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Biomedical subjects

M Devor

Publications and source records attributed to M Devor.

At least 91 records · Page 5Linked to original sources
PubMed1983

Sensory afferent impulses originate from dorsal root ganglia as well as from the periphery in normal and nerve injured rats.

Single units were recorded in dorsal roots or in the sciatic nerve of anaesthetised rats. It was shown by making sections, by stimulation and by collision that some ongoing nerve impulses were originating from the dorsal root ganglia and not from the central or peripheral ends of the axons. In a sample of 2731 intact or acutely sectioned myelinated sensory fibres, 4.75% +/- 3.7% contained impulses generated within the dorsal root ganglia. In 2555 axons sectioned in the periphery 2-109 days before, this percentage rose to 8.6% +/- 4.8%. There was a considerable variation between animals; 0-14% in intact and acutely sectioned nerves and 1-21% in chronically sectioned nerves. The conduction velocity of the active fibres did not differ significantly from the conduction velocity of unselected fibres. The common pattern of ongoing activity from the ganglion was irregular and with a low frequency (about 4 Hz) in contrast to the pattern of impulses originating in a neuroma which usually have a higher frequency with regular intervals. Slight mechanical pressure on the dorsal root ganglion increased the frequency of impulses. Unmyelinated fibres were also found to contain impulses originating in the dorsal root ganglion. In intact or acutely sectioned unmyelinated axons, the percentage of active fibres 4.4% +/- 3.5% was approximately the same as in myelinated fibres but there were no signs of an increase following chronic section. Fine filament dissection of dorsal roots and of peripheral nerves and collision experiments showed that impulses originating in dorsal root ganglia were propagated both orthodromically into the root and antidromically into the peripheral nerve. It was also shown that the same axon could contain two different alternating sites of origin of nerve impulses: one in the neuroma or sensory ending and one in the ganglion. These observations suggest that the dorsal root ganglion with its ongoing activity and mechanical sensitivity could be a source of pain producing impulses and could particularly contribute to pain in those conditions of peripheral nerve damage where pain persists after peripheral anaesthesia or where vertebral manipulation is painful.

Afferent Pathways↗
PubMed1983

Autotomy after nerve injury and its relation to spontaneous discharge originating in nerve-end neuromas.

Following transection and ligation of the sciatic and saphenous nerves, rodents frequently scratch and bite their anesthetic foot (autotomy). Many authors have suggested that autotomy is related to uncomfortable paresthesias induced by abnormal afferent discharge known to be generated in myelinated afferents in nerve-end neuromas. We report that preventing the development of ectopic neuroma discharge in rats by treating the severed nerves with colchicine or vinblastine does not prevent, or even detectably reduce, autotomy directed toward the denervated hindlimb. We conclude that abnormal discharge in myelinated afferents is not necessary for the expression of autotomy following nerve injury in rats.

Animals↗
PubMed1981

Collateral reinnervation of rat hindlimb skin does not depend on repeated sensory testing.

After cutaneous nerve injury there is a tendency for afferents in neighboring cutaneous nerves to reinnervate the adjacent denervated zone. Diamond and collaborators have recently claimed [5,8] that collateral sprouting of cutaneous afferents in the hindquarter of adult mammals is substantially accelerated by sensory testing (pinching) of the skin. We examined this claim in hindlimb skin of adult rats. All but the most medial part of the foot was rendered anesthetic by ligation and section of the sciatic nerve. The return of mechanosensation by functional spread of the intact saphenous nerve was examined behaviorally. We were unable to detect any effect of repeated sensory testing on the sensory recovery.

Animals↗
PubMed1981

Effect of peripheral nerve injury on receptive fields of cells in the cat spinal cord.

When the sciatic and saphenous nerves are cut and ligated in adult cats, the immediate effect is the production of a completely anesthetic foot and a region in medial lumbar dorsal horn where almost all cells have lost their natural receptive fields (RFs). Beginning at about 1 week and maturing by 4 weeks, some 40% of cells in the medial dorsal horn gain a novel RF on proximal skin, that is, upper and lower leg, thigh, lower back, or perineum. This new RF is supplied by intact proximal nerves and not by sciatic and saphenous nerve fibers that sprouted in the periphery. During the period of switching of RFs from distal to proximal skin there was no gross atrophy of dorsal horn grey matter and no Fink-Heimer stainable degeneration of central arbors and terminals of peripherally axotomized afferents. In intact animals medial dorsal horn cells showed no sign of response to mechanical stimulation of proximal skin. RFs of some of the cells had spontaneous variations in size and sensitivity, but these were not nearly sufficient to explain the large shifts observed after chronic nerve section. Tetanic electrical stimulation of skin or peripheral nerves often caused RFs to shrink, but never to expand. Although natural stimuli of proximal skin would not excite medial dorsal horn cells in intact or acutely deafferented animals, it was found that electrical stimulation of proximal nerves did excite many of these cells, often at short latencies. In the discussion we justify our working hypothesis that the appearance of novel RFs is due to the strengthening or unmasking of normally present but ineffective afferent terminals, rather than to long-distance sprouting of new afferent arbors within the spinal cord.

Afferent Pathways↗
PubMed1981

Activation of myelinated afferents ending in a neuroma by stimulation of the sympathetic supply in the rat.

The sciatic nerve in rats was cut and ligated, and 5-18 days later pathophysiological properties of the resulting neuroma were studied. We found that afferent fibers ending in the neuroma produced prolonged discharges following repetitive stimulation of the lumbar sympathetic trunk (LST) or i.v. adrenaline. Mean latencies of activation of afferent fibers were 10 +/- 2.1 sec and 12 +/- 3.4 sec (mean +/- S.D.) to LST stimulation and to adrenaline injection, respectively. The alpha-adrenergic antagonist phentolamine blocked responses to LST stimulation and adrenaline. The beta-adrenergic antagonist propranolol had no effect.

Afferent Pathways↗
PubMed1981

The effect of peripheral nerve injury on dorsal root potentials and on transmission of afferent signals into the spinal cord.

The sciatic nerve of adult rats was either cut and ligated or was crushed on one side. The response of the spinal cord to stimulation of the proximal part of the injured nerve was examined at various times after the lesion and compared to the effects of stimulating the intact nerve on the other side. During the first 10 days after nerve section the following measures were not affected: (i) the size of the input volley (compound action potential, CAP, measured on a dorsal root that carried sciatic nerve afferents (L5); (ii) the volley running in the dorsal columns; (iii) the dorsal root potential (DRP) evoked on neighbouring dorsal roots which do not contain sciatic afferents (L2 and L3); (iv) the post-synaptic volleys ascending in the spinal cord. However, by the fourth day after nerve section, there was a decrease of the DRP evoked on the ipsilateral L5 dorsal root by stimulation of the cut nerve. By 10 days this DRP had decreased by 50%. There was also a decrease in the DRP on the L5 root evoked by stimulation of the contralateral intact nerve. Crush lesions of the sciatic nerve did not produce DRP change. Beginning 10--20 days after nerve cut, there was a decrease in the amplitude of the afferent CAP and of all the measures of central response to the afferent volley. We discuss the possibility that the loss of the DRP may be associated with a disinhibition which results in novel receptive fields which we observe in cord cells deafferented by the peripheral nerve section. The decrease of DRP and the appearance of novel receptive fields do not occur if the peripheral nerve is crushed rather than cut.

Afferent Pathways↗
PubMed1981

Plasticity in the spinal cord sensory map following peripheral nerve injury in rats.

The medial part of the L4 and 5 dorsal horn in adult rats is dominated by afferents from the toes and foot. After transection of the sciatic and saphenous nerves, virtually all cells in this region are left without any peripheral receptive field. Beginning 4 to 5 days after nerve section, however, many peripherally deafferented cells take on a novel receptive field on the thigh, lower back, or perineum. The new receptive fields are served by intact nerves ending in proximal skin rather than by misdirected sprouts of cut toe-foot nerves. Thus, peripheral axotomy results in synaptic reorganization in the spinal cord proper. Receptive field reorganization occurs after nerve transection, ligation, or ligation with distal transection but does not occur if the nerve is crushed. If a cut nerve is sutured and regeneration is permitted, spinal reorganization is reversed and the toe-foot afferents regain exclusive dominance of the medial dorsal horn.

Afferent Pathways↗
PubMed1980

Mapping and plasticity of acid phosphatase afferents in the rat dorsal horn.

After peripheral nerve injury in rats, naturally occurring fluoride resistant acid phosphatase (FRAP) disappears from the substantia gelatinosa in that part of the dorsal horn in which the injured nerve afferents terminate. We have taken advantage of this fact to establish the spinal distribution of nerves innervating the skin of the hindlimb. The spinal map of the foot, the distal part of the lower lumbar dermatomes, is in the medial part of the substantia gelatinosa. More proximal skin of the thigh and lower back maps laterally. The zone of disappearance of FRAP after sciatic nerve section did not shrink detectably within the first few months after injury, provided that regeneration of the nerve was prevented. After one year, however, central FRAP activity was at least partially restored. Secondary transection of the sciatic nerve eliminated the new enzyme and transection of neighboring nerves failed to do so. The restored FRAP activity therefore reflects renewed synthesis and transport of enzyme in still injured neurons, and not central sprouting of intact neighboring afferents.

Acid Phosphatase↗
PubMed1979

Two modes of cutaneous reinnervation following peripheral nerve injury.

The return of sensation to the foot following sciatic nerve crush injury was analyzed behaviorally and electrophysiologically in the rat. Functional recovery begins within four days. Its early phase is accounted for by expansion of the functional distribution of intact neighboring fibers of the saphenous n. It occurs even if the sciatic n. is ligated, and it disappears with section of the saphenous n. Accompanying this functional expansion we began to encounter in electrophysiological recordings from the saphenous n., fibers with unusually large receptive fields (RF's) extending onto the plantar surface of the foot, well beyond their limits in intact rats. All of the expanded RF's were high threshold mechanoreceptors. On about the twentieth day after crushing, the regenerating sciatic n. began to make a functional contribution. This was seen by return of sensation to zones not invaded by the saphenous n. and by the onset of sensation in rats in which the saphenous n. had previously been ligated. With return of the sciatic n. the expanded distribution of the saphenous n. went back to its original boundaries. Correspondingly, we could no longer find expanded saphenous n. RF's. We conclude that cutaneous reinnervation begins with the collateral expansion of high threshold afferents from intact neighboring nerves. This alien innervation is later replaced upon regeneration of the original nerve.

Animals↗
PubMed1979

Autotomy following peripheral nerve lesions: experimental anaesthesia dolorosa.

(1) When hindlimb peripheral nerves are cut across in rats and mice, there is a tendency for the animal to attack the anaesthetic limb. We have called this attack "autotomy". In this paper we describe the time course and degree of autotomy following various types of nerve injury. (2) Four different types of lesion were applied to the sciatic nerve of rats. The most serious autotomy was produced by section of the nerve and encapsulation of its cut end in a polythene tube. Section followed by immediate resuturing also produced serious autotomy. Simple ligation of the nerve end was followed by less autotomy than encapsulation or cut and resuture. A crush lesion caused only minimal attack. (3) Section of the saphenous branch of the femoral nerve produced no autotomy. However, if the saphenous and sciatic nerves were ligated at the same time so that the entire foot became anaesthetic there was a great increase of autotomy over that seen when the sciatic nerve alone was ligated. This increase with the double lesion occurred even if the saphenous nerve was ligated more than 100 days after the sciatic nerve had been cut. (4) Mice showed autotomy very similar to that seen in rats but the onset was somewhat faster. (5) Reasons are given to propose that autotomy is triggered by an abnormal afferent barrage generated in the cut end of the nerve. Autotomy from peripheral nerve lesions is a different phenomenon from that seen after dorsal root section. Autotomy occurs under conditions which produce anaesthesia dolorosa in man. This simple model may be suitable for studies of the prevention of irritations originating from chronic lesions of peripheral nerves.

Animals↗