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  • 1
    ISSN: 1432-1106
    Keywords: Respiratory control ; Phrenic nerve ; Motoneuron ; Spinal hemisection ; Serotonin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serotonin reveals ineffective (subthreshold) pathways from the C2 lateral funiculus to ipsilateral phrenic motoneurons in spinalized rats. The objective of the present study was to investigate serotonergic modulation of crossed-spinal pathways to contralateral phrenic motoneurons. Rats (n = 10) were anesthetized (urethane), paralyzed, vagotomized, and artificially ventilated. The spinal cord was hemisected at C1–C2 and, on the intact side, a tungsten stimulating electrode was placed ventral to the C2 dorsal root entry zone in the dorsolateral (∼ 1.1 mm) or the ventrolateral funiculus (∼2.2 mm depth). Single shocks (100–750 μA, 0.1–0.5 ms, 2 Hz) elicited a short-latency (∼ 1.0 ms to peak) excitation in the ipsilateral phrenic nerve, but usually evoked little or no response in the contralateral phrenic nerve at either stimulus site. Following systemic injection of the monoamine oxidase inhibitor pargyline (25 mg/kg) and the serotonin precursor 5-hydroxytryptophan (5–10 mg/kg), complex responses were revealed in the contralateral phrenic nerve, including; (1) spontaneous tonic activity; (2) a short-latency (∼1.0 ms to peak) evoked excitation; and (3) two long-latency (∼2.2 and 7.8 ms to peak) evoked excitations. The longest latency excitation was expressed only when the stimulating electrode was positioned in the dorsolateral funiculus. Contralateral evoked responses were blocked by systemic methysergide (2–6 mg/kg), a broad-spectrum serotonin receptor antagonist. These results indicate that serotonin converts ineffective crossed phrenic pathways in the spinal cord to effective pathways. It remains to be determined whether serotonin is both necessary and sufficient in this modulatory process, or if it is a nonspecific result of increased phrenic motoneuron excitability.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Neuroscience 26 (2003), S. 239-266 
    ISSN: 0147-006X
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Notes: Abstract Breathing is a vital behavior that is particularly amenable to experimental investigation. We review recent progress on three problems of broad interest. (i) Where and how is respiratory rhythm generated? The preBotzinger Complex is a critical site, whereas pacemaker neurons may not be essential. The possibility that coupled oscillators are involved is considered. (ii) What are the mechanisms that underlie the plasticity necessary for adaptive changes in breathing? Serotonin-dependent long-term facilitation following intermittent hypoxia is an important example of such plasticity, and a model that can account for this adaptive behavior is discussed. (iii) Where and how are the regulated variables CO2 and pH sensed? These sensors are essential if breathing is to be appropriate for metabolism. Neurons with appropriate chemosensitivity are spread throughout the brainstem; their individual properties and collective role are just beginning to be understood.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 416 (1990), S. 580-585 
    ISSN: 1432-2013
    Keywords: Pulmonary stretch receptors ; CO2-chemoreceptors ; ventilatory control ; Vagus nerve ; phrenic nerve activity ; sensory interactions ; suprapontine mechanisms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of changes in static airway pressure (P aw) and arterial PCO2 (P aCO2) on phrenic nerve activity were studied in unanesthetized, decerebrate dogs and compared with previous results from chloralose/urethane anestetized dogs using the same experimental preparation (Mitchell et al. 1982; Mitchell and Selby 1987). In ten mid-collicular decerebrate dogs, the lungs were independently ventilated while the left pulmonary artery was occluded and the right vagus nerve was transected. Changes in left lung P aw, therefore, exerted effects on pulmonary stretch receptors without altering blood gases; changes in the inspired gas ventilating the right lung controlled blood gas composition, without altering lung volume feedback. Phrenic burst frequency (f) and integrated amplitude (Phr) were monitored while P aw was varied between 2 and 12 cmH2O at various constant levels of P aCO2 between 31 and 69 mmHg. The major findings of this study are: (1) hypercapnia decreases the slope of the relationship between expiratory duration (t E) and P aw in both decerebrated and anesthetized dogs; (2) hypercapnia increases the inspiratory duration (t I) in decerebrated, but not anesthetized dogs; and (3) hypercapnia decreases the slope of the relationship between f and P aw due to these effects on t E and t I. These results support previous studies indicating that vagal and suprapontine mechanisms exert independent effects on respiratory timing. It is concluded that neither suprapontine influences nor anesthesia are necessary in the mechanism underlying interactions between stretch receptors and CO2-chemoreceptors in modulating t E. Furthermore, decerebration reveals a unique effect of CO2-chemoreceptors on t I, an effect found in anesthetized dogs only after carotid denervation.
    Type of Medium: Electronic Resource
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