Physiological Changes in Sympathetic Ganglia Infected With Pseudorabies Virus

Dempsher, John; Larrabee, Martin G.; Bang, Frederik B.; Bodian, David

doi:10.1152/ajplegacy.1955.182.1.203

Cited by 47 publications

(27 citation statements)

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“…Since this discharge does not occur in the chronically denervated ganglion, and since ChE is located on the presynaptic terminal of the ganglion (Koelle & Koelle, 1959), it has been suggested that the discharge is initiated by the action of ACh on the presynaptic terminals (Voile & Koelle, 1961;Koelle, 1961Koelle, , 1962. Periodic bursts of impulse discharge, generated presynaptically, occur in the sympathetic ganglia infected by pseudorabies virus (Dempsher, Larrabee, Bang & Bodian, 1955;Dempsher & Riker, 1957); this phenomenon is related to the prolonged depolarization of the presynaptic terminals (Dempsher & Zabara, 1960). In normal mammalian sympathetic ganglion, however, neither antidromic impulse discharges nor prolonged depolarization of the preganglionic nerve terminals have ever been recorded even when presynaptic stimulation was continued with the administration of anti-ChEs.…”

Section: Introductionmentioning

confidence: 99%

Cholinergic receptors at sympathetic preganglionic nerve terminals

Koketsu¹,

Nishi²

1968

The Journal of Physiology

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SUMMARY1. In the paravertebral sympathetic chain of bullfrogs, some part of the preganglionic nerve located within the ganglion was depolarized transiently when acetylcholine (ACh) was directly applied to the ganglion, particularly in the presence of an anticholinesterase (anti-ChE). The axonal part of the preganglionic nerve, on the other hand, showed no detectable depolarization following direct application of ACh (with anti-ChEs) to the interganglionic nerve trunk.2. The ACh depolarization was markedly depressed by nicotine, and less markedly by (+ )-tubocurarine, whereas it was not affected by atropine. Nicotine, similar to ACh, transiently depolarized only the intraganglionic portion of the presynaptic fibres.3. The action potentials, recorded from the axonal as well as the terminal parts of the preganglionic nerve, showed spike potentials followed by a marked negative after-potential. The negative after-potential was followed by a positive after-potential which was markedly enhanced by repetitive nerve stimulation.4. A slow negative potential followed the positive after-potential in the repetitive responses of the terminal parts of the preganglionic nerve. The slow negative potential was enhanced by anti-ChEs, eliminated by ACh and nicotine, and unaffected by atropine.5. The amplitude of the action potentials of the terminal parts of the preganglionic nerve, and particularly that of the negative after-potential, was significantly depressed during the development of ACh depolarization as well as the slow negative potential, indicating that the two types of slow depolarization originated in the intraganglionic portion of the presynaptic fibres, presumably somewhere near or at the nerve terminals.6. ACh depolarization similar to that observed with bullfrog sympathetic ganglia was observed with rat superior cervical ganglia. The present K. KOKETSU AND S. NISHI experiments provide evidence that a certain part of the preganglionic nerve terminals is depolarized by the action of the transmitter released from their endings.

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Section: Introductionmentioning

confidence: 99%

Cholinergic receptors at sympathetic preganglionic nerve terminals

Koketsu¹,

Nishi²

1968

The Journal of Physiology

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“…Similar results have been found in vivo, with neurons in the ganglia of PrVinfected mice showing a synchronous and cyclical calcium pattern 38 . This spontaneous and synchronous cyclic activity had already been reported decades ago in neuronal tissues infected by PrV virus 36,44,45 . Abnormal electrical activity is hypothesized to be the cause of the characteristic symptoms caused by alpha-herpesviruses i.e.…”

Section: ! "(+!supporting

confidence: 69%

“…The molecular pathways allowing for regrowth of C. elegans axons following injury have been studied extensively and are becoming well established [44][45][46] . In contrast, relatively few studies have focused…”

Section: Molecular Mediators Of Axonal Fusionmentioning

confidence: 99%

“…How EFF-1 is regulated, such that it mediates dendritic fusion during development but not following injury, is unclear, but may involve context-specific regulation. Just as the growth of an axon has different molecular regulators during development compared with regeneration 13,44,[56][57][58][59] , there may also be distinct mechanisms for regulating fusogens in these two contexts. In contrast, AFF-1 has not been reported to function during neuronal development, and may instead be activated by cellular responses unique to regeneration.…”

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Function and regulation of the fusogen EFF-1 during axonal repair

Linton¹

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In the current clinical environment, treatment options for nerve and spinal cord injuries remain limited. To develop novel therapies, we require a better understanding of axonal repair and its underlying molecular mechanisms. The response of an axon to a transection injury is complex: the axon still attached to the cell body begins a process of regenerative regrowth, whereas a concurrent process of degeneration is activated in the severed axonal fragment. Characterizing ways in which the axon can achieve repair, involving both regeneration and degeneration, is crucial to making progress in a clinical setting.We have studied a means of axonal repair called axonal fusion, which occurs spontaneously in the mechanosensory neurons of the nematode C. elegans. Following axotomy with a UV laser, the regrowing axonal fragment is able to directly fuse with its own severed fragment, re-establishing continuity. When axonal fusion was first described in C. elegans, the molecular pathways involved were unknown, and the only protein associated with the process was the fusogen Epithelial Fusion Failure-1 (EFF-1). EFF-1 is a nematode-specific transmembrane glycoprotein that acts to fuse plasma membranes. It has been studied extensively in other C. elegans tissues, but its function and regulation in neurons have been largely uncharacterized.In this context, we aimed to further understand the role of EFF-1 in axonal repair, focusing on its potential contribution to both regeneration and degeneration, and the mechanisms that regulate its fusogenic activity. We approached these biological questions using a combination of genetic and molecular biology techniques available in the C. elegans model system.The following chapters characterize EFF-1 function and regulation in the C. elegans mechanosensory neuron PLM. Firstly, we demonstrate a cell-autonomous role for EFF-1 in axonal fusion, and show that it has a dynamic localization pattern in the regenerating axon, whereby it is mobilized to the membrane of the regenerating growth cone. We also place it downstream in a pathway of apoptotic clearance molecules that allow recognition of the distal axonal fragment.Secondly, we find that neuronal EFF-1 is regulated by the endocytic GTPase RAB-5, with alterations in RAB-5 activity affecting both EFF-1 localization and its function in axonal fusion.Thirdly, we characterize the genes involved in the degeneration of the distal PLM axon following axotomy, and find a remarkable overlap with the molecules involved in regenerative fusion, possibly including EFF-1. Finally, we discuss an intriguing potential role for EFF-1 in mediating neuronal repair through cell-cell fusion. The research detailed here represents significant progress in understanding how a fusogen mediates axonal repair in vivo. It will potentially contribute to the application of axonal fusion as a novel therapy for patients with nerve injuries.ii Declaration by authorThis thesis is composed of my original work, and contains no material previously published or written by an...

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“…On the other hand, observations of the form of, and effect of drugs upon, the slow potential were carried out by means of Ag-AgCl electrodes, a low-gain direct-coupled pre-amplifier, and a single beam oscilloscope containing a high-gain direct-coupled amplifier. In both methods the excised preparation was maintained in a bathing solution (Dempsher et al 1955) equilibrated with a mixture of 95 % oxygen and 5 % CO2.…”

Section: Methodsmentioning

confidence: 99%

A study of presynaptic slow potentials in virus‐infected sympathetic ganglia of the rat

Dempsher¹,

Zabara²

1960

The Journal of Physiology

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In order to explain the occurrence of spontaneous impulses, originating in presynaptic nerve endings and discharged simultaneously and synchronously in pre-and post-ganglionic nerves of rat sympathetic ganglia infected with pseudo-rabies virus, the following working hypothesis was adopted. Spontaneous impulses originated in presynaptic nerve endings because the virus infection interfered with the normal action of an inhibiting system having its origin in the central nervous system (c.N.s.) and exerting its action upon the presynaptic nerve endings through the release of substances such as gamma aminobutyric acid, adrenaline, and noradrenaline. Interference with the normal action of the inhibitory system resulted in a spontaneous release of acetylcholine (ACh), which stimulated the presynaptic nerve endings to initiate the discharge of impulses in both nerves, antidromic in the preganglionic nerve, orthodromic in the postganglionic nerve (Dempsher, Larrabee, Bang & Bodian, 1955;Dempsher & Riker, 1957;Dempsher, Tokumaru & Zabara, 1959).An inherent weakness of the working concept presented above has been that, although based on experiments in which we used electrophysiological techniques, no electrical event had been described which could actually be located in the presynaptic nerve endings, the suggested site of interaction of excitatory and inhibitory systems. The purpose of this paper is to report experiments supporting the suggestion that the electrical event in the presynaptic nerve endings accompanying interaction of excitatory and inhibitory systems in virus-infected rat sympathetic ganglia is a slowly changing, decreasing potential change, the presynaptic slow potential. METHODS Preparation of the virus inoculum to infect the rat superior cervical ganglion was described in detail in previous publications (Tokumaru, 1957;Dempsher et al. 1959). Briefly, rat superior cervical ganglia were infected following intraocular inoculations of 005 ml. of undiluted suspension of L strain pseudo-rabies virus harvested from infected 14 PHYSIO. CLI

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Physiological Changes in Sympathetic Ganglia Infected With Pseudorabies Virus

Cited by 47 publications

References 0 publications

Cholinergic receptors at sympathetic preganglionic nerve terminals

Cholinergic receptors at sympathetic preganglionic nerve terminals

Function and regulation of the fusogen EFF-1 during axonal repair

A study of presynaptic slow potentials in virus‐infected sympathetic ganglia of the rat

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