Postnatal Maturation of Phrenic, Vagus, and Intercostal Nerves in the Kitten

Marlot, D.; Duron, B

doi:10.1159/000241238

Cited by 29 publications

(10 citation statements)

References 11 publications

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“…For example, it is clear that somatic axons myelinate earlier than sympathetic axons (Marlot and Duron 1979;Schäfer and Friede 1988). Similarly, among motoneuron axons in rat ventral roots, the larger α population myelinates earlier than the smaller γ fibers; most of the α fibers begin to myelinate between E20 and P6, while most of the γ fibers myelinate between P6 and P12 Kaar and Fraher 1985).…”

Section: Discussionmentioning

confidence: 99%

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Development of the rat phrenic nerve and the terminal distribution of phrenic afferents in the cervical cord

Song¹,

Tracey²,

Ashwell³

1999

Anatomy and Embryology

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The development of the right phrenic nerve and the distribution of phrenic nerve afferents to the spinal cord have been examined with the aid of electron microscopy and carbocyanine dye retrograde diffusion along the phrenic nerve, respectively. The formation of fascicles in the right phrenic nerve commenced at E15, while Schwann cells penetrated the nerve from E17 and myelination began at P0. The total number of axons in the right phrenic nerve decreased from E15 (943, 965 in two animals) to E19 (539, 582), remained steady until P0 (564, 594) before rising to almost adult values by P7 (689, 934). The postnatal rise in number of axons appears to be due to a large influx of unmyelinated axons. Carbocyanine dye tracing revealed that at E13, neurons in dorsal root ganglia C 2 to C 6 contributed peripheral processes to the phrenic nerve. Phrenic afferents arrived in the spinal cord by E13 and penetrated the dorsal horn at E14. Three terminal fields for phrenic afferents became apparent by E17. These were:(1) in the central parts of laminae I to V, (2) medially in laminae V to VII or adjacent area X near the central canal, (3) in laminae VIII and IX, around the differentiating phrenic motoneurons. Around the time of birth, some phrenic afferents in the second group were distributed across the midline and could be seen to approach the ventromedial dendritic bundle of phrenic motoneurons on the contralateral side, but these were no longer seen by P4. Just before birth (E21), afferents in the third group divided into two further subsets, supplying the dorsolateral and ventromedial groups of phrenic motoneuron dendritic bundles, respectively. Our findings strongly suggest that phrenic afferent differentiation is largely complete by birth.

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Section: Discussionmentioning

confidence: 99%

“…Many peripheral nerves have been studied around the time of birth (Marlot and Duron 1979;Jenq et al 1986;Schäfer and Friede 1988). However, to our knowledge, no single nerve has been studied from the time of formation of the nerve trunk throughout development.…”

Section: Introductionmentioning

confidence: 99%

Development of the rat phrenic nerve and the terminal distribution of phrenic afferents in the cervical cord

Song¹,

Tracey²,

Ashwell³

1999

Anatomy and Embryology

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“…In fact, mammals generate spontaneous respiratory activity in utero, starting early in the last trimester (Jansen & Chernick, 1983). Furthermore, the distribution and morphology of spinal respiratory motoneurones in the neonate resembles those found in the mature adult (Marlot & Duron, 1979;Smith & Hollyday, 1983;Lindsay, Greer & Feldman, 1991). Therefore, while certain neural components and mechanisms may undergo some postnatal maturation (see Smith et al 1990b), the basic neuronal networks and associated transmitters involved in rhythmogenesis and the transmission of respiratory drive are fully operational in the neonate and likely to resemble those in the adult.…”

Section: Discussionmentioning

confidence: 99%

Role of excitatory amino acids in the generation and transmission of respiratory drive in neonatal rat.

Greer

Smith

Feldman

1991

The Journal of Physiology

240

189

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SUMMARY1. The involvement of excitatory amino acids in the generation and transmission of rhythmic respiratory drive was studied in an in vitro neonatal rat brain stem-spinal cord preparation. The subclasses of excitatory amino acid receptors studied included: (i) N-methyl-D-aspartate (NMDA) receptors, (ii) (R, S)-o-amino-3-hydroxy-5-methylisoxazole-4-propionic acid hydrobromide (AMPA) and kainate (non-NMDA) receptors and (iii) 2-amino-4-phosphonobutyric acid (AP-4)-sensitive receptors. Respiratory motoneurone population discharge was recorded from glossopharyngeal (IX), vagus (X), and hypoglossal (XII) cranial nerves, as well as cervical (C1-C5) and thoracic (T2-T5) spinal ventral roots. This activity is generated in the motoneurone pools that transmit respiratory drive to upper airway, accessory, diaphragm and intercostal muscles. Perturbations of motor nerve discharge were analysed after excitatory amino acid receptor antagonists or agonists were added to bathing solutions surrounding either the spinal cord or brain stem. The excitatory amino acid receptor antagonists included: (i) NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5, 10-imin-H-maleate (MK-801) and (ii) non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The agonists included: (i) NMDA, (ii) non-NMDA receptor agonists AMPA and kainic acid. The effects of perturbations of AP-4-sensitive receptors with AP-4, and of inhibiting excitatory amino acid uptake with dihydrokainic acid (DHK) were also studied.2. Block of non-NMDA receptors in the medulla by CNQX resulted in an antagonist concentration-dependent decrease in the respiratory motoneuronal burst frequency. Non-NMDA receptor activation with kainic acid or AMPA caused a concentration-dependent increase in burst frequency, with competitive interactions with CNQX.3. Inhibition of excitatory amino acid uptake in the medulla with DHK resulted in a reversible, dose-dependent increase in respiratory frequency. A similar increase in respiratory frequency was induced by DHK when medullary NMDA receptors were blocked with MK-801, confirming that endogenously released excitatory amino acids act at non-NMDA receptors to modulate rhythm.4. Non-NMDA receptor block reduced and ultimately abolished the amplitude of MS 8563 J. J. GREER, J. C. SMITH AND J. L. FELDMAN integrated cranial and spinal respiratory motoneuronal discharge when added to the solution bathing the medulla and spinal cord, respectively. 5. NMDA receptor block in the medulla with MK-801 did not perturb the spontaneous respiratory burst frequency, although bath application of NMDA produced a dose-dependent increase in frequency, with non-competitive interactions with MK-801. MK-801 also did not perturb the amplitude of cranial or bulbospinal premotoneurone discharge. Block of NMDA receptors within the spinal cord caused a relatively small (10-30%) decrease in the amplitude of inspiratory motoneurone discharge.6. AP-4 applied to the medullary bathing solution did not affect respiratory r...

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“…Moreover, in kittens, during eupnea there ex ists relatively weak neuronal inspiratory ac tivity [3][4][5] which generally is not reinforced very much by excitatory stimulations such as hypoxia [6] or lung deflation [7], which in adults strengthen inspiratory activity. In var ious experimental procedures (anesthetized or decerebrate preparations) bivagotomy, which in adults reinforces central inspiratory activity, induces prolongation and reinforce ment of expiration in newborn animals [8,9], In spite of marked vagus nerve immaturity observed histologically [10], discharge pat terns of vagal afferent units are similar in kit tens and adult cats. Nevertheless, the inhibi tory action of slowly adapting pulmonary stretch receptors, which exists in all species studied [8,11], is stronger at birth than later during maturation.…”

Section: Introductionmentioning

confidence: 99%

Nonvagal Reflex Apnea in the Newborn Kitten and during the Early Postnatal Period

Khater-Boidin¹,

Wallois²,

Toussaint³

et al. 1994

Neonatology

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The aim of this work was to study the nonvagal mechanisms which might induce apneic reflexes in kittens. Experiments were performed on spontaneously breathing animals (19 kittens at different postnatal ages). Animals were anesthetized (halothane) or decerebrated by transcollicular section of the brainstem. Weakly nociceptive cutaneous stimulations and various oral stimulations were administered in all animals. In 10 kittens, one of the lingual nerves was stimulated electrically. In 3 decerebrate kittens the effects of serotonin on respiratory activity and on muscles innervated by the hypoglossal nerve were studied. All the stimulations produced apneas of variable duration, and expiratory reinforcement was associated with activation of pretracheal muscles. Similar effects were observed after applying serotonin to the floor of the 4th ventricle. Thus serotonin may be involved in the mechanisms that cause some apneas.

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Postnatal Maturation of Phrenic, Vagus, and Intercostal Nerves in the Kitten

Cited by 29 publications

References 11 publications

Development of the rat phrenic nerve and the terminal distribution of phrenic afferents in the cervical cord

Development of the rat phrenic nerve and the terminal distribution of phrenic afferents in the cervical cord

Role of excitatory amino acids in the generation and transmission of respiratory drive in neonatal rat.

Nonvagal Reflex Apnea in the Newborn Kitten and during the Early Postnatal Period

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