Inspiratory augmenting bulbospinal neurons express both glutamatergic and enkephalinergic phenotypes

Stornetta, Ruth L.; Sevigny, Charles P.

doi:10.1002/cne.10486

Cited by 78 publications

(65 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The nonradioactive method used presently to detect vesicular glutamate transporter2 (VGLUT2) has also been described previously (Stornetta et al, 2003;Weston et al, 2004). Finally, the simultaneous detection of two mRNAs by in situ hybridization using FITC-labeled (in the present case for GLYT2) and digoxigenin-labeled (in the present case for VGLUT2) riboprobes was also performed with a previously published method .…”

Section: Methodsmentioning

confidence: 99%

Bötzinger Expiratory-Augmenting Neurons and the Parafacial Respiratory Group

Fortuna¹,

West²,

Stornetta³

et al. 2008

J. Neurosci.

View full text Add to dashboard Cite

In neonatal rat brains in vitro, the rostral ventral respiratory column (rVRC) contains neurons that burst just before the phrenic nerve discharge (PND) and rebound after inspiration (pre-I neurons). These neurons, called parafacial respiratory group (pfRG), have been interpreted as a master inspiratory oscillator, an expiratory rhythm generator or simply as neonatal precursors of retrotrapezoid (RTN) chemoreceptor neurons. pfRG neurons have not been identified in adults, and their phenotype is unknown. Here, we confirm that the rVRC normally lacks pre-I neurons in adult anesthetized rats. However, we show that, during hypercapnic hypoxia, a population of rVRC expiratory-augmenting (E-AUG) neurons consistently develops a pre-I discharge. These cells reside in the Bötzinger region of the rVRC, they express glycine-transporter-2, and their axons arborize throughout the VRC. Hypoxia triggers an identical pre-I pattern in retroambigual expiratory bulbospinal neurons, but this pattern is not elicited in Bötzinger expiratory-decrementing neurons, Bötzinger inspiratory neurons, RTN neurons, and blood pressure-regulating neurons. In conclusion, under hypoxia in vivo, abdominal expiratory premotor neurons of adult rats develop a pre-I pattern reminiscent of that observed in neonate brainstems in vitro. In the rVRC of adult rats, pre-I cells include selected rhythmogenic neurons (glycinergic Bötzinger neurons) but not RTN chemoreceptors. We suggest that the pfRG may not be an independent rhythm generator but a heterogeneous collection of E-AUG neurons (glycinergic Bötzinger neurons, possibly facial motor and premotor neurons), the discharge of which becomes preinspiratory under specific experimental conditions resulting from, in part, a prolonged and intensified activity of postinspiratory neurons.

show abstract

Section: Methodsmentioning

confidence: 99%

Bötzinger Expiratory-Augmenting Neurons and the Parafacial Respiratory Group

Fortuna¹,

West²,

Stornetta³

et al. 2008

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Transient occlusion of the descending aorta just below the diaphragm was used to activate arterial baroreceptors (Brown and Guyenet 1985). Rostral ventral respiratory group (rVRG) respiratory neurons were recorded between Bregma levels -13.0 to -13.4 mm (Schwarzacher et al 1991;Stornetta et al 2003). Cell types are named according to standard descriptive terminology referring to the timing of their discharge relative to that of the phrenic nerve (Schwarzacher et al 1991).…”

Section: In Vivo Recordingsmentioning

confidence: 99%

Activation of 5-Hydroxytryptamine Type 3 Receptor-Expressing C-Fiber Vagal Afferents Inhibits Retrotrapezoid Nucleus Chemoreceptors in Rats

Moreira

Takakura²,

Colombari³

et al. 2007

Journal of Neurophysiology

Self Cite

View full text Add to dashboard Cite

Moreira TS, Takakura AC, Colombari E, Guyenet PG. Activation of 5-hydroxytryptamine type 3 receptor-expressing C-fiber vagal afferents inhibits retrotrapezoid nucleus chemoreceptors in rats. J Neurophysiol 98: 3627-3637, 2007. First published October 10, 2007 doi:10.1152/jn.00675.2007. Retrotrapezoid nucleus (RTN) chemoreceptors are regulated by inputs from the carotid bodies (CB) and from pulmonary mechanoreceptors. Here we tested whether RTN neurons are influenced by 5-hydroxytryptamine type 3 receptor-expressing C-fiber vagal afferents. In urethan-anesthetized rats, selective activation of vagal C-fiber afferents by phenylbiguanide (PBG) eliminated the phrenic nerve discharge (PND) and inhibited RTN neurons (n ϭ 24). PBG had no inhibitory effect in vagotomized rats. Muscimol injection into the solitary tract nucleus, commissural part, reduced inhibition of PND and RTN by PBG (73%), blocked activation of PND and RTN by CB stimulation (cyanide) but had no effect on inhibition of PND and RTN by lung inflation. Bilateral injections of muscimol into interstitial solitary tract nucleus (NTS) reduced the inhibition of PND and RTN by PBG (53%), blocked the inhibitory effects of lung inflation but did not change the activation of PND and RTN neurons by CB stimulation. PBG and lung inflation activated postinspiratory neurons located within the rostral ventral respiratory group (rVRG) and inhibited inspiratory and expiratory neurons. Bilateral injections of muscimol into rVRG eliminated PND and partially decreased RTN neuron inhibition by PBG (32%). In conclusion, activation of cardiopulmonary C-fiber afferents inhibits the activity of RTN chemoreceptors. The pathway relays within a broad medial region of the NTS and involves the rVRG to a limited degree. The apnea triggered by activation of cardiopulmonary C-fiber afferents may be due in part to a reduction of the activity of RTN chemoreceptors.

show abstract

“…A large number of bulbospinal premotor neurons in the preBötC, which discharge later in the respiratory cycle compared with early inspiratory neurons, also express NKRs Stornetta et al 2003b).…”

Section: Introductionmentioning

confidence: 99%

Neurokinin Receptor-Expressing Pre-Bötzinger Complex Neurons in Neonatal Mice Studied In Vitro

Hayes¹,

Negro²

2007

Journal of Neurophysiology

View full text Add to dashboard Cite

Hayes JA, Del Negro CA. Neurokinin receptor-expressing preBötzinger complex neurons in neonatal mice studied in vitro. J Neurophysiol 97: 4215-4224, 2007. First published April 4, 2007 doi:10.1152/jn.00228.2007. Breathing in mammals depends on inspiratory-related neural activity generated in the pre-Bötzinger complex (preBötC), where neurokinin receptor-expressing neurons (NKR ϩ ) have been hypothesized to play a critical rhythmogenic role. Currently, the extent to which the preBötC is populated by rhythmogenic NKR ϩ neurons and whether neurons without neurokinin receptor expression (NKR Ϫ ) share similar electrical properties with NKR ϩ neurons are not well understood. These interrelated problems must be resolved to understand the widespread excitatory effects of neuropeptides and the mechanism of respiratory rhythmogenesis. We recorded and imaged inspiratory neurons in neonatal mouse slices that isolate the preBötC and generate respiratory motor output in vitro. Using tetramethylrhodamine conjugated to the endogenous NKR agonist substance P (TMR-SP) to tag neurons that express NKRs, we show that early inspiratory neurons with small whole cell capacitance (C M ) are 36% TMR-SP ϩ and 64% TMR-SP Ϫ . Also, late inspiratory neurons with large C M are 67% TMR-SP ϩ and 33% are TMR-SP Ϫ . Thus NKR ϩ and NKR Ϫ neurons exhibit the same phenotypic properties, which suggests that they may share functional roles also. Substance P (SP) alone evoked a voltage-insensitive inward current (I SP ) that reversed at -19 mV and was associated with an increase in membrane conductance in both NKR ϩ and NKR Ϫ neurons. Gap junctions may be needed to confer SP sensitivity to neurons that appear to lack NKR expression. We propose that cell death in NKR ϩ preBötC neurons, by targeted lesion or neurodegeneration, may impair breathing behavior by killing less than one half of the rhythmogenic preBötC neurons and a large number of respiratory premotoneurons.

show abstract

Inspiratory augmenting bulbospinal neurons express both glutamatergic and enkephalinergic phenotypes

Cited by 78 publications

References 59 publications

Bötzinger Expiratory-Augmenting Neurons and the Parafacial Respiratory Group

Bötzinger Expiratory-Augmenting Neurons and the Parafacial Respiratory Group

Activation of 5-Hydroxytryptamine Type 3 Receptor-Expressing C-Fiber Vagal Afferents Inhibits Retrotrapezoid Nucleus Chemoreceptors in Rats

Neurokinin Receptor-Expressing Pre-Bötzinger Complex Neurons in Neonatal Mice Studied In Vitro

Contact Info

Product

Resources

About