Chronic pain induces cell type-specific alterations in the intrinsic excitability of spinal cord lamina II circuits in female rats.
TL;DR
It is demonstrated that chronic pain induces firing pattern-dependent adaptations in intrinsic excitability, with selective enhancement of responsiveness in IB neurons, which may contribute to persistent amplification of nociceptive signaling by reshaping microcircuit dynamics within the superficial dorsal horn, thereby facilitating pathological nociceptive transmission during established pain states.
Abstract
Chronic pain is associated with maladaptive plasticity within nociceptive circuits of the spinal dorsal horn (SDH). However, whether this reorganization selectively targets specific neuronal populations remains unresolved. Addressing this question has been technically challenging because reliable measurements of somatic excitability in spinal neurons are difficult to obtain under experimental pain conditions, where tissue integrity and recording stability are frequently compromised. In this comparative study, we examined neuronal excitability in two electrophysiologically distinct lamina II populations; tonic and initial burst (IB) firing neurons, under basal conditions and across three chronic pain models: complete Freund's adjuvant (CFA), spinal nerve ligation (SNL), and streptozotocin (STZ). Our results demonstrate that chronic pain induces firing pattern-dependent adaptations in intrinsic excitability, with selective enhancement of responsiveness in IB neurons. This interpretation is reinforced by principal component analysis (PCA), which partitions IB and tonic neurons into distinct electrophysiological domains. This subtype-specific plasticity may contribute to persistent amplification of nociceptive signaling by reshaping microcircuit dynamics within the superficial dorsal horn, thereby facilitating pathological nociceptive transmission during established pain states.