Requirement of α7 nicotinic acetylcholine receptors for amyloid beta protein-induced depression of hippocampal long-term potentiation in CA1 region of rats in vivo

Synapse ◽  
2011 ◽  
Vol 65 (11) ◽  
pp. 1136-1143 ◽  
Author(s):  
Shao-Feng Li ◽  
Mei-Na Wu ◽  
Xiao-Hui Wang ◽  
Li Yuan ◽  
Dong Yang ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Long Term Potentiation ◽  
Amyloid Beta Protein ◽  
Nicotinic Acetylcholine ◽  
Ca1 Region ◽  
Term Potentiation ◽  
Α7 Nicotinic Acetylcholine Receptors

scholarly journals Gating of Long-Term Potentiation by Nicotinic Acetylcholine Receptors at the Cerebellum Input Stage

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64828 ◽  
Author(s):  
Francesca Prestori ◽  
Claudia Bonardi ◽  
Lisa Mapelli ◽  
Paola Lombardo ◽  
Rianne Goselink ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Long Term Potentiation ◽  
Nicotinic Acetylcholine ◽  
Input Stage ◽  
Term Potentiation

Nicotine Enhances the Depressive Actions of Aβ1–40 on Long-Term Potentiation in the Rat Hippocampal CA1 Region In Vivo

2003 ◽  
Vol 89 (6) ◽  
pp. 2917-2922 ◽  
Author(s):  
D. B. Freir ◽  
C. E. Herron
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
High Affinity ◽  
Ca1 Region ◽  
Α7 Nachr ◽  
Term Potentiation ◽  
Significant Depression

Hippocampal long-term potentiation (LTP) is a form of synaptic plasticity used as a cellular model of memory. Beta amyloid (Aβ) is involved in Alzheimer's disease (AD), a neurode-generative disorder leading to cognitive deficits. Nicotine is also claimed to act as a cognitive enhancer. Aβ is known to bind with high affinity to the α7-nicotinic acetylcholine receptor (nAChR). Here we have investigated the effect of intracerebroventricular (icv) injection of the endogenous peptide Aβ1–40 on LTP in area CA1 of urethananesthetized rats. We also examined the effect of Aβ12–28 (icv), which binds with high affinity to the α7-nAChR and the specific α7-nAChR antagonist methyllycaconitine (MLA) on LTP. We found that Aβ12–28 had no effect on LTP, whereas MLA depressed significantly LTP, suggesting that activation of the α7-nAChR is a requirement for LTP. Within the in vivo environment, where other factors may compete with Aβ12–28 for binding to α7-nAChR, it does not appear to modulate LTP. To determine if the depressive action of Aβ1–40 on LTP could be modulated by nicotine, these agents were also co-applied. Injection of 1 or 10 nmol Aβ1–40 caused a significant depression of LTP, whereas nicotine alone (3 mg/kg) had no effect on LTP. Co-injection of nicotine with Aβ1–40 1 h prior to LTP induction caused a further significant depression of LTP compared with Aβ1–40 alone. These results demonstrate that nicotine enhances the deficit in LTP produced by Aβ1–40. This then suggests that nicotine may exacerbate the depressive actions of Aβ on synaptic plasticity in AD.

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