Effects of axotomy on the distribution of passive electrical properties of cat motoneurones.

Gustafsson, Bengt; Pinter, Martin J.

doi:10.1113/jphysiol.1984.sp015474

Cited by 53 publications

(25 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A lowering of the somadendritic threshold has been noted by several investigators (4, 5, 7), indicating a possible increase in the density of Na+ channels in the somatic membrane. Although a significant reduction in current is needed to fire motoneurons after axotomy (7), as we have also observed, at least part of this reduction is the result of an increase in motoneuron-input resistance (24,25), again confirmed by us. However, there is additional evidence supporting the idea that partial spikes are part of a more general phenomenon, that new Na+ channels are incorporated into somatic as well as remote dendritic membranes following axotomy.…”

Section: Resultssupporting

confidence: 69%

Sodium-dependent regenerative responses in dendrites of axotomized motoneurons in the cat.

Sernagor¹,

Yarom²,

Werman³

1986

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Ten days after extradural axotomy, partial spikes are found in >20% of cat L7 motoneurons, while 15-21 days after axotomy the incidence increases to 60%. These responses are produced in excitable (hot) spots in the dendrites by synaptic excitation. Intracellular injection of a lidocaine derivative and effective blocker of Na+ channels from within neurons, results in elimination of partial spikes before blocking somadendritic spikes. Partial spikes appear rather abruptly '.10 days after axotomy in our hands, are present in 23.6% of 106 neurons 10-14 days after axotomy, and the incidence more than doubles to 60.0% of 90 neurons 15-21 days after axotomy. Initially, a number of experiments were carried out in Abbreviations: EPSP, excitatory postsynaptic potential; PBST, posterior biceps-semitendinosus; LGS, lateral gastrocnemiussoleus; MG, medial gastrocnemius. 7966The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

show abstract

Section: Resultssupporting

confidence: 69%

Sodium-dependent regenerative responses in dendrites of axotomized motoneurons in the cat.

Sernagor¹,

Yarom²,

Werman³

1986

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Peripheral nerve lesions are known to induce several morphological (16), biochemical (20)(21)(22)(23), and physiological (17)(18)(19) changes in a-motoneurons. The alterations in a-motoneuron physiological properties seen after sciatic nerve lesions are known to be reversible upon target reinnervation (33)(34)(35) and have been ascribed primarily to the loss of functional contact with the muscular targets, since they can be reproduced by the intramuscular administration of botulinum toxin (36) and are not prevented by chronic electric stimulation (37).…”

Section: Discussionmentioning

confidence: 99%

“…After peripheral nerve lesions, motoneurons undergo complex morphological (16), physiological (17)(18)(19), and biochemical (20)(21)(22)(23)) changes. We have tested whether the presumptive Renshaw neurons might respond to peripheral nerve injuries by modulating their calbindin-expression as a result of the reduced motoneuronal activity and the consequent reduced need for Ca2+-buffering power.…”

mentioning

confidence: 99%

Presumptive Renshaw cells contain decreased calbindin during recovery from sciatic nerve lesions.

Sanna

Celio²,

Bloom³

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

A subpopulation of calbindin-immunoreactive neurons in lamnina VII of the spinal cord has been identified by its location as Renshaw cells, the anatomical substrate for recurrent inhibition. The expression of calbindin (28 kDa) in these calbindin-containing rat ventral horn interneurons was studied with immunocytochemistry after sciatic nerve injuries.One week after axotomy calbindin immunoreactivity was strongly reduced on the lesioned side between levels L4 and L6, while calbindin-containing neurons and fibers were still numerous contralateraily and cranially to the lesioned levels. Low-affinity nerve growth factor receptor (LNGFR) immunoreactivity was used as marker for peripherally lesioned a-motoneurons, since previous studies showed that motoneurons express LNGFR during regeneration after sciatic nerve injuries (22, 24). MATERIALS AND METHODSSciatic Nerve Lesions. For this study, six female SpragueDawley rats weighing 200-220 g were anesthetized intraperitoneally with a mixture of ketamine, acepromazine, and xylazine, and their right sciatic nerve was crushed with forceps at the mid-thigh level three times for 5 sec and left in place. Six other animals received a sciatic nerve cut with removal ofa 2-cm segment to prevent reconnection ofthe two stumps. Six sham-operated rats were used as controls. Three further rats received an intramuscular injection of 5 ng of botulinum toxin A (Sigma) in 5 ,u of saline in the right tibialis anterior muscle. Three control rats received an injection of saline. Four normal unperturbed rats were also used.Immunohistochemistry. Rats were deeply anesthetized and perfused intracardially with ice-cold heparinized 0.1 M phosphate buffer (pH 7.4) followed by 250 ml of ice-cold 4% paraformaldehyde in phosphate buffer.Spinal cords were treated as described (24). Briefly, the spinal cord was removed after laminectomy, anchored to a dental wax sheet to prevent curvature or distortions, and postfixed in 4% paraformaldehyde in phosphate buffer for 16 hr at 4°C. The spinal cords were then rinsed in phosphate buffer for 24 hr and cryoprotected in 10% and 30% sucrose in phosphate buffer for 24 hr each. Prior to sectioning, the spinal cords were divided under the dissecting microscope into three segments by cuts across the dorsal roots at C8 and T10; in the present study, only the caudal segment was analyzed. The dorsal root entry zone on the right side of Li was marked with a small cut for orientation. The spinal cord segments were then sectioned on a freezing microtome, and individual sections (40 ,um) were collected and stored at 4°C in Millonig's buffer until immunocytochemistry.Sections were incubated free floating at room temperature in 0.1 M Tris (pH 7.4) containing 1.4% NaCl and 10%o (vol/vol) heat-inactivated horse serum (Tris-serum) for 30 min. The sections were then treated in Tris-serum with a mouse anti-calbindin monoclonal antibody (25) used at a dilution of 1:6000 overnight or with the mouse anti-LNGFR monoclonal antibody (26) 192-IgG used at 5 ug/ml for 30 hr. LNGFR...

show abstract

“…Carlson et al, 1979) but undergo several changes that, in some respects, result in motor neurons resuming an immature phenotype (for review, see Titmus and Faber, 1990). These include changes in gene expression, particularly of genes encoding metabolic and cytoskeletal proteins, remodeling of dendritic branches, removal of some synaptic inputs, and changes in passive and active membrane electrical properties (Gustafsson and Pinter, 1984;Pinter and Vanden Noven, 1989;Koliatsos et al, 1990;Funakoshi et al, 1993;Wu, 1996). It was thus of interest to determine whether gap junctional coupling, widespread among developing motor neurons, was also reestablished among axotomized adult motor neurons.…”

mentioning

confidence: 99%

Nerve Injury Induces Gap Junctional Coupling among Axotomized Adult Motor Neurons

et al. 2000

View full text Add to dashboard Cite

Neonatal spinal motor neurons are electrically and dye-coupled by gap junctions, but coupling is transient and disappears rapidly after birth. Here we report that adult motor neurons become recoupled by gap junctions after peripheral nerve injury. One and 4-6 weeks after nerve cut, clusters of dyecoupled motor neurons were observed among axotomized, but not control, lumbar spinal motor neurons in adult cats. Electrical coupling was not apparent, probably because of the electrotonic distance between dendrodendritic gap junctions and the somatic recording location. Analyses of gap junction protein expression in cat and rat showed that the repertoire of connexins expressed by normal adult motor neurons, Cx36, Cx37, Cx40, Cx43, and Cx45, was unchanged after axotomy. Our results suggest that the reestablishment of gap junctional coupling among axotomized adult motor neurons may occur by modulation of existing gap junction proteins that are constitutively expressed by motor neurons. After injury, interneuronal gap junctional coupling may mediate signaling that maintains the viability of axotomized motor neurons until synaptic connections are reestablished within their targets.

show abstract

Effects of axotomy on the distribution of passive electrical properties of cat motoneurones.

Cited by 53 publications

References 21 publications

Sodium-dependent regenerative responses in dendrites of axotomized motoneurons in the cat.

Sodium-dependent regenerative responses in dendrites of axotomized motoneurons in the cat.

Presumptive Renshaw cells contain decreased calbindin during recovery from sciatic nerve lesions.

Nerve Injury Induces Gap Junctional Coupling among Axotomized Adult Motor Neurons

Contact Info

Product

Resources

About