Muscarinic control of the excitability of hindlimb motoneurons in chronic spinal‐transected salamanders

Abstract

The excitability of spinal motoneurons (MNs) is regulated by acetylcholine via the activation of muscarinic receptors. The objective of the present study was to determine whether this cholinergic modulation of MN excitability is altered following a chronic spinal cord transection. Juvenile salamanders (Pleurodeles waltlii) were spinally transected at the mid-trunk level, and patch-clamp recordings from hindlimb MNs in spinal cord slices were performed 9-30 days after transection, with and without bath application of muscarine (20 mum). Our results showed that the input-output relationship was larger in MNs recorded 2 weeks after spinal transection than in MNs recorded 3-4 weeks after spinal transection. They further revealed that muscarine increased both the gain of MNs and the proportion of MNs that could exhibit plateau potentials and afterdischarges, whereas it decreased the amplitude of the medium afterhypolarizing potential. Moreover, muscarine had no effect on the hyperpolarization-activated cation current (I(h)), whereas it increased the inward rectifying K(+) current (I(Kir)) in MNs recorded > or = 2 weeks after spinal transection. We conclude that following chronic spinal cord injury, the muscarinic modulation of some intrinsic properties of MNs previously reported in acute spinal-transected animals [S. Chevallier et al. (2006)The Journal of Physiology, 570, 525-540] was preserved, whereas that of other intrinsic properties of MNs was suppressed, either transiently (I(Kir)) or definitively (I(h)). These alterations in muscarinic modulation of MN excitability may contribute to the spontaneous recovery of locomotion displayed in long-term chronic spinal-transected salamanders.

Inward rectifier potassium (Kir) current in dopaminergic periglomerular neurons of the mouse olfactory bulb

“…A similar effect has been reported in a variety of preparations, ranging from mammal atrial myocytes (Sakmann et al, 1983), to thalamic reticular neurons (Mccormick and Prince, 1986), spinal motoneurons (Chevallier et al, 2008), interneurons of striatum (Calabresi et al, 1998), neocortex (Xiang et al, 1998), and hippocampus (McQuiston and Madison, 1999). …”

Noradrenergic modulation of intrinsic and synaptic properties of lumbar motoneurons in the neonatal rat spinal cord

“…These differences between hypoglossal and lumbar locomotor motoneurons could result from distinct NAergic receptor sub-type expression and/or intracellular coupling (Rekling et al, 2000). The K IR channels contribute to the resting membrane potential and neuronal excitability and for these reasons, they constitute the main targets of numerous G-protein coupled receptors (see for examples Bertrand et al, 2003a,b; Derjean et al, 2003; Chevallier et al, 2008). In the neonatal rat spinal cord, it has been shown that serotonin as NA increases the motoneuron excitability partly via the inhibition of K IR -like current (Kjaerulff and Kiehn, 2001).…”

From lamprey to salamander: an exploratory modeling study on the architecture of the spinal locomotor networks in the salamander

“…Adding to the above studies we extended the model by the addition of a hyperpolarization activated h-current (I h ) and a persistent sodium current (I NaP ) since it has been demonstrated that blocking these channels can, respectively, slow down or abolish oscillatory behavior (Ryczko et al 2010a). I h was further demonstrated to be present in salamander motoneurons (Chevallier et al 2006(Chevallier et al , 2008b. The default diameter of our tentative salamander locomotor CPG interneurons was chosen as 30 µm (Jovanovic and Burke 2004).…”