Brainstem network controlling descending drive to phrenic motoneurons in rat

Dobbins, Elizabeth G.; Feldman, Jack L.

doi:10.1002/cne.903470106

Cited by 444 publications

(376 citation statements)

References 97 publications

Supporting

Mentioning

339

Contrasting

Unclassified

Order By: Relevance

“…Although manipulation of vagal afferents directly affects both phrenic and hypoglossal motor outflow, repeated modulation only triggers plasticity of hypoglossal function; it never affects phrenic activity. Anatomical tracing data show that noradrenergic LC neurons densely innervate hypoglossal motoneurons (Aldes et al, 1992), but they do not directly innervate phrenic motoneurons (Dobbins and Feldman, 1994). In fact, findings suggest that phrenic motoneurons do not receive direct noradrenergic inputs.…”

Section: Discussionmentioning

confidence: 93%

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

Tadjalli¹,

Duffin²,

Peever³

2010

J. Neurosci.

View full text Add to dashboard Cite

The respiratory control system is not just reflexive, it is smart, it learns, and, in fact, it has a memory. The respiratory system listens to and carefully remembers how previous stimuli affect breathing. Respiratory memory is laid down by adjusting synaptic strength between respiratory neurons. For example, repeated hypoxic bouts trigger a form of respiratory memory that functions to strengthen the ability of respiratory motoneurons to trigger contraction of breathing muscles. This type of respiratory plasticity is known as long-term facilitation (LTF). Although chemical feedback, such as hypoxia, initiates LTF, it is unknown whether natural modulation of mechanical feedback (from vagal inputs) also causes motor plasticity. Here, we used reverse microdialysis, electrophysiology, neuropharmacology, and histology to determine whether episodic modulation of vagally mediated mechanical feedback is able to induce respiratory LTF in anesthetized adult rats. We show that repeated obstructive apneas disrupt vagal feedback and trigger LTF of hypoglossal motoneuron activity and genioglossus muscle tone. This same stimulus does not cause LTF of diaphragm activity. Hypoxic episodes do not cause apnea-induced LTF; instead, LTF is triggered by modulation of vagal feedback. Unlike hypoxia-induced respiratory plasticity, vagusinduced LTF does not require 5-HT 2 receptors but instead relies on activation of ␣1-adrenergic receptors on hypoglossal motoneurons. In summary, we identify a novel form of hypoxia-and 5-HT-independent respiratory motor plasticity that is triggered by physiological modulation of vagal feedback and is mediated by ␣1-adrenergic receptor activation on (or near) hypoglossal motoneurons.

show abstract

Section: Discussionmentioning

confidence: 93%

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

Tadjalli¹,

Duffin²,

Peever³

2010

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…In addition, anatomical evidence that RVM neurons directly project to medullary and spinal cord cardiovascular sites suggests that RVM neurons elicit increases in arterial pressure by inhibiting parasympathetic control of the heart at the level of the medulla, and by activating direct descending pathways to spinal cord sympathetic preganglionic neurons [22,41,42]. Moreover, the RVM may also function in the control of respiration through direct connections to the phrenic nucleus [43,44]. Based on these facts, the present results suggest the possibility that self-touch regulates the autonomic nervous system, producing an antisympathetic effect in even a pain-free and stress-free situation.…”

Section: Discussionmentioning

confidence: 99%

The Neural Basis of Self-Touch in a Pain-Free Situation

Kikuchi¹,

Shirato²,

Machida³

et al. 2018

Neuropsychiatry

View full text Add to dashboard Cite

Objective:Self-touch is thought to be an act of coping with harmful or stressful situations, based on the mechanism which suppresses somatosensory perception as well as somatosensory cortex activity, and sympathetic activity. In addition, this suppression can be observed in even nonpainful and non-stressful situations. However, its detailed neural mechanism remains unknown. Several studied have shown, not only that the descending pain modulatory system (DPMS) plays critical roles in painful situations, but also that there is intrinsic functional connectivity in the DPMS in even non-painful situations. Based on these findings, we hypothesized that the neural system consisting of the anterior cingulate cortex (ACC), amygdala and rostral ventromedial medulla (RVM) would play a basic role in self-touch, and we here investigated interactive effects of these regions in a pain-free self-touch situation. Methods:We used functional magnetic resonance imaging (fMRI) to investigate brain activity induced by mere self-touch (rubbing the left hand with the right) in a pain-free and stress-free situation, and carried out the Physio-Physiological Interaction (PPI) analysis to investigate the modulatory effects of brain activity. Results:PPI analysis showed that the rostral ACC (rACC) modulated activity in the RVM and left cerebellum (CB) via the right amygdala, such that the modulation linearly suppressed RVM and left CB activity. Furthermore, the latter was positively correlated with right primary somatosensory cortex (SI) activity. Moreover, we also showed that coherent activity in the bilateral secondary somatosensory cortex (SII) modulated activity of both the left temporoparietal junction (TPJ) and RVM, with the latter also suppressed by the modulation in a linear fashion. Conclusion:These findings suggest that self-touch exerts inhibitory effects on sensory afferents and sympathetic activity through the ACC-amygdala-RVM (AAR) system, and that bilateral sensorimotor integration plays an important role in the effect based on the bodily self.

show abstract

“…1) (Moreno et al, 1992;Dobbins and Feldman 1994;Lipski et al, 1994). Although most crossed pathways decussate in the brainstem, an apparently ineffective synaptic pathway crosses the spinal midline caudal to C2 (i.e., the "crossed phrenic pathway") (Goshgarian, 1981;Moreno et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Synaptic Pathways to Phrenic Motoneurons Are Enhanced by Chronic Intermittent Hypoxia after Cervical Spinal Cord Injury

Fuller¹,

Johnson²,

et al. 2003

View full text Add to dashboard Cite

Spinal hemisection at C2 reveals caudal synaptic pathways that cross the spinal midline (crossed phrenic pathways) and can restore inspiratory activity in ipsilateral phrenic motoneurons. Intermittent hypoxia induces plasticity in the cervical spinal cord, resulting in enhanced inspiratory phrenic motor output. We hypothesized that chronic intermittent hypoxia (CIH) (alternating 11% O 2 and air; 5 min periods; 12 hr per night; 7 nights) would strengthen crossed phrenic pathways. Experiments were performed on anesthetized, vagotomized, paralyzed, ventilated, and spinally injured (C2 hemisection) rats that were exposed to either normoxia or CIH before acute injury (preconditioning) or after chronic injury (postconditioning). Spontaneous inspiratory bursts or compound action potentials evoked via stimulation of the ventrolateral funiculus (contralateral to injury) were recorded in both phrenic nerves. Spontaneous or evoked activity in crossed phrenic pathways were minimal or absent in all acutely injured rats regardless of preconditioning. In rats postconditioned with normoxia, crossed phrenic inspiratory bursts were observed occasionally during baseline conditions and always during chemoreceptor stimulation (hypoxia and hypercapnia). However, CIH postconditioned rats had substantially larger crossed phrenic inspiratory bursts during baseline, hypoxia, and hypercapnia (all p Ͻ 0.05 vs normoxic group). Short-latency (0.7 msec) evoked crossed phrenic potentials were also enhanced by CIH conditioning in chronically injured rats ( p Ͻ 0.05). We conclude that CIH induced spinal cord plasticityenhanced phrenic motor output. This plasticity required preconditions established by chronic spinal injury.

show abstract

Brainstem network controlling descending drive to phrenic motoneurons in rat

Cited by 444 publications

References 97 publications

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

The Neural Basis of Self-Touch in a Pain-Free Situation

Synaptic Pathways to Phrenic Motoneurons Are Enhanced by Chronic Intermittent Hypoxia after Cervical Spinal Cord Injury

Contact Info

Product

Resources

About