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Membrane potential changes of phrenic motoneurons during fictive vomiting, coughing, and swallowing in the decerebrate cat.

1. The patterns of membrane potential changes of phrenic motoneurons were compared during fictive vomiting, fictive coughing, and fictive swallowing in decerebrate, paralyzed cats. These fictive behaviors were identified by motor nerve discharge patterns similar to those recorded from the muscles of nonparalyzed animals. Phrenic motoneurons (n = 54) were identified by antidromic activation from the thoracic phrenic nerve. Intracellular recordings were obtained from 27 motoneurons during fictive vomiting, 40 during fictive coughing, and 27 during fictive swallowing. Sixteen motoneurons were recorded during both fictive coughing and fictive swallowing, eight during both fictive coughing and fictive vomiting, and two during both fictive vomiting and fictive swallowing. Seven motoneurons were studied during all three behaviors. 2. Fictive vomiting, typically evoked by electrical stimulation of abdominal vagal afferents, was characterized by a series of bursts of coactivation of phrenic and abdominal motor nerves, culminating in an expulsion phase in which abdominal discharge was prolonged both with respect to phrenic discharge and to abdominal discharge during the preceding retching phase. During fictive vomiting, phrenic motoneurons depolarized abruptly, and the amplitude of depolarization was significantly greater than during control inspirations. They then repolarized slowly throughout the phrenic burst, rapidly repolarizing at the end of each phrenic burst during retching and reaching a level similar to that observed during expiration. During the expulsion phase, the pattern was initially the same. However, after the cessation of phrenic discharge, the membrane potential repolarized slowly until the end of the abdominal burst, exhibiting greater synaptic noise than during expiration. One phrenic motoneuron, presumably innervating the periesophageal region of the diaphragm, received a strong hyperpolarization just before the onset of the emetic episode and fired for shorter periods during fictive vomiting than did other phrenic motoneurons.(ABSTRACT TRUNCATED AT 250 WORDS)

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[Reticular structures of the cat brain participating in startle reflexes in response to somatic stimuli of different modalities].

Characteristics and reticular mechanisms of two types of late reflex responses (equivalents of the startle reflex) evoked by weak (tactile stimuli) and strong (high-threshold peripheral nerve stimulation) stimulations were studied in chloralose-anesthetized cats; these responses were designated as "tactile" (T) and "spino-bulbo-spinal" (SBS) reflexes, respectively. Some differences in the peripheral and central (brainstem) organization of these reflexes were found. In particular, the existence of the rostro-caudal differentiation of reticular structures involved in these types of reflexes was revealed using differential lesions of the brainstem reticular formation as well as its pharmacologic blockades (by means of microinjections of sodium chloride or procaine); the T-reflex was found to relay mainly through the pontine RF level, while the SBS-reflex--predominantly through the bulbar RF. Possible functional significance of the revealed differentiation in organization of some motor and sensory functions of the brainstem are discussed.

Animals↗

Bladder contractions alter inspiratory termination by superior laryngeal and intercostal nerve stimulation.

Gradual distension of the urinary bladder evokes spontaneous bladder contractions (SBCs), which are associated with reduced inspiratory activity in the phrenic and other inspiratory motor nerves. We examined the influence of isovolumetric SBCs on the threshold for termination of phrenic inspiration by electrical stimulation of superior laryngeal and/or mid-thoracic intercostal nerves (ICN) in decerebrate, vagotomized, paralyzed, ventilated cats. Although SBCs reduced phrenic inspiratory activity, the threshold for inspiratory termination by nerve stimulation was increased. The results emphasize the complexity of the synaptic connections among brain stem neurons governing micturition and breathing.

Animals↗

[Cyriax's syndrome. A cause of diagnostic error in abdominal pains].

The slipping rib syndrome is characterized by upper abdominal pain due to irritation of the intercostal nerve by incomplete dislocation of the costal cartilage of the 8th, 9th, or 10th ribs. Twenty-three new cases are reported and the literature is reviewed. Diagnosis is only clinical. The pain is precipitated by movement and certain postures; it is faithfully reproduced by pressure on one particular point of the costal margin and is relieved by local injection of an anaesthetic. Pain from a slipping rib is usually attributed to visceral causes, which is a source of diagnostic errors.

Abdomen↗

[Horseradish peroxidase localization of the cell bodies of the sympathetic and parasympathetic neurones controlling the lower oesophageal sphincter in the cat (author's transl)].

The localization of the parasympathetic preganglionic and sympathetic postganglionic neuronal cell bodies innervating the lower oesophageal sphincter (l.o.s.) has been investigated in cats, using the technique of horseradish peroxidase (HRP) retrograde axonal transport. HRP was injected into the sphincteric muscle layers (under aseptic conditions). The animals were sacrificed 72 hours later and fixed by perfusion via the aorta. The medulla oblongata and the sympathetic chains from the stellate to T12 ganglia were removed and processed for HRP identification. 1. Labelled cell bodies were identified in the medulla, the stellate and other thoracic ganglia and in the caeliac ganglia. 2. In the medulla, the labelled neurones were located mainly in the vagal dorsal motor nucleus and, to a lesser extent, in the nucleus ambiguus. A few cell bodies were observed between both nuclei. The medullary labelled cell bodies are presumably those of the preganglionic vagal neurones innervating the l.o.s. 3. In the stellate ganglia, the labelled neurones were exclusively located in the ventromedial area. It is likely that they correspond to the postganglionic adrenergic neurones of the sympathetic pathway controlling the lower oesophageal sphincter, the axons of which leave the ganglia through cardiac branches and pass in the thoracic vagus nerve to reach the sphincter (see GONELLA et al., 1979). 4. Labelled neurones were no longer observed in the medulla and in the stellate ganglia when HRP was injected in the l.o.s. after a thoracic bilateral vagotomy. 5. Labelled neurones were also observed in other thoracic ganglia from T3 to T11, most of them lying in T9 and T10. They are probably the postganglionic neurones of a second sympathetic pathway controlling the lower oesophageal sphincter, via the splanchnic nerve (see GONELLA et al., 1979). 6. A homogenous distribution of labelled neurones has been observed in the caeliac ganglia. Its functional significance is discussed.

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Morphometric evaluation of primary sensory neurons in experimental p-bromophenylacetylurea intoxication.

To evaluate the three-dimensional pathology of lumbar primary sensory neurons in p-bromophenylacetylurea intoxication, the number and size distribution of neurons and of myelinated fibers were evaluated at the L-6 spinal ganglion level and at proximal and distal levels of sural nerve and thoracic (proximal) and cervical (distal) levels of Goll's tract, respectively, 2 and 6 weeks after the intoxication in rats. The number and size distribution of ganglion neuron cell bodies were not significantly different between intoxicated and control rats. The distal level of sural nerve had significantly fewer large myelinated fibers than did control, and a significantly higher frequency of fibers undergoing degeneration. Proximal levels of sural nerve showed similar, but less severe changes. Similarly, the myelinated fibers of Goll's tract were significantly more affected at cervical than at thoracic level. Therefore, by morphometric criteria both centrally and peripherally directed myelinated fibers are most affected distally and less affected proximally while neuron cell bodies are not affected at all. These three-dimensional morphological changes must be taken into consideration in formulating possible mechanisms for the development of this neuropathy.

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