Hernandez-Melesio MA, Gonzalez-Esquivel D, Ortiz-Plata A, Sanchez-Mendoza A, Sanchez-Garcia A, Alcaraz-Zubeldia M, Rios C, Perez-Severiano F (2011) Molsidomine modulates the cNOS activity in an experimental model of cholinergic damage induced by 192-IgG saporin. Neurosci Lett 491(2):133-137. doi: 10.1016/j.neulet.2011.01.023
Summary: Nitric oxide (NO) is required for the survival of cholinergic neurons in the basal forebrain. Delivery of nerve growth factor (NGF) is related to the modulation of NO – as excessive NO can lead to excitotoxicity. The authors administered molsidomine to rats that had previously received 220 ng of 192-IgG-SAP (Cat. #IT-01) into the medial septum. Molsidomine is a NO donator, and produced a significant recovery of NO activity in lesioned animals, indicating a potential therapeutic pathway.
Related Products: 192-IgG-SAP (Cat. #IT-01)