The Journal of Neuroscience, April 5, 2006, ():
Sympathetic Sprouting Drives Hippocampal Cholinergic Reinnervation That Prevents Loss of a Muscarinic Receptor-Dependent Long-Term Depression at CA3–CA1 Synapses
J. Neurosci. Scheiderer et al.
26: 3745
Supplemental data
Files in this Data Supplement:
- supplemental material
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Supplemental Figure 1. Blockade of mLTD by pirenzepine and analysis of paired-pulse
facilitation ratios.
(A) 75 nM pirenzepine, a concentration selective for blocking M1 receptors, prevents mLTD (99 ± 4% of baseline, n=5, p>0.01). (B) 10 μM pirenzepine prevents both mLTD (87 + 4% of baseline, n=5, p>0.06) as well as the transient depression during CCh application (92 + 3% of baseline, n=5, p>0.08), demonstrating that this concentration is not selective for M1 receptors. (C) The PPF ratio is not altered during mLTD expressed when induced with either CCh or McN (CCh: 1.5 ± 0.03 during mLTD expression vs 1.5 ± 0.01 during baseline transmission, n=7, p>0.05; McN: 1.6 ± 0.05 during mLTD expression vs 1.6 ± 0.04 during baseline n=6, p>0.05). (D) The PPF ratio increases during application of CCh but not during McN application (1.5 ± 0.01 during baseline vs 2.0 ± 0.03 during CCh application, n=7, p<0.05; 1.6 ± 0.04 during baseline vs 1.8 ± 0.20 during McN application, n=6, p>0.05).
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Supplemental Figure 2. Images demonstrating lesion of medial septum.
Images on top show representative examples of a sham electrolytic medial septum lesion (top left, medial septum indicated by arrow) and an electrolytic lesion of medial septum (top right). At 4 weeks post electrolytic lesion, animals were sacrificed and sections of septum were stained for the loss of AChE using the copper-thiocholine method to detect acetylcholinesterase. Notice (arrow, top right panel) that the medial septum has been physically destroyed as a result of the electrolytic stimulation. The bottom set of images shows a sham medial septal lesion (bottom left, medial septum indicated by aorrow) and a complete lesion of the medial septum induced by intraseptal injection of 192 IgG-saporin (right). At 12 weeks post injection, animals were sacrificed and sections of septum were stained for loss of AChE. Notice the loss of cholinergic neurons in the bottom right panel indicating a successful lesion of medial septum.
- supplemental material
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Supplemental Figure 3. Effects of cholinergic denervation and sympathetic ingrowth on mLTD expression separated by lesion method.
(A-B) mLTD of the same magnitude is expressed in slices from animals with either (A) sham electrolytic medial septal lesions or (B) sham 192 IgG-saporin (sham electrolytic lesions: 77 ± 2% of baseline, n=6 slices/3 animals; sham 192 IgG-saporin lesions: 82 ± 3% of baseline, n=5 slices/3 animals; p>0.1 when comparing lesion methods). (C-D) mLTD is lost in slices from animals with either (C) electrolytic or (D) 192 IgG-saporin induced medial septal lesions when the SCG have been removed bilaterally to prevent ingrowth (electrolytic lesions: 99 ± 3% of baseline n=7slices/3 animals; 192 IgG-saporin lesions: 95 ± 2% of baseline, n=3 slices/2 animals; p>0.4 when comparing lesion methods). (E-F) mLTD is at control levels in slices from animals with either (E) electrolytic or (F) 192 IgG-saporin medial septal lesion (F) when the SCG are left intact to allow ingrowth to occur (electrolytic lesions: 79±3 % of baseline, n=9 slices/5 animals; 192 IgG-saporin lesions: 79 ± 5% of baseline, n=7 slices/4 animals; p>0.9 when comparing lesion methods).
