author(s):  
Nicholas M. Mellen ◽  
William K. Milsom ◽  
Jack L. Feldman
Keyword(s):  
Brain Stem ◽  
Motor Neurons ◽  
Respiratory Rhythm ◽  
Field Potential ◽  
Respiratory Arrest ◽  
Motor Output ◽  
Neonatal Rat ◽  
Bötzinger Complex ◽  
Neonatal Rat Brain

This study was designed to examine the possibility that respiratory arrest during hypothermia occurs at the level of premotor or motor neurons rather than at the level of the central rhythm generator itself. Specifically, we sought to determine the consequences of hypothermic cooling until respiratory arrest, and subsequent rewarming, on neurons in the pre-Bötzinger Complex, as an indication of the output of the entire rhythmogenic network; and from cervical spinal (phrenic) ventral roots, as an indication of motor neuron output, in an in vitro neonatal rat brain stem-spinal cord preparation. We found that hypothermia led to a slowing of the respiratory rhythm with little or no decrease in the magnitude of phrenic motor output or the field potential of pre-Bötzinger Complex neurons. Ultimate arrest occurred abruptly and simultaneously in recordings from both sites, indicating that the arrest was due to failure of the central rhythm-generating network, primarily due to removal of a conditional excitation. On being rewarmed, the motor output recorded at both sites was usually fractionated, initially suggesting that changes occurred in network synchronization either during cooling or during reactivation following hypothermic arrest.

Octopamine induces steady-state reflex reversal in crayfish thoracic ganglia

1996 ◽  
Vol 76 (1) ◽  
pp. 93-108 ◽  
Author(s):  
P. Skorupski
Keyword(s):  
Spontaneous Activity ◽  
Motor Neurons ◽  
Motor Output ◽  
Reflex Response ◽  
Neuron Activity ◽  
Chordotonal Organ ◽  
Nerve Activity ◽  
Group 2 ◽  
Stimulation Of ◽  
Group 1

1. This paper investigates the effect of octopamine on spontaneous and reflex motor output of crayfish leg motor neurons. Octopamine modulated spontaneous activity, both rhythmic and tonic, and dramatically modulated the pattern of reflex motor output elicited by stimulating identified proprioceptors of the basal limb. 2. Spontaneous reciprocal motor patterns, involving alternating bursts of promotor and remotor motor neuron activity, were reversibly abolished by octopamine. The threshold concentration for this effect was approximately 1 microM. 3. At concentrations greater than approximately 10 microM octopamine inhibited spontaneous promotor nerve activity in both bursting and nonbursting preparations. In some experiments promotor inhibition was correlated with the induction of tonic remotor nerve activity. The EC50 for complete inhibition of promotor nerve activity by octopamine was 20-30 microM. 4. Reflexes mediated by two basal limb proprioceptors, the thoracocoxal muscle receptor organ (TCMRO; which signals leg promotion) and the thoracocoxal chordotonal organ (TCCO; which signals leg remotion) were analyzed in a number of promotor and remotor motor neurons. In both cases assistance reflexes (excitation of promotors by the TCCO and remotors by the TCMRO) were restricted to subgroups of the motor pool. Among remotor motor neurons, the first two units recruited during bursts of spontaneous activity were members of the assistance reflex group (group 1). A third unit, sometimes recruited during more intense spontaneous bursts, was excited by TCCO stimulation and was therefore a member of the resistance reflex group (group 2). Other resistance group remotors were also excited by the TCCO, but this input normally remained subthreshold. 5. Stimulation of the TCCO afferent nerve elicited excitatory postsynaptic potentials (EPSPs) in group 2 (resistance group) remotor motor neurons at a latency compatible with a monosynaptic connection. The same stimulation excited group 1 (assistance group) promotor motor neurons, but at a greater and more variable latency. Thus the remotor resistance reflex from the TCCO is probably monosynaptic, but the promotor assistance reflex, also elicited by TCCO stimulation, is likely to be di- or polysynaptic. Assistance group (group 1) remotor motor neurons are inhibited by mechanical stimulation of the TCCO, or electrical stimulation of its nerve. 6. Octopamine had selective effects on individual remotor units. First, assistance group remotor motor neurons were affected in two ways. One unit was inhibited, so that reflex spiking in response to TCMRO stimulation was abolished. A second unit was not inhibited, but its reflex response mode changed, so that instead of responding to TCMRO input with an assistance reflex, it responded to TCCO input with a resistance reflex. Second, among motor neurons that normally respond to TCCO input with resistance reflexes, these responses were enhanced by octopamine. 7. Promotor motor neurons were inhibited by octopamine and reflex responses were also affected selectively. Responses to TCCO input (assistance reflexes) were abolished; whereas, responses to TCMRO input (resistance reflexes) were relatively less affected. 8. Intracellular recordings revealed that the majority of remotor motor neurons depolarized in the presence of octopamine. In preparations where these could be classified on the basis of TCMRO/ TCCO inputs, all were identified as group 2 (resistance group). A minority of remotor motor neurons were hyperpolarized by octopamine. All of these were identified as group 1 (assistance group), with strong TCMRO input. 9. The majority of promotor motor neurons were depolarized by octopamine. This depolarization was nevertheless inhibitory since it reversed slightly positive to rest and was associated with a substantial fall in inp

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

1996 ◽  
Vol 81 (5) ◽  
pp. 1865-1877 ◽  
Author(s):  
Walter M. St. John
Keyword(s):  
Mammalian Species ◽  
Respiratory Rhythm ◽  
Rhythmic Activity ◽  
Neonatal Rat ◽  
Rhythm Generation ◽  
Bötzinger Complex ◽  
Per Se ◽  
Respiratory Rhythm Generation

St. John, Walter M. Medullary regions for neurogenesis of gasping: noeud vital or noeuds vitals? J. Appl. Physiol. 81(5): 1865–1877, 1996.—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.

Developmental Changes in the Hypoxic Response of the Hypoglossus Respiratory Motor Output In Vitro

1997 ◽  
Vol 78 (1) ◽  
pp. 383-392 ◽  
Author(s):  
J. M. Ramirez ◽  
U.J.A. Quellmalz ◽  
B. Wilken
Keyword(s):  
Respiratory Rhythm ◽  
Rhythmic Activity ◽  
Motor Output ◽  
Developmental Changes ◽  
Induced Response ◽  
Biphasic Response ◽  
Hypoxic Response ◽  
Cellular Analysis ◽  
Respiratory Network

Ramirez, J. M., U.J.A. Quellmalz, and B. Wilken. Developmental changes in the hypoxic response of the hypoglossus respiratory motor output in vitro. J. Neurophysiol. 78: 383–392, 1997. The transverse brain stem slice of mice containing the pre-Bötzinger complex (PBC), a region essential for respiratory rhythm generation in vitro, was used to study developmental changes of the response of the in vitro respiratory network to severe hypoxia (anoxia). This preparation generates, at different postnatal stages [postnatal day (P)0–22], spontaneous rhythmic activity in hypoglossal (XII) rootlets that are known to occur in synchrony with periodic bursts of neurons in the PBC. It is assumed that this rhythmic activity reflects respiratory rhythmic activity. At all examined stages anoxia led to a biphasic response: the frequency of rhythmic XII activity initially increased (“primary augmentation”) and then decreased (“secondary depression”). In neonates (P0–7), anoxia did not significantly affect the amplitude of integrated XII bursts. Secondary depression never led to a cessation of rhythmic activity. In mice older than P7, augmentation was accompanied by a significant increase in the amplitude of XII bursts. A significant decrease of the amplitude of XII bursts occurred during secondary depression. This depression led always to cessation of rhythmic activity in XII rootlets. The anoxia-induced response of the respiratory rhythmic XII motor output is biphasic and changes during development in a similar way to the in vivo respiratory network. Whether this biphasic response is due to a biphasic response of the respiratory rhythm generator and/or to a biphasic modulation of the XII motor nucleus remains unresolved and needs further cellular analysis. We propose that the transverse slice is a useful model system for examination of the mechanisms underlying the hypoxic response.

Follicle-stimulating hormone-dependent estrogen secretion by rat Sertoli cells in vitro: Modulation by calcium

1991 ◽  
Vol 125 (3) ◽  
pp. 280-285 ◽  
Author(s):  
J. Alan Talbot ◽  
Ann Lambert ◽  
Robert Mitchell ◽  
Marek Grabinski ◽  
David C. Anderson ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Culture Medium ◽  
Follicle Stimulating Hormone ◽  
Dibutyryl Camp ◽  
Immature Rat ◽  
Estradiol Secretion ◽  
Old Rats ◽  
Stimulating Hormone

Abstract We have investigated the role of Ca2+ in the control of FSH-induced estradiol secretion by Sertoli cells isolated from 8-10 days old rats. Exogenous Ca2+ (4-8 mmol/1) inhibited FSH-stimulated E2 secretion such that, with 8 mmol/l Ca2+ and FSH (8 IU/l) E2 secretion decreased from 2091±322 to 1480±84 pmol/l (p<0.002), whilst chelation of Ca2+ in the culture medium with EGTA (3 mmol/l) increased E2 secretion from 360±45 to 1242±133 pmol/l) in the absence of FSH. Further, EGTA (3 mmol/l) markedly potentiated FSH (8 IU/l), forskolin (1 μmol/l) and dibutyryl cAMP (1 mmol/l)-stimulated E2 secretion. Addition of the Ca2+ ionophores, ionomycin (2-5 μmol/l) and A23187 (2 μmol/l), inhibited FSH (8 IU/l)-stimulated E2 secretion by >80%. The effect of ionomycin was totally reversible, whereas that of A23187 was irreversible. Ionomycin (5 μmol/l) had no effect on EGTA-induced E2 secretion in the absence of FSH, but reduced EGTA-provoked E2 secretion by 59% in the presence of FSH (8 IU/l). Similarly, forskolin- and dibutyryl cAMP-provoked E2 production was inhibited 46-50% by ionomycin (5 μmol/l). We conclude that FSH-induced E2 secretion from immature rat Sertoli cells is modulated by intra- and extracellular Ca2+.

Panax notoginseng saponins attenuate neuroinflammation through TXNIP-mediated NLRP3 inflammasome activation in aging rats

2020 ◽  
Vol 21 ◽  
Author(s):  
Zhiyong Zhou ◽  
Menghan He ◽  
Qingqing Zhao ◽  
Dongfan Wang ◽  
Changcheng Zhang ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Panax Notoginseng ◽  
Control Group ◽  
Inflammasome Activation ◽  
Panax Notoginseng Saponins ◽  
Aging Rats ◽  
Nlrp3 Inflammasome Activation ◽  
Bv2 Microglia ◽  
Old Rats

Introduction:: Microglia-mediated inflammatory responses play a crucial role in aging-related neurodegenerative diseases. The TXNIP/NLRP3 pathway is a key pathway leading to microglial activation. Panax notoginseng saponins (PNS) have been widely used for the treatment of stroke in China. Objective:: This study evaluates the anti-neuroinflammatory effect of PNS and investigates the mechanism via TXNIPmediated NLRP3 inflammasome activation in aging rats. Materials and Methods:: Eighteen-month-old Sprague-Dawley rats were randomly divided into the aging control group and PNS treated groups (n=15 each group). For PNS-treated groups, rats were administrated food with PNS at the doses of 10 mg/kg and 30 mg/kg for consecutive 6 months until they were 24-month old. Rats from the aging control group were given the same food without PNS. Two-month-old rats were purchased and given the same food until 6-month old as the adult control group (n = 15). Then, the cortex and hippocampus were rapidly harvested and deposited. H&E staining was used to assess histo-morphological changes. Western blotting was carried out to detect the protein expression. Immunofluorescence was employed to measure the co-localization of NLRP3, TXNIP and Iba-1. In vitro model was established by LPS+ATP coincubation in the BV2 microglia cell line. Results:: Aging rats exhibited increased activation of microglia, accompanied by a high level of IL-1β expression. Meanwhile, aging rats showed enhanced protein expression of TXNIP and NLRP3 related molecules, which co-localized with microglia. PNS treatment effectively reduced the number of degenerated neurons and reversed the activation of the TXNIP/NLRP3 inflammatory pathway. In vitro results showed that PNS up to 100 μg / ml had no significant toxicity on BV2 microglia. Discussion:: PNS (25, 50 μg/ml) effectively reduced the inflammatory response induced by LPS and ATP co-stimulation, thus inhibiting the expression of TXNIP/NLRP3 pathway-related proteins. Conclusion:: PNS treatment improved aging-related neuronal damage through inhibiting TXNIP mediated NLRP3 inflammasome activation, which provided a potential target for the treatment of inflammatory-related neurodegenerative diseases.

Sodium Currents in Neurons From the Rostroventrolateral Medulla of the Rat

2003 ◽  
Vol 90 (3) ◽  
pp. 1635-1642 ◽  
Author(s):  
Ilya A. Rybak ◽  
Krzysztof Ptak ◽  
Natalia A. Shevtsova ◽  
Donald R. McCrimmon
Keyword(s):  
Sodium Channels ◽  
Sodium Current ◽  
Cell Voltage ◽  
Kinetic Properties ◽  
Persistent Sodium Current ◽  
Sodium Currents ◽  
Bötzinger Complex ◽  
Window Current ◽  
Bursting Activity

Rapidly inactivating and persistent sodium currents have been characterized in acutely dissociated neurons from the area of rostroventrolateral medulla that included the pre-Bötzinger Complex. As demonstrated in many studies in vitro, this area can generate endogenous rhythmic bursting activity. Experiments were performed on neonate and young rats (P1-15). Neurons were investigated using the whole cell voltage-clamp technique. Standard activation and inactivation protocols were used to characterize the steady-state and kinetic properties of the rapidly inactivating sodium current. Slow depolarizing ramp protocols were used to characterize the noninactivating sodium current. The “window” component of the rapidly inactivating sodium current was calculated using mathematical modeling. The persistent sodium current was revealed by subtraction of the window current from the total noninactivating sodium current. Our results provide evidence of the presence of persistent sodium currents in neurons of the rat rostroventrolateral medulla and determine voltage-gated characteristics of activation and inactivation of rapidly inactivating and persistent sodium channels in these neurons.

scholarly journals In vitro analysis of the origin and maintenance of O-2Aadult progenitor cells.

1992 ◽  
Vol 116 (1) ◽  
pp. 167-176 ◽  
Author(s):  
D Wren ◽  
G Wolswijk ◽  
M Noble
Keyword(s):  
Adult Life ◽  
Cell Types ◽  
Adult Rats ◽  
Optic Nerves ◽  
Limited Life ◽  
Old Rats ◽  
Vitro Analysis

We have been studying the differing characteristics of oligodendrocyte-type-2 astrocyte (O-2A) progenitors isolated from optic nerves of perinatal and adult rats. These two cell types display striking differences in their in vitro phenotypes. In addition, the O-2Aperinatal progenitor population appears to have a limited life-span in vivo, while O-2Aadult progenitors appear to be maintained throughout life. O-2Aperinatal progenitors seem to have largely disappeared from the optic nerve by 1 mo after birth, and are not detectable in cultures derived from optic nerves of adult rats. In contrast, O-2Aadult progenitors can first be isolated from optic nerves of 7-d-old rats and are still present in optic nerves of 1-yr-old rats. These observations raise two questions: (a) From what source do O-2Aadult progenitors originate; and (b) how is the O-2Aadult progenitor population maintained in the nerve throughout life? We now provide in vitro evidence indicating that O-2Aadult progenitors are derived directly from a subpopulation of O-2Aperinatal progenitors. We also provide evidence indicating that O-2Aadult progenitors are capable of prolonged self renewal in vitro. In addition, our data suggests that the in vitro generation of oligodendrocytes from O-2Aadult progenitors occurs primarily through asymmetric division and differentiation, in contrast with the self-extinguishing pattern of symmetric division and differentiation displayed by O-2Aperinatal progenitors in vitro. We suggest that O-2Aadult progenitors express at least some properties of stem cells and thus may be able to support the generation of both differentiated progeny cells as well as their own continued replenishment throughout adult life.

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