Pontine cholinergic mechanisms enhance trigeminally evoked respiratory suppression in the anesthetized rat

1999 ◽  
Vol 87 (3) ◽  
pp. 1059-1065 ◽  
Author(s):  
Mathias Dutschmann ◽  
Horst Herbert
Keyword(s):  
Rem Sleep ◽  
Minute Volume ◽  
Emg Activity ◽  
Vascular Responses ◽  
Anesthetized Rats ◽  
Neuronal Mechanisms ◽  
Before And After ◽  
Reticular Nuclei ◽  
Respiratory Responses ◽  
Stimulation Of

In the present study, we investigated in anesthetized rats the influences of the pontine rapid-eye-movement (REM) sleep center on trigeminally induced respiratory responses. We evoked the nasotrigeminal reflex by electrical stimulation of the ethmoidal nerve (EN5) and analyzed the EN5-evoked respiratory suppression before and after injections into the pontine reticular nuclei of the cholinergic agonist carbachol. After injections of 80–100 nl of carbachol (20 mM), we observed a decrease in respiratory rate, respiratory minute volume, and blood pressure but an increase in tidal volume. In those cases in which carbachol injections alone caused these REM sleep-like autonomic responses, we also observed that the EN5-evoked respiratory suppression was significantly potentiated. Unfortunately, carbachol injections failed to depress genioglossus electromyogram (EMG) effectively, because the EMG activity was already strongly depressed by the anesthetic α-chloralose. We assume that pontine carbachol injections in our anesthetized rats cause autonomic effects that largely resemble REM sleep-like respiratory and vascular responses. We therefore conclude that the observed potentiation of EN5-evoked respiratory suppression after carbachol might be due to REM sleep-associated neuronal mechanisms. We speculate that activation of sensory trigeminal afferents during REM sleep might contribute to pathological REM sleep-associated respiratory failures.

Active upper airway closure during induced central apneas in lambs is complete at the laryngeal level only

2003 ◽  
Vol 95 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Pierre-Hugues Fortier ◽  
Philippe Reix ◽  
Julie Arsenault ◽  
Dominique Dorion ◽  
Jean-Paul Praud
Keyword(s):  
Upper Airway ◽  
Emg Activity ◽  
Airway Closure ◽  
Internal Branch ◽  
Laryngeal Nerves ◽  
Before And After ◽  
Subglottal Pressure ◽  
Central Apneas ◽  
Afferent Innervation ◽  
Stimulation Of

We tested the hypotheses that active upper airway closure during induced central apneas in nonsedated lambs 1) is complete and occurs at the laryngeal level and 2) is not due to stimulation of the superior laryngeal nerves (SLN). Five newborn lambs were surgically instrumented to record thyroarytenoid (TA) muscle (glottal constrictor) electromyographic (EMG) activity with supra- and subglottal pressures. Hypocapnic and nonhypocapnic central apneas were induced before and after SLN sectioning in the five lambs. A total of 174 apneas were induced, 116 before and 58 after sectioning of the internal branch of the SLN (iSLN). Continuous TA EMG activity was observed in 88% of apneas before iSLN section and in 87% of apneas after iSLN section. A transglottal pressure different from zero was observed in all apneas with TA EMG activity, with a mean subglottal pressure of 4.3 ± 0.8 cmH2O before and 4.7 ± 0.7 cmH2O after iSLN section. Supraglottal pressure was consistently atmospheric. Sectioning of both iSLNs had no effects on the results. We conclude that upper airway closure during induced central apneas in lambs is active, complete, and occurs at the glottal level only. Consequently, a positive subglottal pressure is maintained throughout the apnea. Finally, this complete active glottal closure is independent from laryngeal afferent innervation.

scholarly journals Selective optogenetic stimulation of the retrotrapezoid nucleus in sleeping rats activates breathing without changing blood pressure or causing arousal or sighs

2015 ◽  
Vol 118 (12) ◽  
pp. 1491-1501 ◽  
Author(s):  
Peter G. R. Burke ◽  
Roy Kanbar ◽  
Kenneth E. Viar ◽  
Ruth L. Stornetta ◽  
Patrice G. Guyenet
Keyword(s):  
Blood Pressure ◽  
Rem Sleep ◽  
Lentiviral Vector ◽  
Catecholaminergic Neurons ◽  
Optogenetic Stimulation ◽  
Retrotrapezoid Nucleus ◽  
Brainstem Nucleus ◽  
Before And After ◽  
Spinal Injections ◽  
Stimulation Of

Combined optogenetic activation of the retrotrapezoid nucleus (RTN; a CO2/proton-activated brainstem nucleus) with nearby catecholaminergic neurons (C1 and A5), or selective C1 neuron stimulation, increases blood pressure (BP) and breathing, causes arousal from non-rapid eye movement (non-REM) sleep, and triggers sighs. Here we wished to determine which of these physiological responses are elicited when RTN neurons are selectively activated. The left rostral RTN and nearby A5 neurons were transduced with channelrhodopsin-2 (ChR2+) using a lentiviral vector. Very few C1 cells were transduced. BP, breathing, EEG, and neck EMG were monitored. During non-REM sleep, photostimulation of ChR2+ neurons (20s, 2-20 Hz) instantly increased V̇e without changing BP (13 rats). V̇e and BP were unaffected by light in nine control (ChR2−) rats. Photostimulation produced no sighs and caused arousal (EEG desynchronization) more frequently in ChR2+ than ChR2− rats (62 ± 5% of trials vs. 25 ± 2%; P < 0.0001). Six ChR2+ rats then received spinal injections of a saporin-based toxin that spared RTN neurons but destroyed surrounding catecholaminergic neurons. Photostimulation of the ChR2+ neurons produced the same ventilatory stimulation before and after lesion, but arousal was no longer elicited. Overall (all ChR2+ rats combined), ΔV̇e correlated with the number of ChR2+ RTN neurons whereas arousal probability correlated with the number of ChR2+ catecholaminergic neurons. In conclusion, RTN neurons activate breathing powerfully and, unlike the C1 cells, have minimal effects on BP and have a weak arousal capability at best. A5 neuron stimulation produces little effect on breathing and BP but does appear to facilitate arousal.

Modulation of renin by thromboxane: studies with thromboxane synthase inhibitor, receptor antagonists, and mimetic

1989 ◽  
Vol 257 (4) ◽  
pp. F554-F560 ◽  
Author(s):  
W. J. Welch ◽  
C. S. Wilcox ◽  
K. R. Dunbar
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Plasma Renin ◽  
Renal Hemodynamics ◽  
Thromboxane Synthase ◽  
Anesthetized Rats ◽  
Before And After ◽  
Synthase Inhibitor ◽  
By Products ◽  
Stimulation Of

The regulation of plasma renin activity (PRA) by thromboxane (Tx) A2 was studied in anesthetized rats by measuring PRA before and after administration of drugs that block cyclooxygenase (CO) (indomethacin [INDO], 5 mg/kg), thromboxane synthase (TS) (UK 38485 [UK], 100 mg/kg), or Tx receptors (SQ 29548 [SQ], 8 mg/kg or L 641953 [L], 50 mg/kg) or that activate Tx receptors (U 46619 [U], 10 ng.kg-1.min-1). PRA (ng ANG I.ml-1.h-1) was unaffected by vehicle; it was reduced by INDO (25 +/- 2 to 13 +/- 3, n = 13, P less than 0.001) but was increased by UK (24 +/- 3 to 50 +/- 6, n = 18, P less than 0.005), SQ (27 +/- 4 to 44 +/- 7, n = 6, P less than 0.05), and L (32 +/- 4 to 51 +/- 7, n = 10, P less than 0.05). U reduced PRA in each rat (17 +/- 3 to 10 +/- 3, n = 6, P less than 0.005). UK caused dose-dependent stimulation of PRA (mean effective dose 50 mg/kg) and inhibition of TxB2 excretion (mean inhibitory dose 15 mg/kg). After INDO, SQ no longer changed PRA (-1 +/- 10, n = 7). Prolonged administration of SQ for 4-6 days (20 mg.kg-1.day-1 ip) did not change Na+ or K+ balances, blood pressure, renal hemodynamics, or urine flow. However, SQ stimulated PRA (P less than 0.007) independent of prior salt intake. In conclusion in anesthetized rats 1) PRA is stimulated by products of CO but inhibited by products of TS and by a Tx mimetic; 2) stimulation of PRA by SQ depends on ongoing PG and Tx synthesis; 3) rise in PRA with Tx antagonists is not closely related to changes in salt balance, blood pressure, or renal hemodynamics.

Antiparasitic Treatment of Patients with P. falciparum Malaria Reduces the Ability of Patient Serum to Induce Tissue Factor by Decreasing NF-κB Activation

1995 ◽  
Vol 73 (01) ◽  
pp. 039-048 ◽  
Author(s):  
A Bierhaus ◽  
Ch J Hemmer ◽  
N Mackman ◽  
R Kutob ◽  
R Ziegler ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Falciparum Malaria ◽  
De Novo ◽  
Neutralizing Antibody ◽  
Mobility Shift ◽  
Before And After ◽  
Tf Gene ◽  
Electrophoretic Mobility Shift Assays ◽  
Antiparasitic Treatment ◽  
Stimulation Of

SummarySerum from patients with P. falciparum malaria at day 1 (pretherapy) induces tissue factor (TF) in cultured endothelial cells. TF induction depends on de novo transcription as shown in Nuclear Run On assays. Electrophoretic mobility shift assays demonstrated binding of AP-1 and NF- κB/Rel proteins to their recognition sites in the TF promotor. After therapy (day 28), stimulation of TF antigen by patient serum is reduced by 70%. When serum obtained before and after therapy was compared, a decrease of NF-κB activation was evident. Activation of NF-κB-like proteins was in part dependent on TNFα in patient serum, since a TNFα neutralizing antibody reduced induction of TF transcription and translation and induction of NF-κB-like proteins. Induction of TF activity was suppressed by pDTC, an inhibitor of NF-κB activation. When different promotor constructs of the TF gene were tested, induction was dependent upon the presence of the intact NF-κB-like binding site in the TF promotor. A mutant with deleted NF-κB, but intact AP-1 sites was not inducible. Mutation of the AP-1 sites did not prevent induction, but reduced inducibility by pretherapy serum. Therefore, NF-κB/Rel proteins are responsible for induction of TF transcription by pretherapy serum, but AP-1 is needed for highest inducibility. The effect of antiparasitic therapy on the induction of TF by serum from patients with complicated P. falciparum malaria is dependent on a therapy-mediated loss of activation of NF-κB-like proteins in post-treatment patient serum.

scholarly journals Hippocampus-retrosplenial cortex interaction is increased during phasic REM and contributes to memory consolidation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Daniel Gomes de Almeida-Filho ◽  
Bruna Del Vechio Koike ◽  
Francesca Billwiller ◽  
Kelly Soares Farias ◽  
Igor Rafael Praxedes de Sales ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Memory Consolidation ◽  
Retrosplenial Cortex ◽  
Contextual Fear Conditioning ◽  
Oscillatory Activity ◽  
Theta Oscillation ◽  
Contextual Fear ◽  
Before And After ◽  
Freely Behaving ◽  
Phasic Rem Sleep

AbstractHippocampal (HPC) theta oscillation during post-training rapid eye movement (REM) sleep supports spatial learning. Theta also modulates neuronal and oscillatory activity in the retrosplenial cortex (RSC) during REM sleep. To investigate the relevance of theta-driven interaction between these two regions to memory consolidation, we computed the Granger causality within theta range on electrophysiological data recorded in freely behaving rats during REM sleep, both before and after contextual fear conditioning. We found a training-induced modulation of causality between HPC and RSC that was correlated with memory retrieval 24 h later. Retrieval was proportional to the change in the relative influence RSC exerted upon HPC theta oscillation. Importantly, causality peaked during theta acceleration, in synchrony with phasic REM sleep. Altogether, these results support a role for phasic REM sleep in hippocampo-cortical memory consolidation and suggest that causality modulation between RSC and HPC during REM sleep plays a functional role in that phenomenon.

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