Skip to main content
. Author manuscript; available in PMC: 2005 Sep 13.
Published in final edited form as: Neuron. 2002 Dec 5;36(5):855–868. doi: 10.1016/s0896-6273(02)01067-x

Figure 7. Exogenous Adenosine and Adenosine Released from Electrically Stimulated Axons Promote Myelination of DRG Axons by OPCs.

Figure 7

(A) Immunocytochemical staining for MBP was used to compare the effects of chronic adenosine treatment on myelination after 14 days in coculture. In contrast to control cultures (a), OPCs in adenosine-treated cultures displayed multiple parallel processes enriched in MBP (green) and undergoing early stages of myelin formation (b).

(B) The number of MBP+ oligodendrocytes with multiple parallel processes in adenosine-treated cultures increased 292% as compared with controls (p < 0.004, t test, n = 14 cultures). Data shown are normalized with respect to the total number of MBP+ cells/field. Similar results were obtained when expressed as the percentage of total OPCs/field (426% increase with adenosine treatment; 7.8% ± 1.3% versus 1.8% ± 0.69%; p < 0.004, n = 14).

(C) Cocultures treated with adenosine receptor antagonists (AdoA) (5 μM MRS 1191, 500 nM ZM241385, and 10 μM DPCPX) developed significantly fewer MPB+ oligodendrocytes with multiple parallel processes after 3–4 days in coculture (p < 0.0001, n = 26 cultures). Electrical stimulation for 24 hr (10 Hz) increased the number of MBP+ oligodendrocytes with multiple parallel processes as compared with controls (0 Hz) after 3–4 days in coculture (p < 0.01; n = 28), and this effect was blocked by stimulation in the presence of adenosine receptor antagonists (10 Hz with AdoA) (p < 0.00001, n = 31). Adding the antagonists after the 24 hr stimulus (10 Hz before AdoA) resulted in significantly more MBP+ cells with multiple parallel processes than when the antagonists were added during the stimulus (10 Hz with AdoA) (p < 0.0001, n = 27 cultures), indicating an effect of the antagonist in antagonizing an activity-dependent axon-derived signal. All conditions contained the non-NMDA glutamate receptor antagonist CNQX (20 μM), thus excluding the possible involvement of these glutamate receptors. Similar results were obtained in the absence of CNQX (see Results). *p < 0.0001 versus 0 Hz; **p < 0.01 versus 0 Hz; ***p < 0.00001 versus 10 Hz; ****p < 0.0001 versus AdoA.