Electrophysiological demonstration of the projection from expiratory neurones in rostral medulla to contralateral dorsal respiratory group.
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Biomedical subjects
Publications and source records attributed to J Lipski.
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The latency from the stimulus (S) to the IS and SD components of the antidromic spike was measured in motoneurones and spinocerebellar tract cells following displacement of the membrane potential either by current pulses or by synaptic potentials. Changes in the latency to the SD spike (S-SD delay) were mainly caused by changes in the IS-SD delay and varied from 10 to 100 musec per mV change in membrane potential, depending on the initial value of the IS-SD delay. Changes in the S-IS delay were also observed and these changes could, especially in spinocerebellar cells, give a significant contribution to the change in the total delay. EPSPs shortened the S-SD delay as efficiently as current-evoked depolarizations of similar magnitude while IPSPs were often more effective in prolonging the delay than current-evoked hyperpolarizations. This difference was related to the larger conductance increase during IPSPs than during IPSPs and to the longer IS-SD delays at hyperpolarized potentials. The presented data contribute to the understanding of the method which uses extracellular recording of antidromic latency changes as an indirect measure of intracellular membrane potential changes. Our results show that the recording of antidromic latency changes is a particularly sensitive method for detecting inhibition of neurones.
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(1) Glass microelectrodes were used to record extracellularly the activity of single dorsal (in the region of nucleus tractus solitarius (NTS)) inspiratory neurons in either chloralose- or pentobarbitone-anaesthetized, paralyzed cats. (2) In the lateral and ventral part of NTS, 89 cells were localized which responded antidromically to stimulation applied to the contralateral spinal cord (C3). Seventy were not excited by lung inflation and were classified as Ralpha, while 19 excited by that stimulus were classified as Rbeta. Usually Rbeta neurons fired both during each pump-induced lung inflation and during the central inspiratory excitation (CIE). (3) A technique similar to Merrill's recording small variations in the antidromic latency measured to the SD spike was used to ascertain excitability of Ralpha and Rbeta cells during the CIE time and during lung inflation in expiration. The technique was extended by averaging antidromic latency patterns within many respiratory cycles. (4) In the majority of Ralpha cells the averaging revealed a shortening of the antidromic latency during lung inflation in expiration, which indicated a subthreshold depolarization. Lengthening of the antidromic latency by this stimulus was never observed. These results are in disagreement with the concept of a direct inhibitory input from Rbeta to Ralpha neurons. (5) It is concluded that the dorsal Ralpha and Rbeta neurons differ less in their properties than was previously assumed on the basis of classical extracellular techniques. The inhibitory influence of pulmonary stretch receptor input on inspiratory discharge of Ralpha cells seems to be exerted through an indirect action on the source of the CIE.
1. Inhibitory post-synaptic potentials evoked by adequate stimulation of group Ia muscle spindle afferents of homonymous and synergistic muscles and by selective electrical stimulation of tendon organ afferents were analysed in motoneurones of triceps surae and plantaris. 2. Selective activation of Ia afferents was verified to occur with brief stretches of triceps surae and plantaris 35 micrometer or less in amplitude with an initial muscle tension of 5 N; stretches of 30--35 micrometer were estimated to activate 80--90% of Ia afferents in these muscles. Under the same conditions the lowest thresholds for group Ib tendon organ afferents were about 40 micrometer. 3. Stretches less than or equal to 30 micrometer evoked i.p.s.p.s in 80% of triceps surae and plantaris motoneurones; lowest thresholds for evoking i.p.s.p.s wef triceps surae and plantaris motoneurones; lowest thresholds for evoking i.p.s.p.s were 10 micrometer or less. However, such low thresholds for stretch-evoked i.p.s.p.s, lower than the thresholds for activation of Ib afferents, were found mainly in spinalized, unanaesthetized (after decerebration) or lightly anaesthetized animals. The latencies of these i.p.s.p.s indicated disynaptic and trisynaptic coupling between Ia afferents and motoneurones. The i.p.s.p.s were evoked (i) from the homonymous and synergistic muscles stretched together, (ii) from the homonymous muscles alone and (iii) from the synergistic muscles alone. 4. Control experiments showed that i.p.s.p.s could be evoked by stretches sub-threshold for discharging motoneurones, thus showing that those i.p.s.p.s were not mediated by Renshaw cells. The stretch-evoked i.p.s.p.s disappeared after sectioning the nerves from the corresponding muscles, further excluding their mediation by afferents other than group Ia afferents from thf stretched muscle. 5. In order to selectively activate tendon organ afferents, thresholds for excitation of Ia afferents by electrical stimuli were increased to a level above the threshold for Ib afferents by prolonged muscle vibration (Coppin, Jack & MacLennan, 1970). I.p.s.p.s evoked by stimuli near threshold for Ib afferents appeared with latencies indicating disynaptic coupling. Later (trisynaptic) components of Ib i.p.s.p.s required somewhat stronger stimuli. 6. Amplitudes of Ia i.p.s.p.s evoked by muscle stretches activating about 80% of muscle spindle afferents were compared with amplitudes of Ib i.p.s.p.s due to less than 50% of tendon organ afferents of the same muscles. The Ia i.p.s.p.s were much smaller (16--35%) than the Ib i.p.s.p.s. The amplitudes of such Ia and Ib i.p.s.p.s constituted about 10 and 25--66%, respectively, of the maximal i.p.s.p.s evoked by electrical stimulation of all group I afferents. 7. We conclude that inhibition of motoneurones may be evoked from Ia muscle spindle afferents from homonymous and synergistic muscles as well as from Ib tendon organ afferents...
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1. An investigation has been made into the connexions between the carotid body chemoreceptors and the dorsal respiratory neurones of the cat's medulla.2. In confirmation of previous work these neurones were found to be all inspiratory in firing pattern and to fall into two categories, Ralpha (forty-four units) which fire only with the central inspiratory rhythm and Rbeta (thirty-two neurones) that are also excited by lung inflation. Both categories were shown to be excited by stimuli delivered to the carotid bodies during inspiration but, with a single exception, not during expiration.3. When Rbeta neurones were made to fire tonically in expiration by maintained lung inflation, chemoreceptor activation inhibited this discharge in 7/11 cases, the remainder being unaffected.4. Iontophoretically applied DL-homocysteic acid or glutamate made both Ralpha and Rbeta neurones fire tonically in expiration. Chemoreceptor stimulation during expiration inhibited this activity in all neurones tested (nine Ralpha and three Rbeta cells).5. Using the measurement of the antidromic latency to spinal stimulation as an index of membrane potential, evidence was obtained that any subthreshold influence of the chemoreceptors on dorsal respiratory neurones during expiration was inhibitory (9/18 cases).6. It is concluded that chemoreceptors do not even subliminally excite dorsal inspiratory neurones during expiration; such influence as they have then is inhibitory. Possible reasons for this difference in chemoreceptor influence during inspiration and expiration are discussed. It is suggested that chemoreceptor excitation reaches them only as part of an enhanced central inspiratory drive from an as yet unknown source.
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Holter electrocardiographic monitoring in 55 symptomatic patients with syncope, palpitations or dizziness uncovered significant arrhythmias in 30 patients (55 percent). By providing an observation period of at least 24 hours including a period of sleep, the procedure aided detection and diagnosis in both symptomatic and asymptomatic patients of transient arrhythmias or conduction abnormalities not documented by routine electrocardiograms. Bradyarrhythmias accounted for the majority of arrhythmias recorded in 21 or 30 symptomatic patients (70 percent); 15 had sinus bradycardia (35 to 55 beats/min) alone and 6 also had long episodes of sinus arrest of up to 5 seconds. Two had sinus bradycardia with periods of atrioventricular block with Wenckebach phenomenon. Five patients had a tachycardia-bradycardia syndrome; three had other episodic arrhythmias and one had pacemaker failure. In 15 (60 percent) of the 25 patients without arrhythmias, monitoring did not document the cause of symptoms. Holter monitoring is of considerable value in assessing the efficacy and adequacy of drug treatment, especially in patients with known heart disease, and in detecting pacemaker malfunction. However, very long periods of monitoring may be needed to make a diagnosis in those with only sporadic symptoms.
Bilateral electrolytic lesion of the area of the nucleus tractus solitarii (NTS) in rats produced a sustained increase in blood pressure and reduced the hypotensive response to a single dose of clonidine (30 mug/kg, i.v.). The same dose of clonidine evoked a much larger drop in blood pressure in another group of rats in which an equialent increase in blood pressure was produced by bilateral section of the vagosympathetic trunks and occlusion of both carotid arteries. It is concluded that the dorsal part of the medulla oblongata in the area of NTS is an important link in the hypotensive action of clonidine.
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In paralyzed cats under chloralose-urethane anaesthesia the medulla oblongata was searched with dye-filled microelectrodes for neurons responding to electrical stimulation of the carotid sinus nerve (CSN) and distension of the isolated carotid sinus (CS). 89 cells localized in the solitary tract nucleus and in the reticular formation ventrally and ventrolaterally to the nucleus exhibited mainly an excitatory input from the CSN. 16 could be also antidromically excited from the cervical spinal cord at C4 level. 11 of these were shown to be excited by a pressure rise in the CS. The latencies of the antidromically driven units ranged from 1.2-2.8 msec and the calculated conduction velocity of the descending fibres was 29 plus or minus 5.2 m/sec. The possibility of involvement of these bulbo-spinal neurons in the inhibition of the preganglionic sympathetic neurons at the spinal cord level is discussed.
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Electrical stimulation within the medulla of cats revealed that myelinated primary afferent fibres of the sinus nerve terminated within the immediate vicinity of the tractus solitarius and its nucleus. 2. The activity of neurones within this area was also evoked on sinus nerve stimulation, although few (17%) were activated within a latency compatible with monosynaptic excitation. Additional projections over polysynaptic pathways have been shown to the parahypoglossal area and to the area of the nucleus ambiguus. 3. These three areas were shown to contain neurones whose activity was enhanced by stimulation of the baroreceptor endings of the ipsilateral carotid sinus. 4. No evidence for a projection of sinus nerve afferents to the medial reticular formation (an area extending medially from the hypoglossal nucleus and nerve tract and including the paramedian reticular nucleus) was obtained in either antidromic or orthodromic studies. 5. The organization of the central pathway of the carotid sinus baroreceptor reflex is discussed in the light of these results.
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