Inhibitory postsynaptic potentials in lumbar motoneurons remain depolarizing after neonatal spinal cord transection in the rat.

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Jean-Xavier C, Pflieger JF, Liabeuf S, Vinay L

Inhibitory postsynaptic potentials in lumbar motoneurons remain depolarizing after neonatal spinal cord transection in the rat.

J Neurophysiol. 2006 Nov;96(5):2274-81. Epub 2006 Jun 28.

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16807348 [ View in PubMed

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Abstract

GABA and glycine are excitatory in the immature spinal cord and become inhibitory during development. The shift from depolarizing to hyperpolarizing inhibitory postsynaptic potentials (IPSPs) occurs during the perinatal period in the rat, a time window during which the projections from the brain stem reach the lumbar enlargement. In this study, we investigated the effects of suppressing influences of the brain on lumbar motoneurons during this critical period for the negative shift of the reversal potential of IPSPs (E(IPSP)). The spinal cord was transected at the thoracic level on the day of birth [postnatal day 0 (P0)]. E(IPSP), at P4-P7, was significantly more depolarized in cord-transected than in cord-intact animals (E(IPSP) above and below resting potential, respectively). E(IPSP) at P4-P7 in cord-transected animals was close to E(IPSP) at P0-P2. K-Cl cotransporter KCC2 immunohistochemistry revealed a developmental increase of staining in the area of lumbar motoneurons between P0 and P7 in cord-intact animals; this increase was not observed after spinal cord transection. The motoneurons recorded from cord-transected animals were less sensitive to the experimental manipulations aimed at testing the functionality of the KCC2 system, which is sensitive to [K(+)](o) and blocked by bumetanide. Although bumetanide significantly depolarized E(IPSP), the shift was less pronounced than in cord-intact animals. In addition, a reduction of [K(+)](o) affected E(IPSP) significantly only in cord-intact animals. Therefore influences from the brain stem may play an essential role in the maturation of inhibitory synaptic transmission, possibly by upregulating KCC2 and its functionality.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Bumetanide	Solute carrier family 12 member 4	Protein	Humans	Yes	Inhibitor	Details