Sriyani Pathirathna

TL;DR: It is found that, in parallel with the development of diabetes-induced pain, T-type current density increased by twofold in medium-size cells from L4–L5 dorsal root ganglia (DRG) with a depolarizing shift in steady-state inactivation, and increased cellular excitability manifested as a lower threshold for burst firing in diabetic than in control cells.

TL;DR: The finding that T-type currents are upregulated in a CCI model of peripheral neuropathy and earlier pharmacological and molecular studies suggest that T -type channels may be potentially useful therapeutic targets for the treatment of neuropathic pain associated with partial mechanical injury to the sciatic nerve.

TL;DR: It is demonstrated that potent peripheral analgesia induced by 5α‐reduced neurosteroid is mediated in part by effects on T‐type Ca2+ channels, which strongly suggest that GABAA channels do not contribute to baseline pain transmission, but they can enhance anti‐nociception mediated by blockade of T‐ type Ca2- channels.

TL;DR: The results indicate that pharmacological antagonism of T-channels is potentially an important novel therapeutic approach for the management of painful diabetic neuropathy.