Suppression of abnormally increased excitability of monosynaptic spinal reflex arcs by riluzole |
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Authors: | E A Makii A G Rodinskii |
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Institution: | (1) Ministry of Public Health of Ukraine, Dnepropetrovsk State Medical Academy, Ukraine |
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Abstract: | We studied the effects of a neuroprotector, riluzole, on the evoked mass activity of spinal neuronal mechanisms and on action
potentials (APs) recorded from the sciatic nerve in intact rats and rats with the manifestations of postdenervational and
4-aminopyridine (4-AP)-induced hyperreflexia, as well as in animals in the superreflexia state (induced by combined action
of denervation and 4-AP). We measured the parameters of monosynaptic reflex discharges (monosynaptic reflexes, MRs) recorded
from the ventral root (VR), of the spinal dorsal surface potential (DSPs), and of mass APs evoked in afferent and efferent
fibers of the SN before and 10, 30, 60, and 120 min after injection of riluzole. It was found that in intact animals riluzole
significantly (by 60–70%) decreased the amplitude of VR MRs and those of the afferent peak and N1 component of DSPs. Riluzole exerted smaller suppressive effects on mass APs in the afferent fibers of the SN; the effect
on APs in the SN efferent fibers was the minimum (a 4 to 5% decrease). Under conditions of increased sensitivity of the motoneuronal
postsynaptic membrane to the transmitter (postdenervational hyperreflexia) and an increased release of glutamate from presynaptic
elements (4-AP-induced hyperreflexia), as well as under superreflexia conditions, the dynamics of suppression of the evoked
spinal activity by riluzole showed relatively moderate differences from those in intact animals. Under the above conditions,
riluzole in the same manner decreased the amplitude of VR MRs. In the superreflexia state, the agent blocked the development
of additional components of these dramatically increased potentials (in the above state, their amplitude increased by nearly
nine times, on average, and this resulted in the generation of such components). We believe that the inhibitory effect of
riluzole on glutamatergic neurotransmission in the spinal cord is based, first of all, on blocking of excitation in afferent
presynaptic terminals. The possibility to use riluzole for correction of abnormally increased hyperexcitability of the spinal
neuronal systems is discussed.
Neirofiziologiya/Neurophysiology, Vol. 37, Nos. 5/6, pp. 416–423, September–December, 2005. |
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Keywords: | riluzole spinal hyperreflexia superreflexia monosynaptic discharges dorsal surface potential sciatic nerve mass action potentials |
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