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. 2014 Mar 4;5:3374. doi: 10.1038/ncomms4374

Figure 2. Muscarinic receptor-dependence of LTD in vivo.

Figure 2

(a,b) Systemic injection of scopolamine (0.2 mg kg−1, i.p.), a muscarinic acetylcholine receptor antagonist, completely prevented LFS-induced LTD, whereas application of the nicotinic acetylcholine receptor antagonist mecamylamine (5 mg kg−1, i.p.) did not affect LTD induction. Open triangle, i.p.; hash, intracerebroventricular (i.c.v.). As summarized in (b) the EPSP decreased significantly to 72.0±4.4% in the vehicle control group and the mecamylamine group (67.1±4.9%, n=4, P<0.05 compared with Pre, P>0.05 compared with vehicle) but not in the scopolamine group (96.5±6.4%, n=6, P>0.05 compared with Pre, P<0.05 compared with vehicle); paired t and one-way ANOVA-Tukey. (c,d) LFS-900-induced LTD was also significantly reduced by treatment with the M1-selective mAChR antagonist pirenzepine (triangle, 50 nmol in 5 μl). As summarized in (d), the EPSP decreased to 67.5±4.5% and 90.4±2.1%, n=4, in vehicle- and pirenzepine-injected animals, respectively (P<0.05 compared with Pre and between groups; t-test). (e,f) Application of LFS-900 before the injection of scopolamine (triangle, 0.2 mg kg−1, i.p.) induced robust LTD (71.7±7.2%, n=6, P<0.05 compared with Pre; paired t). (g,h) The acetylcholinesterase inhibitor donepezil lowered the threshold to induce LTD. (g) The application of weak LFS (bar, LFS-300; 300 high-intensity pulses at 1 Hz) induced a transient synaptic depression in vehicle-injected animals (triangle), whereas the same protocol triggered a robust and stable LTD after acute injection of donepezil (1 mg kg−1, subcutaneously). (h) Veh: 101.8±6.3%; donepezil: 70.5±7.1% at 3 h after LFS. *P<0.05, t-test, n=4 per group. Values are mean±s.e.m. Calibration bars: vertical, 2 mV; horizontal, 10 ms.