Ventral root evoked entrainment of disinhibited bursts across early postnatal development in mice

Highlights • Ventral root evoked entrainment of disinhibited bursts can be elicited in P24 spinal cord preparations. • Disinhibited bursting and dorsal root evoked entrainment can be elicited even at P39. • Ventral root evoked entrainment shows a decline from P0−15, and the coefficient of variation increases during this period. • Ventral root evoked entrainment decays after a trial and shows some recovery after long periods following a trial. • Dopamine D2 receptor antagonists and mGluR1 agonists can enhance ventral root evoked entrainment.
Early in the postnatal period, motoneuron axon stimulation can excite motor networks in the spinal cord. Here we tested if these excitatory effects changed across early postnatal development up to postnatal day (P) 24 by when mice are capable of weight-bearing locomotion and locomotor networks are considered functionally mature. This was accomplished in the isolated spinal cord preparation using ventral root evoked entrainment of disinhibited bursts. Ventral root evoked entrainment was defined and characterized over the first 2 weeks of postnatal development, and was found to decline over this period, but entrainment could still be detected in mice as old as P24. Disinhibited bursting could be elicited, and dorsal root evoked entrainment could be recorded as late as P39 and remained unchanged in effectiveness, suggesting that poor tissue viability may not be the cause of the decline in ventral root evoked entrainment. Pharmacological experiments performed on younger animals established that dopamine D2 receptor antagonists and mGluR1 agonists both enhanced ventral root evoked entrainment. In conclusion, the motoneuronal inputs to spinal motor networks via the excitatory pathway is modulated by dopamine and metabotropic glutamate receptors and may be under powerful inhibitory control, which may explain why there is a developmental decline in entrainment.