Chapter 21 Possible functions of transmitter-controlled plateau potentials in α motoneurones
References (35)
- et al.
Transmitter-controlled properties of α-motoneurones causing long-lasting motor discharge to brief excitatory inputs
Responses of neurons in isolated preparations of the mammalian central nervous system
Prog. Neurobiol.
(1986)- et al.
Serotonergic facilitation of facial motoneuron excitation
Brain Res.
(1979) - et al.
Serotonin-induced depolarization of rat facial motoneurons in vivo: Comparison with amino acid transmitters
Brain Res.
(1982) - et al.
Facilitation of spinal motoneurone excitability by 5-hydroxytryptamine and noradrenaline
Brain Res.
(1980) - et al.
Pharmacological antagonism of facilitatory but not inhibitory effects of serotonin and norepinephrine on excitability of spinal motoneurones
Neuropharmacology
(1983) - et al.
The time course of the disappearance of noradrenaline and 5-hydroxytryptamine in the spinal cord after transection
Acta Physiol. Scand.
(1964) - et al.
The brain nucleus locus coeruleus: restricted afferent control of a broad efferent network
Science
(1986) - et al.
Response of muscle spindle primary endings to static stretch in acute and chronic spinal cats
Am. J. Vet. Res.
(1980) - et al.
Plateau potentials in α-motoneurones induced by intravenous injection of L-DOPA and clonidine in the spinal cat
J. Physiol. (London)
(1988)
Tonic stretch reflexes and their dependence of polysynaptic excitation from muscle spindle Ia afferents
Maintained changes in motoneuronal excitability by short-lasting synaptic inputs in the decerebrate cat
J. Physiol. (London)
Central generation of locomotion in vertebrates
Bistable firing properties of soleus motor units in freely moving rats
Acta Physiol. Scand.
Bi-stable firing pattern of soleus motor units in rats during quiet standing
J. Physiol. (London)
Firing patterns of motor units in normal rats
Nature (London)
Cat hindlimb motoneurones during locomotion. II. Normal activity patterns
J. Neurophysiol.
Cited by (83)
Emergence of spiral and antispiral patterns and its CGLE analysis in leech-heart interneuron model with electromagnetic induction
2024, Applied Mathematical ModellingIncreased Axon Initial Segment Length Results in Increased Na<sup>+</sup> Currents in Spinal Motoneurones at Symptom Onset in the G127X SOD1 Mouse Model of Amyotrophic Lateral Sclerosis
2021, NeuroscienceCitation Excerpt :In models of spinal cord injury it is now well documented that hyperreflexia and spasticity appear as a consequence of increased motoneurone excitability in addition to local changes in spinal cord circuitry. This includes a reduction of inhibition (Norton et al., 2008), reductions in post-activation depression of excitatory Ia afferent synapses on motoneurones (Schindler-Ivens and Shields, 2000), increases in Na+ and Ca2+ PICs (Eken et al., 1989; Murray et al., 2010; Bellardita et al., 2017), and an upregulation or constitutive activity of serotonergic and noradrenergic receptors (Murray et al., 2010; Rank et al., 2011). Spasticity is also observed in SOD1 models of ALS (Dentel et al., 2013; Modol et al., 2014), and many of the changes observed following spinal cord injury have also been observed in SOD1 models, including the G127X.
Role of chloride cotransporters in the development of spasticity and neuropathic pain after spinal cord injury
2020, Neuronal Chloride Transporters in Health and DiseaseMotor Neuron Excitability Attenuation as a Sequel to Lumbosacral Manipulation in Subacute Low Back Pain Patients and Asymptomatic Adults: A Cross-Sectional H-Reflex Study
2018, Journal of Manipulative and Physiological TherapeuticsCitation Excerpt :However, using conditioning H-reflex protocols to measure changes in postactivation depression, reciprocal inhibition, presynaptic inhibition, and Renshaw cell inhibition within the Ia afferent-alpha motoneuron pathway may provide insights on neural adaptations that occur after SMT for patients with LBP.24,25 Reliable and valid cat models that are being used to study the effects of SM on afferent discharges may be extended to study the mechanistic relationship among bistability properties of motoneuron membranes, hypertonicity, and SM-like loads.19,36-39 Experimental models to induce and interrupt muscle cramps in humans may also provide insights on the mechanistic relationship among bistability properties of motoneuron membranes from motor unit discharge rates, hypertonicity, and HVLA SM.40-42
The time course of serotonin 2C receptor expression after spinal transection of rats: An immunohistochemical study
2013, NeuroscienceCitation Excerpt :The hyperreflexia, in the chronic phase, is characterized by exaggerated cutaneous reflexes and velocity-dependent stretch reflexes, also termed spasticity (Lance, 1980; Dietz, 2000; Nielsen et al., 2007). Experiments in cats (Eken et al., 1989) and rats (Bennett et al., 1999, 2001a,b; Li et al., 2004) have suggested that the appearance of plateau potentials generated by persistent inward currents (PICs) in motoneurons is one of the mechanisms underlying the hyperexcitability observed in the chronic spinal phase. In a rat model with a complete transection at sacral 2 (S2) level Bennett and colleagues have demonstrated that the magnitude of PICs in motoneurons below the lesion is increased and the motoneurons become 30-fold supersensitive to 5-HT or 5-HT2A/C receptor agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) (Harvey et al., 2006a; Li et al., 2007).
The time course of serotonin 2A receptor expression after spinal transection of rats: An immunohistochemical study
2011, NeuroscienceCitation Excerpt :In both cases the tonic/maintained discharge also seems to be dependent on the recruitment of plateau potentials in the motoneurons (Crone et al., 1988; Hounsgaard et al., 1988). The return of tonic stretch reflexes (and general hyper-reflexia) following a chronic spinal transection (>2 weeks) has been related to the return of plateau potentials in motoneurons–but now without the descending serotonergic innervation (see Eken et al., 1989; Bennett et al., 2001a,b). There may be several reasons for the return of plateau potentials and the development of a spastic syndrome.