Modulation of Afterhyperpolarization by Recurrent Inhibition

Abstract

Afterhyperpolarization (AHP) is a major determinant of motoneuron (MN) firing rate. However, it is not the sole factor since it is shaped by excitatory and inhibitory synaptic conductances during different motor tasks. One likely candidate is recurrent inhibition which shared similar timing with the known undershoot of MN action potentials following antidromic stimulation of peripheral nerve. That observation prompted us to directly examine the extent by which recurrent inhibition contributes to MN hyperpolarization. Data were obtained by in vivo intracellular recordings from identified lumbar MNs. Recordings were obtained from 63 MNs in 16 adult rats acutely deafferented and Isoflurane anesthetized. In each MN, action potentials were evoked either by suprathreshold current injection or by antidromic electrical stimulation of the whole peripheral nerve activating the autogenic recurrent inhibition circuit. Changes in the degree of peak hyperpolarization, rate to negative peak, and rate of decay were investigated. Recurrent inhibition added an average increase of 646μV to the peak hyperpolarization ranging from 18μV to 3.46mV. That corresponds to an average increase of 46.5% and up to 1.64 times of original AHP amplitudes. The mean rate of rise increased by 1.53 times (P<0.0001) and the mean rate of decay increased by 1.4 times (P=0.0018). Collectively, recurrent inhibition addition to AHP resulted in significantly larger and faster hyperpolarization following action potentials. That modification is likely to influence firing (rate, the ability to fire for longer durations) and provides direct evidence that further validates the method used to measure recurrent inhibition in humans which pre‐requires that recurrent inhibition magnitude is not negligible when compared to that of AHP.