Supplementary Figure 5: DH-CBD does not restore diminished glycinergic transmission in spinal slices from the α1Q266I mutant mice.
From: Presynaptic glycine receptors as a potential therapeutic target for hyperekplexia disease
(a) Trace records of Gly sIPSC in spinal slices from the WT and α1Q266I mutant mice with and without sustained perfusion of DH-CBD (20 μM) for 6 min. (b) The average frequency and amplitude of Gly sIPSC in spinal slices from the WT and α1Q266I mutant mice with and without sustained perfusion of DH-CBD (20 μM) for 6 min (n=10-12). WT VS Q266I, p=0.045, unpaired t-test; Q266I VS Q266I+DH-CBD, p=0.55, unpaired t-test. (c) The average amplitude of Gly sIPSC in spinal slices obtained from the WT and α1Q266I mutant mice with and without sustained perfusion of DH-CBD (20 μM) for 6 min (n=10-12). WT VS Q266I, p=0.048, unpaired t-test; Q266I VS Q266I+DH-CBD, p=0.63, unpaired t-test.
