Bursting Deep Dorsal Horn Neurons: Potential Contributor to Muscle Spasms

Theeradej Thaweerattanasinp

doi:https://doi.org/10.21985/N2CH50

Work

Bursting Deep Dorsal Horn Neurons: Potential Contributor to Muscle Spasms

Public Deposited

Download PDF

Download All Files (.zip)

Loss of inhibitory control from descending serotonergic (5-HT) fibers deregulates the excitability of spinal motoneurons and interneurons following spinal cord injury (SCI). Exaggerated synaptic activity triggers long-lasting excitatory postsynaptic potentials (long EPSPs) in hyperexcitable motoneurons to ultimately drive muscle spasms at the chronic stage of SCI. Deep dorsal horn (DDH) neurons with burst firing behavior could play a role in generating the long EPSPs. Modifying the 5-HT or glutamatergic transmission could influence the firing activity of the bursting DDH neurons and thus muscle spasms following SCI. Using extracellular electrophysiology, we investigate the firing behaviors of DDH neurons in the isolated sacral spinal cords of adult mice following acute and chronic spinal transection while administering NMDA or 5-HT1B/1D receptor agonist zolmitriptan. We also quantify polysynaptic reflexes in the ventral roots during NMDA administration. Upon dorsal root stimulation, DDH neurons can exhibit one of the three major firing response types with distinct evoked and spontaneous firing behaviors: bursting, single spiking, or spontaneously tonic firing. The bursting DDH neurons likely contribute to generating the long EPSPs due to their burst firing behavior and a slight increase in their excitability over time following SCI. Moreover, during zolmitriptan and NMDA administration, only the bursting DDH neurons exhibit significant changes in their firing properties. Zolmitriptan suppresses the bursting DDH neurons by, for example, reducing their evoked spike count, with stronger effects over time following SCI. In contrast, NMDA facilitates them by, for example, enhancing their spontaneous firing rate, with weaker effects over time following SCI. In addition, NMDA can induce bursting activity in the ventral roots with no significant change in the magnitudes of its effect over time following SCI. These results support the functional contribution of the bursting DDH neurons to generation of the long EPSPs and muscle spasms, whose mechanisms may function independently from NMDA-induced bursting ventral root activity following chronic SCI.

Last modified