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Title: Changes in spinal inhibitory networks induced by furosemide in humans
Authors: Wanalee Klomjai
Lackmy-Vall´ee, Alexandra
Katz, Rose
Bussel, Bernard
Bensmail, Djamel
Lamy, Jean-Charles
Roche, Nicolas
Mahidol University. Faculty of Physical Therapy
Keywords: spinal;human
Issue Date: 2014
Citation: The Journal of Physiology. Vol.592, No.13 (2014), 2865-2879
Abstract: Abstract During neural development in animals, GABAergic and glycinergic neurons are first excitatory, and then become inhibitory in the mature state. This developmental shift is due mainly to strong expression of the cation-chloride K–Cl cotransporter 2 (KCC2) and down-regulation of Na–K–Cl cotransporter 1 (NKCC1) during maturation. The down-regulation of co-transporter KCC2after spinal cord transection inanimals leads to the depolarising (excitatory) action ofGABA and glycine and thus results in a reduction of inhibitory synaptic efficiency. Furosemide, a loop diuretic, has been shown to selectively and reversibly block inhibitory postsynaptic potentials without affecting excitatory postsynaptic potentials in animal spinal neurons. Moreover, this diuretic has been also demonstrated to block the cation-chloride co-transporters. Here, we used furosemide to demonstrate changes in spinal inhibitory networks in healthy human subjects. Non-invasive electrophysiological techniques were used to assess presynaptic inhibition, postsynaptic inhibition and the efficacy of synaptic transmission between muscle afferent terminals and soleus motoneurons in the spinal cord. Orally administered furosemide, at doses commonly used in the clinic (40mg), significantly reduced spinal inhibitory interneuronal activity for at least 70 min fromintake compared to control experiments in the same subjects while no changes were observed in the efficacy of synaptic transmission between muscle afferent terminals and soleus motoneurons. The reduction of inhibition was dose-dependent. Our results provide indirect evidence that reversible changes in the cation-chloride transport system induce modulations of inhibitory neuronal activity at spinal cord level in humans.
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