Modifiability of spinal synapses.

Mendell, Lorne M.

doi:10.1152/physrev.1984.64.1.260

Cited by 254 publications

(99 citation statements)

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“…The effects of training or clonidine observed in this study can then be attributed to changes occurring in spinal pathways and not to an alteration in peripheral sensory events or muscle fibers. There is now growing evidence that reflex pathways are not "hard-wired" (Forssberg and Svartengren, 1983), and that they can display a certain level of plasticity in response to central or peripheral lesions or operant conditioning (Mendell, 1984;Durkovic, 1996;Wolpaw, 1997;Wolpaw and Tennissen, 2001). The recovery of stepping with treadmill training has been attributed solely to plasticity of the CPG (Lovely et al, 1986;Rossignol, 1996;Harkema, 2001).…”

Section: Discussionmentioning

confidence: 99%

Spinal Cats on the Treadmill: Changes in Load Pathways

2003

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Treadmill training and clonidine, an ␣-2 noradrenergic agonist, have been shown to improve locomotion after spinal cord injury. We speculate that transmission in load pathways, which are involved in body support during stance, is specifically modified by training. This was evaluated by comparing two groups of spinal cats; one group (n ϭ 11) was trained to walk until full-weight-bearing (3-4 weeks), and the other (shams; n ϭ 7) was not. During an acute experiment, changes in group I pathways, monosynaptic excitation, disynaptic inhibition, and polysynaptic excitation were investigated by measuring the response amplitude in extensor motoneurons before and after clonidine injection. Monosynaptic excitation was not modified by clonidine but was decreased significantly by training. Disynaptic inhibition was significantly decreased by clonidine in both groups, but more significantly in trained cats, and significantly reduced by training after clonidine. Also, clonidine could reverse group IB inhibition into polysynaptic excitation in both groups but more frequently in trained cats. We also investigated whether fictive stepping revealed additional changes. In trained cats, the phase-dependent modulation of all three responses was similar to patterns reported previously, but in shams, modulation of monosynaptic and polysynaptic responses was not. Overall, training appears to decrease monosynaptic excitation and enhance the effects of clonidine in the reduction of disynaptic inhibition and reversal to polysynaptic excitation. Because it is believed that polysynaptic excitatory group I pathways transmit locomotor drive to extensor motoneurons, we suggest that the latter changes would facilitate the recruitment of extensor muscles for recovering weight-bearing during stepping.

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Section: Discussionmentioning

confidence: 99%

Spinal Cats on the Treadmill: Changes in Load Pathways

2003

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“…20 On the basis of clinical observations a widely accepted conclusion was drawn for the pathophysiology of spasticity such that exaggerated re¯exes are responsible for the observed muscle hypertonia, and therefore the movement disorder. Hyper¯exia is due to the neuronal reorganisation which occurs following central lesions in both cat 21 and man. 22 Novel connections may cause changes in the strength of re¯ex excitability.…”

Section: Clinical Spasticitymentioning

confidence: 99%

“…In addition, supersensitivity caused by the denervation may occur. 21 Although recent observations have indicated that central nervous lesions do not cause sprouting of primary a erents in either cat 23 or man, 24 changes in the reduction of pre-synaptic inhibition of group Ia ®bres occur 25 which correlate with the enhanced excitability of tendon tap re¯exes. In addition, reduction of pre-synaptic inhibition of group Ia a erents is stronger in patients with paraplegia compared to those with hemiplegia.…”

Section: Clinical Spasticitymentioning

confidence: 99%

Spastic movement disorder

Dietz¹

2000

Spinal Cord

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This review deals with the neuronal mechanisms underlying spastic movement disorder, assessed by electrophysiological means with the aim of ®rst, a better understanding of the underlying pathophysiology and second, the selection of an adequate treatment. For the patient usually one of the ®rst symptoms of a lesion within the central motor system represents the movement disorder, which is most characteristic during locomotion in patients with spasticity. The clinical examination reveals exaggerated tendon tap re¯exes and increased muscle tone typical of the spastic movement disorder. However, today we know that there exists only a weak relationship between the physical signs obtained during the clinical examination in a passive motor condition and the impaired neuronal mechanisms being in operation during an active movement. By the recording and analysis of electrophysiological and biomechanical parameters during a functional movement such as locomotion, the signi®cance of, for example, impaired re¯ex behaviour or pathophysiology of muscle tone and its contribution to the movement disorder can reliably be assessed. Consequently, an adequate treatment should not be restricted to the cosmetic therapy and correction of an isolated clinical parameter but should be based on the pathophysiology and signi®cance of the mechanisms underlying the disorder of functional movement which impairs the patient. Spinal Cord (2000) 38, 389 ± 393

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“…During early postnatal life, synaptic refinements are well known to occur in the central (Hubel and Wiesel, 1965;Mendell, 1984;Fregnac et al, 1988;Reiter and Stryker, 1988;Constantine-Paton et al, 1990) and peripheral (Redfern, 1970;Ridge and Betz, 1984;Dan and Poo, 1992;Balice-Gorden and Lichtman, 1994;Colman et al, 1997) nervous systems. This synaptic remodeling serves to refine initial coarse-grained and exuberant neuronal connections and results in formation of highly tuned neural circuits (Purves and Lichtman, 1985;Goodman and Shatz, 1993).…”

Section: Abstract: Synaptic Plasticity; Developmental Synaptic Deprementioning

confidence: 99%

“…A few weeks after birth, this segmental reflex begins to disappear and is replaced by the newly developed spinobulbospinal reflex as the principal mechanism for excretion (de Groat, 1975;Fukuda et al, 1981;Kruse and de Groat, 1990;de Groat et al, 1993). This is also a critical period for the establishment of synaptic refinements (Purves and Lichtman, 1985) as well as for the functional maturation of descending pathways to the spinal cord (Gilbert and Stelzner, 1979;Mendell, 1984). Because the neuronal connections at developing synapses appear to be refined by competition between multiple synaptic inputs converging on the same target cell (Purves and Lichtman, 1985;Goodman and Shatz, 1993), it is possible that the segmental autonomic pathway operating in the early postnatal life is suppressed by competition with the descending projection from the brain for synaptic connections to parasympathetic preganglionic neurons (PGNs).…”

mentioning

confidence: 99%

Developmental Synaptic Depression Underlying Reorganization of Visceral Reflex Pathways in the Spinal Cord

Araki

Groat

1997

J. Neurosci.

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During development, neuronal connectivity has a remarkable plasticity. Synaptic refinement in the spinal autonomic nucleus might be involved in the elimination of primitive segmental reflexes and the emergence of mature spinobulbospinal reflexes, which occurs a few weeks after birth. To address this possibility, we examined the postnatal changes of segmental excitatory synaptic transmission by applying the whole-cell recording technique to parasympathetic preganglionic neurons in slice preparations of the rat lumbosacral spinal cord. The mean magnitude of unitary excitatory synaptic currents evoked in preganglionic neurons by stimulation of single interneurons remained unchanged during the first two postnatal weeks but was reduced by 50% during the third postnatal week. This reduction in synaptic efficacy was associated with a decrease in the amount of transmitter release from interneurons. Moreover, this developmental depression of segmental synaptic transmission was prevented by spinal cord transection at the thoracic level on postnatal day 14. Thus, developmental modification of excitatory synapses on preganglionic neurons appears to be attributable to competition between segmental interneuronal and descending bulbospinal inputs, which results in the developmental reorganization of parasympathetic excretory reflex pathways. Key words: synaptic plasticity; developmental synaptic depression; glutamatergic excitatory synaptic currents; spinal autonomic nucleus; parasympathetic preganglionic neurons; micturition reflex; chronic spinal transection; quantal analysisDuring early postnatal life, synaptic refinements are well known to occur in the central (Hubel and Wiesel, 1965;Mendell, 1984;Fregnac et al., 1988;Reiter and Stryker, 1988;Constantine-Paton et al., 1990) and peripheral (Redfern, 1970;Ridge and Betz, 1984;Dan and Poo, 1992;Balice-Gorden and Lichtman, 1994;Colman et al., 1997) nervous systems. This synaptic remodeling serves to refine initial coarse-grained and exuberant neuronal connections and results in formation of highly tuned neural circuits (Purves and Lichtman, 1985;Goodman and Shatz, 1993). In spinal autonomic reflex pathways, synaptic refinement could be involved in the elimination of primitive segmental reflexes and the emergence of mature reflex patterns. In neonates of many species, excretory f unctions (micturition and defecation) are mediated exclusively by the segmental parasympathetic reflex pathway, which is activated when the mother licks the perineum of the neonate (Beach, 1966;de Groat et al., 1975;Thor et al., 1989). A few weeks after birth, this segmental reflex begins to disappear and is replaced by the newly developed spinobulbospinal reflex as the principal mechanism for excretion (de Groat, 1975;Fukuda et al., 1981;Kruse and de Groat, 1990;de Groat et al., 1993). This is also a critical period for the establishment of synaptic refinements (Purves and Lichtman, 1985) as well as for the functional maturation of descending pathways to the spinal cord (Gilbert and Stelzner, 1979;Men...

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Modifiability of spinal synapses.

Cited by 254 publications

References 0 publications

Spinal Cats on the Treadmill: Changes in Load Pathways

Spinal Cats on the Treadmill: Changes in Load Pathways

Spastic movement disorder

Developmental Synaptic Depression Underlying Reorganization of Visceral Reflex Pathways in the Spinal Cord

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