scholarly journals Mossy Fiber Long-Term Potentiation Deficits in BACE1 Knock-Outs Can Be Rescued by Activation of  7 Nicotinic Acetylcholine Receptors

2010 ◽  
Vol 30 (41) ◽  
pp. 13808-13813 ◽  
Author(s):  
H. Wang ◽  
L. Song ◽  
A. Lee ◽  
F. Laird ◽  
P. C. Wong ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Nicotinic Acetylcholine ◽  
Term Potentiation

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

Blockade of nicotinic acetylcholine receptors suppresses hippocampal long-term potentiation in wild-type but not ApoE4 targeted replacement mice

2005 ◽  
Vol 82 (6) ◽  
pp. 771-777 ◽  
Author(s):  
Sung Hwan Yun ◽  
Kyung A. Park ◽  
Patrick Sullivan ◽  
Joseph F. Pasternak ◽  
Mary Jo LaDu ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Long Term Potentiation ◽  
Wild Type ◽  
Nicotinic Acetylcholine ◽  
Term Potentiation

scholarly journals Lynx1 Prevents Long-Term Potentiation Blockade and Reduction of Neuromodulator Expression Caused by Aβ1-42 and JNK Activation

Acta Naturae ◽  
2018 ◽  
Vol 10 (3) ◽  
pp. 57-61 ◽  
Author(s):  
M. L. Bychkov ◽  
N. A. Vasilyeva ◽  
M. A. Shulepko ◽  
P. M. Balaban ◽  
M. P. Kirpichnikov ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Learning And Memory ◽  
Nicotinic Acetylcholine Receptors ◽  
Cortical Neurons ◽  
Acetylcholine Receptors ◽  
Long Term Potentiation ◽  
Water Soluble ◽  
Amyloid Peptide ◽  
Term Potentiation

Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels. Many neurodegenerative diseases are accompanied by cognitive impairment associated with the dysfunction of nAChRs. The human membrane-tethered prototoxin Lynx1 modulates nAChR function in the brain areas responsible for learning and memory. In this study, we have demonstrated for the first time that the -amyloid peptide A1-42 decreases Lynx1 mRNA expression in rat primary cortical neurons, and that this decrease is associated with the activation of c-Jun N-terminal kinase (JNK). In addition, we have demonstrated that the Lynx1 expression decrease, as well as the blockade of the long-term potentiation underlying learning and memory, caused by A1-42, may be prevented by incubation with a water-soluble Lynx1 analogue. Our findings suggest that the water-soluble Lynx1 analogue may be a promising agent for the improvement of cognitive deficits in neurodegenerative diseases.

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