Parafacial neurons in the human brainstem express specific markers for neurons of the retrotrapezoid nucleus

Author(s):  
J. Levy ◽  
F. Droz‐Bartholet ◽  
M. Achour ◽  
P. Facchinetti ◽  
B. Parratte ◽  
...  

2011 ◽  
Vol 163 (1-2) ◽  
pp. 131
Author(s):  
B. Falquetto ◽  
A.C. Takakura ◽  
T.S. Moreira






1997 ◽  
Vol 82 (2) ◽  
pp. 469-479 ◽  
Author(s):  
Manjapra R. Akilesh ◽  
Matthew Kamper ◽  
Aihua Li ◽  
Eugene E. Nattie

Akilesh, Manjapra R., Matthew Kamper, Aihua Li, and Eugene E. Nattie. Effects of unilateral lesions of retrotrapezoid nucleus on breathing in awake rats. J. Appl. Physiol. 82(2): 469–479, 1997.—In anesthetized rats, unilateral retrotrapezoid nucleus (RTN) lesions markedly decreased baseline phrenic activity and the response to CO2 (E. E. Nattie and A. Li. Respir. Physiol. 97: 63–77, 1994). Here we evaluate the effects of such lesions on resting breathing and on the response to hypercapnia and hypoxia in unanesthetized awake rats. We made unilateral injections [24 ± 7 (SE) nl] of ibotenic acid (IA; 50 mM), an excitatory amino acid neurotoxin, in the RTN region ( n = 7) located by stereotaxic coordinates and by field potentials induced by facial nerve stimulation. Controls ( n = 6) received RTN injections (80 ± 30 nl) of mock cerebrospinal fluid. A second control consisted of four animals with IA injections (24 ± 12 nl) outside the RTN region. Injected fluorescent beads allowed anatomic identification of lesion location. Using whole body plethysmography, we measured ventilation in the awake state during room air, 7% CO2 in air, and 10% O2 breathing before and for 3 wk after the RTN injections. There was no statistically significant effect of the IA injections on resting room air breathing in the lesion group compared with the control groups. We observed no apnea. The response to 7% CO2 in the lesion group compared with the control groups was significantly decreased, by 39% on average, for the final portion of the 3-wk study period. There was no lesion effect on the ventilatory response to 10% O2. In this unanesthetized model, other areas suppressed by anesthesia, e.g., the reticular activating system, hypothalamus, and perhaps the contralateral RTN, may provide tonic input to the respiratory centers that counters the loss of RTN activity.



2007 ◽  
Vol 98 (1) ◽  
pp. 374-381 ◽  
Author(s):  
Ana C. Takakura ◽  
Thiago S. Moreira ◽  
Gavin H. West ◽  
Justin M. Gwilt ◽  
Eduardo Colombari ◽  
...  

The retrotrapezoid nucleus (RTN) contains central respiratory chemoreceptors that are inhibited by activation of slowly adapting pulmonary stretch receptors (SARs). Here we examine whether RTN inhibition by lung inflation could be mediated by a direct projection from SAR second-order neurons (pump cells). Pump cells ( n = 56 neurons, 13 rats) were recorded in the nucleus of solitary tract (NTS) of halothane-anesthetized rats with intact vagus nerves. Pump cells had discharges that coincided with lung inflation as monitored by the tracheal pressure. Their activity increased when end-expiratory pressure was raised and stopped instantly when ventilation was interrupted in expiration. Many pump cells could be antidromically activated from RTN (12/36). Nine of those were labeled with biotinamide. Of these nine cells, eight contained glutamic acid decarboxylase 67 (GAD67) mRNA and seven were found to reside in the lower half of the interstitial subnucleus of NTS (iNTS). Using the retrograde tracer cholera toxin-B, we confirmed that neurons located in or close to iNTS innervate RTN (two rats). Many such neurons contained GAD67 mRNA and a few contained glycine transporter2 (GLYT2) mRNA. Anterograde tract tracing with biotinylated dextranamide (four rats) applied to iNTS also confirmed that this region innervates RTN by a predominantly GABAergic projection. This work confirms that many rat NTS pump cells are located in and around the interstitial subnucleus at area postrema level. We demonstrate that a GABAergic subset of these pump cells innervates the RTN region. We conclude that these inhibitory neurons probably contact RTN chemoreceptors and mediate their inhibition by lung inflation.





2010 ◽  
Vol 13 (4) ◽  
pp. 291-299 ◽  
Author(s):  
Erin Rudzinski ◽  
Raj P. Kapur


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