Disuse enhances synaptic efficacy in spinal mononeurones.

Gallego, Roberto; Kuno, Motoý; Núñez, Rosa; Snider, William D.

doi:10.1113/jphysiol.1979.sp012807

Cited by 91 publications

(76 citation statements)

References 40 publications

(51 reference statements)

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“…Since a similar decrease occurs even in the heteronymous motoneurones whose axons are left intact (Eccles et al 1959;Gallego et al 1979), these changes cannot be attributed to the effects of axotomy of the motoneurones. It has been suggested that decreased synaptic transmission following section of the peripheral nerve is due to the deprivation of impulse activity (disuse) in the sensory pathway (Eccles et al 1959; also, see Eccles & McIntyre, 1953).…”

Section: Introductionmentioning

confidence: 90%

“…The procedures used for recording monosynaptic e.p.s.p.s from motoneurones have been described in detail elsewhere (Gallego et al 1979). Briefly, after a lumbosacral laminectomy intracellular recordings from motoneurones were made with glass micro-electrodes filled with 2 M-potassium acetate.…”

Section: Methodsmentioning

confidence: 99%

“…It has been suggested that decreased synaptic transmission following section of the peripheral nerve is due to the deprivation of impulse activity (disuse) in the sensory pathway (Eccles et al 1959; also, see Eccles & McIntyre, 1953). However, daily stimulation of the central end of the cut sensory fibres cannot prevent the decrease in central synaptic efficacy (Gallego et al 1979). Furthermore, chronic conduction block of an intact peripheral nerve with tetrodotoxin causes an increase, rather than a decrease, in synaptic efficacy (Gallego et al 1979).…”

Section: Introductionmentioning

confidence: 99%

“…However, daily stimulation of the central end of the cut sensory fibres cannot prevent the decrease in central synaptic efficacy (Gallego et al 1979). Furthermore, chronic conduction block of an intact peripheral nerve with tetrodotoxin causes an increase, rather than a decrease, in synaptic efficacy (Gallego et al 1979). The normal function of motoneurone synapses formed by primary afferent fibres thus appears to rely on at least two distinct factors: (1) the axonal continuity of the sensory fibres, interruption of which causes central synaptic depression, and (2) the presence of sensory impulse activity, elimination of which results in synaptic enhancement.…”

Section: Introductionmentioning

confidence: 99%

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Enhancement of synaptic function in cat motoneurones during peripheral sensory regeneration

Gallego

Kuno

Núñez

et al. 1980

The Journal of Physiology

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SUMMARY1. Monosynaptic excitatory post-synaptic potentials (e.p.s.p.s) were recorded from medial (m.g.) and lateral gastrocnemius (1.g.) motoneurones in the cat 2-30 weeks after crushing the m.g. nerve.2. The mean amplitudes of homonymous and heteronymous e.p.s.p.s evoked from the m.g. nerve were initially depressed (2-3 weeks after injury) and subsequently reached levels greater than normal for a period (8-12 weeks) before slowly declining to about 70 % of the normal values (by week 30).3. Monosynaptic e.p.s.p.s evoked in m.g. motoneurones from the intact 1.g. nerve showed neither initial depression nor subsequent alterations following crush of the m.g. nerve.4. By the eighth week after nerve crush, about 70 % of Group I and Group II sensory fibres in the m.g. nerve responded to muscle stretch, about 15 % had regenerated into the muscle but did not respond to muscle stretch, and the remainder failed to regenerate across' the neuroma formed by the nerve crush.5. Homonymous, monosynaptic e.p.s.p.s produced by impulses in single sensory fibres responding to stretch of the m.g. muscle were recorded 8 weeks after crush of the m.g. nerve. Their amplitude distribution was indistinguishable from that obtained in normal, unoperated cats. Thus, there was no evidence that functionally reinnervated sensory fibres are responsible for the enhanced phase of composite e.p.s.p.s observed during peripheral regeneration.6. When the m.g. nerve had been sectioned and prevented from regenerating into the muscle for 8 weeks, the amplitudes of homonymous and heteronymous e.p.s.p.s evoked from the m.g. nerve were significantly smaller than those observed in control animals. Thus, there was no evidence that non-regenerating sensory fibres are responsible for the enhanced phase of composite e.p.s.p.s after nerve crush.7. It is suggested that the sensory fibres responsible for abnormally large composite e.p.s.p.s following nerve crush are those that regenerate into the muscle but do not achieve functional reinnervation. This possibility is discussed in relation to the increase in central synaptic efficacy observed after prolonged disuse of the sensory pathway.

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Section: Introductionmentioning

confidence: 90%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Enhancement of synaptic function in cat motoneurones during peripheral sensory regeneration

Gallego

Kuno

Núñez

et al. 1980

The Journal of Physiology

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“…Similar to nerve crush, chronic tetrodotoxin blockade of AP conduction in peripheral nerves reduces or elim-inates impulse invasion of IA synapses and enlarges EPSPs at IA-MN synapses (Gallego et al, 1979;Manabe et al, 1989;Webb and Cope, 1992). These observations led Kuno (1995) and coworkers to hypothesize that synapses can be strengthened by presynaptic "disuse."…”

Section: Introductionmentioning

confidence: 98%

Enhanced Transmission at a Spinal Synapse TriggeredIn Vivoby an Injury Signal Independent of Altered Synaptic Activity

Bichler¹,

Nakanishi²,

Wang³

et al. 2007

J. Neurosci.

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Peripheral nerve crush initiates a robust increase in transmission strength at spinal synapses made by axotomized group IA primary sensory neurons. To study the injury signal that initiates synaptic enhancement in vivo, we designed experiments to manipulate the enlargement of EPSPs produced in spinal motoneurons (MNs) by IA afferents 3 d after nerve crush in anesthetized adult rats. If nerve crush initiates IA EPSP enlargement as proposed by reducing impulse-evoked transmission in crushed IA afferents, then restoring synaptic activity should eliminate enlargement. Daily electrical stimulation of the nerve proximal to the crush site did, in fact, eliminate enlargement but was, surprisingly, just as effective when the action potentials evoked in crushed afferents were prevented from propagating into the spinal cord. Consistent with its independence from altered synaptic activity, we found that IA EPSP enlargement was also eliminated by colchicine blockade of axon transport in the crushed nerve. Together with the observation that colchicine treatment of intact nerves had no short-term effect on IA EPSPs, we conclude that enhancement of IA-MN transmission is initiated by some yet to be identified positive injury signal generated independent of altered synaptic activity. The results establish a new set of criteria that constrain candidate signaling molecules in vivo to ones that develop quickly at the peripheral injury site, move centrally by axon transport, and initiate enhanced transmission at the central synapses of crushed primary sensory afferents through a mechanism that can be modulated by action potential activity restricted to the axons of crushed afferents.

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Neuromuscular propagation after fatiguing contractions of the paralyzed soleus muscle in humans

1998

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Disuse enhances synaptic efficacy in spinal mononeurones.

Cited by 91 publications

References 40 publications

Enhancement of synaptic function in cat motoneurones during peripheral sensory regeneration

Enhancement of synaptic function in cat motoneurones during peripheral sensory regeneration

Enhanced Transmission at a Spinal Synapse TriggeredIn Vivoby an Injury Signal Independent of Altered Synaptic Activity

Neuromuscular propagation after fatiguing contractions of the paralyzed soleus muscle in humans

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