α7-Type Nicotinic Acetylcholine Receptor and Prodynorphin mRNA Expression after Administration of (−)-Nicotine and U-50,488H in β-Amyloid Peptide (25-35)-Treated Mice

2004 ◽  
Vol 1025 (1) ◽  
pp. 508-514 ◽  
Author(s):  
M HIRAMATSU ◽  
M WATANABE ◽  
S BABA ◽  
R KOJIMA ◽  
T NABESHIMA
Keyword(s):  
Mrna Expression ◽  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Amyloid Peptide ◽  
Nicotinic Acetylcholine ◽  
Β Amyloid ◽  
Β Amyloid Peptide ◽  
Prodynorphin Mrna

scholarly journals Cortical α7 Nicotinic Acetylcholine Receptor and β-Amyloid Levels in Early Alzheimer Disease

2009 ◽  
Vol 66 (5) ◽  
Author(s):  
Milos D. Ikonomovic ◽  
Lynn Wecker ◽  
Eric E. Abrahamson ◽  
Joanne Wuu ◽  
Scott E. Counts ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Nicotinic Acetylcholine ◽  
Β Amyloid

β-Amyloid Peptide Activates Non-α7 Nicotinic Acetylcholine Receptors in Rat Basal Forebrain Neurons

2003 ◽  
Vol 90 (5) ◽  
pp. 3130-3136 ◽  
Author(s):  
Wen Fu ◽  
Jack H. Jhamandas
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Basal Forebrain ◽  
Single Channel ◽  
Amyloid Peptide ◽  
Nicotinic Acetylcholine ◽  
Whole Cell ◽  
Β Amyloid ◽  
Forebrain Neurons ◽  
Β Amyloid Peptide ◽  
Α7 Nachrs

Alzheimer's disease (AD) is a progressive neurodegenerative condition characterized by profound deficits in memory and cognitive function. Neuropathological hallmarks of the disease include a loss of basal forebrain cholinergic neurons and the deposition of β-amyloid peptide (Aβ) in neuritic plaques. At a cellular level, considerable attention has focused on a study of Aβ interactions with the neuronal nicotinic acetylcholine receptor (nAChR) subtypes. In this study, using cell-attached and outside-out single channel recordings from acutely dissociated rat basal forebrain neurons, we report that Aβ and nicotine activate nAChRs with two distinct levels of single-channel conductance. Whole cell recordings from these neurons reveal Aβ and nicotine, in a concentration-dependent and reversible manner, evoke brisk depolarizing responses and an inward current. The effects of Aβ on both single channel and whole cell are blocked by the noncompetitive nAChR antagonist mecamylamine and competitive nAChR antagonist dihydro-beta-erythroidine, but not the specific α7-selective nAChR antagonist methyllycaconitine, indicating that Aβ activated non-α7 nAChRs on basal forebrain neurons. In addition, the non-α7 nAChR agonists UB-165, epibatidine, and cytisine, but not the selective α7 agonist AR-R17779, induced similar responses as Aβ and nicotine. Thus non-α7 nAChRs may also represent a novel target in mediating the effects of Aβ in AD.

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