Autoantibodies (aAb) targeting Contactin-associated protein 2 (Caspr2) have been implicated in neuropathic pain, yet the precise underlying pathomechanism is not completely understood. Caspr2 is part of a protein complex named the voltage-gated potassium channel (VGKC) complex located at the juxtaparanodal region of the nodes of Ranvier in the peripheral nervous system. Dorsal root ganglia (DRG) may serve as mediating neurons transmitting nociceptive signals from the periphery to the central nervous system. Therefore, changes in the excitability of DRG neurons might contribute to the pathology of Caspr2 aAbs. Here, we verified the expression of Caspr2 and potassium channels of the Kv-subtype (Kv1.1, Kv1.2) in DRG neurons. Patient sera were classified into four groups, depending on the IgG subclasses and the pain phenotype. IgG subclasses were exhibited through immunocytochemical stainings. The impact of Caspr2 aAb on the VGKC complex in DRG neurons was investigated through electrophysiological measurements of potassium currents. Short- and long-term effects of Caspr2 aAb on the function of associated Kv channels were measured through whole-cell patch clamp recordings. Caspr2 aAb of different subclassifications caused significantly decreased potassium current amplitudes measured by current-voltage analyses. The recordings showed variability in the obtained traces arguing for various potassium channel subtypes contributing to the observed currents. Using a specific κM-Conotoxin RIIIJ (κM-RIIIJ), we were able to verify a significant contribution of potassium channels including the Kv1.1 and Kv1.2 subunits. Our findings suggest that an increase of DRG excitability upon Caspr2 aAb underlies the pathomechanism of Caspr2 aAb associated with neuropathic pain.