Results: 5

1.
Figure 3

Figure 3. From: ?-Amyloid peptide blocks the response of ?7-containing nicotinic receptors on hippocampal neurons.

Noncompetitive blockade of hippocampal α7-nAChRs by Aβ1–42. Individual cells were tested at 10 mM ACh and one or more additional concentrations of ACh before and after application of 10 nM Aβ1–42. Results were normalized to those obtained with 10 mM ACh and then pooled for each data point (n = 5–7). Increasing the concentration of ACh did not overcome the partial block achieved with the concentration of Aβ1–42 used.

Qing-song Liu, et al. Proc Natl Acad Sci U S A. 2001 April 10;98(8):4734-4739.
2.
Figure 5

Figure 5. From: ?-Amyloid peptide blocks the response of ?7-containing nicotinic receptors on hippocampal neurons.

1–42 blockade of nicotine-induced increases in spontaneous mEPSC frequency in hippocampal neurons. (A) Whole-cell perforated-patch–clamp recording from a neuron showing that the rate of spontaneous mEPSCs (Top) is increased by application of 1 μM nicotine (Middle) as shown previously (16) and that the nicotine-induced increase can be blocked by 100 nM Aβ1–42 (Aβ; Bottom). Tetrodotoxin and bicucculine were present to block action potentials and GABAA receptors, respectively. (B) Same neuron as in A, showing that Aβ1–42 does not depress the basal rate of spontaneous mEPSCs. (C) Cumulative distribution plots showing that 100 nM Aβ1–42 prevents 1 μM nicotine (Nic) from increasing the frequency of spontaneous mEPSCs but that the peptide has no effect on the basal rate (Left); in contrast, neither nicotine nor Aβ1–42 has any effect on the amplitude distribution of the spontaneous mEPSCs (Right).

Qing-song Liu, et al. Proc Natl Acad Sci U S A. 2001 April 10;98(8):4734-4739.
3.
Figure 2

Figure 2. From: ?-Amyloid peptide blocks the response of ?7-containing nicotinic receptors on hippocampal neurons.

Effects of 100 nM Aβ1–42 on other ionotropic receptors. Cells were voltage-clamped at −60 mV. (A) Representative example showing the slowly desensitizing, αBgt-resistant ACh responses of a neuron with non-α7-nAChRs before (Left) and during (Right) application of Aβ1–42. (B) Compiled data showing the absence of significant Aβ1–42 blockade on peak responses from non-α7-nAChRs (non-α7), glutamate receptors (Glu), and GABAA receptors (GABA) on rat hippocampal neurons and the presence of blockade for α7-nAChRs on chick ciliary ganglion neurons (CGα7). Mean initial responses (in nanoamperes) from Left to Right were 0.8 ± 0.2 (n = 6), 3.2 ± 0.7 (7), 4.3 ± 1.2 (4), and 4.5 ± 0.5 (8).

Qing-song Liu, et al. Proc Natl Acad Sci U S A. 2001 April 10;98(8):4734-4739.
4.
Figure 1

Figure 1. From: ?-Amyloid peptide blocks the response of ?7-containing nicotinic receptors on hippocampal neurons.

Specific blockade of α7-nAChRs by β-amyloid peptides. (A) ACh responses characteristic of hippocampal α7-nAChRs before (Left), during (Center), and 5 min after (Right) a 3-min exposure to 100 nM rat Aβ1–42. (B) Concentration dependence for the Aβ1–42 blockade of the α7-nAChR response (n = 6–8 for each value). (C) Effects of the rat (r) and human (h) Aβ1–42 and Aβ1–40 peptides (all at 100 nM; n = 8) on the α7-nAChR response. Negative control: hAβ40–1 (100 nM; n = 6); vehicle (n = 6) was extracellular recording solution plus 0.005% acetic acid. Both here and in the other figures, results were normalized to the peak response obtained from the same cell before peptide application (normalized current).

Qing-song Liu, et al. Proc Natl Acad Sci U S A. 2001 April 10;98(8):4734-4739.
5.
Figure 4

Figure 4. From: ?-Amyloid peptide blocks the response of ?7-containing nicotinic receptors on hippocampal neurons.

1–42 blockade of chimeric α7-nAChR/5HT3 receptors. HEK293 cells were transfected with either the chimeric α7-nAChR/5HT3 receptor (A) or wild-type 5HT3 receptor (B) constructs and were examined 2 days later with whole-cell patch–clamp recording to compare responses elicited by ACh or 5-HT in the absence (Left) and presence (Right) of 100 nM Aβ1–42 for cells voltage-clamped at −60 mV. The black bar of the construct represents the α7 domain; the gray bar represents 5HT3 wild-type domain; M indicates transmembrane domain. The peptide produced significant (and equivalent) inhibition of chimeric responses elicited by either 0.3 or 1 mM ACh but not wild-type responses elicited by 1 mM 5HT (C). The peak amplitude of the response in Aβ1–42 was normalized to the initial response from the same cell in each case (n = 10 for each; P < 0.001).

Qing-song Liu, et al. Proc Natl Acad Sci U S A. 2001 April 10;98(8):4734-4739.

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