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  4. Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters

Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters

Weisshaar CL, Kras JV, Pall PS, Kartha S, Winkelstein BA (2017) Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters. Neurosci Lett 655:82-89. doi: 10.1016/j.neulet.2017.07.006 PMID: 28689926

Objective: To investigate the role of peptidergic afferents in the development and maintenance of mechanical hyperalgesia, dysregulated nociceptive signaling, and spinal hyperexcitability that develop after mechanical injury to the facet joint

Summary: Isolectin-B4 saporin (IB4- SAP) was injected into the facet joint to ablate non-peptidergic cells, and the facet joint later underwent a ligament stretch known to induce pain. Administering IB4-SAP prior to a painful injury prevented the development of mechanical hyperalgesia that is typically present. Intra-articular IB4-SAP also prevented the upregulation of the glutamate transporters GLT-1 and EAAC1 in the ventral posterolateral nucleus of the thalamus and reduced thalamic neuronal hyperexcitability at day 7.

Usage: Rats received a bilateral intra-articular injections of 5µg in the C6/C7 facet joints of IB4-SAP (5 µg, IT-10) in 10μL of PBS to ablate the IB4-binding neurons. Saporin (PR-01) was used as control.

Related Products: IB4-SAP (Cat. #IT-10), Saporin (Cat. #PR-01)

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