Table 1.
Regulation by Aβ of cholinergic control of neurotransmitter release.
| Aβ species | Concentration and timing | Effects of Aβ on neurotransmitter release | Experimental model/brain area | References |
|---|---|---|---|---|
| Dopamine | ||||
| Soluble Aβ1−40 and Aβ1−42 | 1–10 μM/60–80 min (for in vivo experiments); 100 nM/up to 10 min (for in vitro experiments) | Low micromolar concentrations (1 μM) of Aβ prevented the muscarinic receptor-activated dopamine release in rat nucleus accumbens. The [3H]dopamine release, evoked by carbachol, was decreased by 100 nM Aβ in isolated nerve endings of the nucleus accumbens. Moreover, Aβ1−42 (100 nM) significantly reduced the dopamine release evoked by carbachol. |
In vivo (brain dialysis) and in vitro (isolated synaptosomes) models/rat nucleus accumbens | Preda et al., 2008 |
| Aβ1−40 | 100 nM | Treatment with 100 nM Aβ1−40 prevented both nicotinic and muscarinic cholinergic modulation of dopamine release. | Synaptosomes/rat nucleus accumbens | Olivero et al., 2014 |
| Aβ1−40 and Aβ1−42 | 10–100 nM/up to 12 min | In nerve endings, Aβ impaired the muscarinic control of dopamine release in both the nucleus accumbens and caudate putamen. | Synaptosomes/caudate-putamen-nucleus accumbens | Mura et al., 2010 |
| GABA | ||||
| Monomers of Aβ1−40 and Aβ1−42 | 100 nM/up to 17 min | In isolated nerve endings, Aβ blocked GABA release by acting on muscarinic receptor subtypes (M3 and M5). Instead, Aβ was ineffective on muscarinic receptor subtypes negatively modulating the stimulated transmitter release (M2 and M4). | Synaptosomes/rat nucleus accumbens | Grilli et al., 2010 |
| Monomers of Aβ1−40 | 100 nM, 1 μM, and 10 μM/40–60 min (for in vivo experiments); 100 pM, 1 nM, and 100 nM/up to 10 min (for in vitro experiments) | While perfusion of 10 μM Aβ blocked the nicotine-induced release of GABA, perfusion of 100 nM Aβ potentiated the nicotine-evoked GABA overflow. In isolated nerve endings, 100 nM Aβ blocked the nicotine-induced release of GABA and 100 nM Aβ inhibited the release of GABA induced by the 4β2 selective agonist 5IA85380. |
In vivo (microdialysis) and in vitro (synaptosomes in superfusion) techniques/hippocampus | Mura et al., 2012 |
| Glycine | ||||
| Aβ1−40 | 10 μM/40–60 min (for in vivo experiments); 10 nM and 100 nM/up to 10 min (for in vitro experiments) | Perfusion of 10 μM Aβ1−40 reduced the nicotine-induced glycine overflow and also the glycine overflow induced by the α7 selective agonist PHA543613. In isolated nerve endings, both 10 and 100 nM Aβ inhibited the nicotine-induced glycine release; 100 nM Aβ inhibited the release of glycine evoked by the α7 selective agonist carbachol and by the α4β2 selective agonist 5IA85380. |
In vitro (synaptosomes in superfusion) and in vivo (microdialysis) approaches/hippocampus | Zappettini et al., 2012 |
| Aspartate | ||||
| Monomers of Aβ1−40 | 100 nM, 1 μM, and 10 μM/40–60 min (for in vivo experiments); 100 pM, 1 nM, and 100 nM/up to 10 min (for in vitro experiments) | Perfusion of 10 and 1 μM Aβ inhibited the nicotine-induced release of aspartate. In isolated nerve endings, 100 nM Aβ inhibited the nicotine-induced release of aspartate; 100 nM Aβ inhibited the release of aspartate that was induced by the α7 selective agonist carbachol; 100 nM Aβ inhibited the release of aspartate induced by the α4β2 selective agonist 5IA85380; 100 pM Aβ potentiated the carbachol-induced release of aspartate. |
In vivo (microdialysis) and in vitro (synaptosomes in superfusion) techniques/hippocampus | Mura et al., 2012 |
| Glutamate | ||||
| Monomers of Aβ1−40 | 100 nM, 1 μM, and 10 μM/40–60 min (for in vivo experiments); 100 pM, 1 nM, and 100 nM/up to 10 min (for in vitro experiments) | Perfusion of 10 and 1 μM Aβ inhibited the nicotine-induced release of glutamate. In isolated nerve endings, 100 nM Aβ inhibited the nicotine-induced release of glutamate and the release of glutamate induced by the α7 selective agonist carbachol. Instead, 1 nM Aβ potentiated the release of glutamate induced by carbachol; 100 nM Aβ inhibited the release of glutamate induced by the α4β2 selective agonist 5IA85380; 100 pM Aβ potentiated the carbachol-induced release of glutamate. |
In vivo (microdialysis) and in vitro (synaptosomes in superfusion) techniques/hippocampus | Mura et al., 2012 |