scholarly journals Selective Activation of M4Muscarinic Acetylcholine Receptors Reverses MK-801-Induced Behavioral Impairments and Enhances Associative Learning in Rodents

2014 ◽  
Vol 5 (10) ◽  
pp. 920-942 ◽  
Author(s):  
Michael Bubser ◽  
Thomas M. Bridges ◽  
Ditte Dencker ◽  
Robert W. Gould ◽  
Michael Grannan ◽  
...  
2008 ◽  
Vol 74 (6) ◽  
pp. 1496-1511 ◽  
Author(s):  
Nicole A. Horenstein ◽  
Fedra M. Leonik ◽  
Roger L. Papke

Toxins ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 751
Author(s):  
Joyce A. Nieva ◽  
Bernd Krock ◽  
Urban Tillmann ◽  
Jan Tebben ◽  
Christian Zurhelle ◽  
...  

Gymnodimines and spirolides are cyclic imine phycotoxins and known antagonists of nicotinic acetylcholine receptors (nAChRs). We investigated the effect of gymnodimine A (GYM A) and 13-desmethyl spirolide C (SPX 1) from Alexandrium ostenfeldii on rat pheochromocytoma (PC12) cells by monitoring intracellular calcium levels ([Ca]i). Using whole cells, the presence of 0.5 µM of GYM A or SPX 1 induced an increase in [Ca]i mediated by acetylcholine receptors (AChRs) and inhibited further activation of AChRs by acetylcholine (ACh). To differentiate the effects of GYM A or SPX 1, the toxins were applied to cells with pharmacologically isolated nAChRs and muscarinic AChRs (mAChRs) as mediated by the addition of atropine and tubocurarine, respectively. GYM A and SPX 1 activated nAChRs and inhibited the further activation of nAChRs by ACh, indicating that both toxins mimicked the activity of ACh. Regarding mAChRs, a differential response was observed between the two toxins. Only GYM A activated mAChRs, resulting in elevated [Ca]i, but both toxins prevented a subsequent activation by ACh. The absence of the triketal ring system in GYM A may provide the basis for a selective activation of mAChRs. GYM A and SPX 1 induced no changes in [Ca]i when nAChRs and mAChRs were inhibited simultaneously, indicating that both toxins target AChRs.


Peptides ◽  
2008 ◽  
Vol 29 (10) ◽  
pp. 1708-1715 ◽  
Author(s):  
Arthur A. Nery ◽  
Cleber A. Trujillo ◽  
Claudiana Lameu ◽  
Katsuhiro Konno ◽  
Vitor Oliveira ◽  
...  

2021 ◽  
pp. 107053
Author(s):  
Patrick Miller-Rhodes ◽  
Nadine Piazza ◽  
Anna Mattle ◽  
Eric Teboul ◽  
Megan Ehmann ◽  
...  

Insects ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 420 ◽  
Author(s):  
Bernd Grünewald ◽  
Paul Siefert

Acetylcholine (ACh) is the major excitatory neurotransmitter in the insect central nervous system (CNS). However, besides the neuronal expression of ACh receptors (AChR), the existence of non-neuronal AChR in honeybees is plausible. The cholinergic system is a popular target of insecticides because the pharmacology of insect nicotinic acetylcholine receptors (nAChRs) differs substantially from their vertebrate counterparts. Neonicotinoids are agonists of the nAChR and are largely used in crop protection. In contrast to their relatively high safety for humans and livestock, neonicotinoids pose a threat to pollinating insects such as bees. In addition to its effects on behavior, it becomes increasingly evident that neonicotinoids affect developmental processes in bees that appear to be independent of neuronal AChRs. Brood food (royal jelly, worker jelly, or drone jelly) produced in the hypopharyngeal glands of nurse bees contains millimolar concentrations of ACh, which is required for proper larval development. Neonicotinoids reduce the secreted ACh-content in brood food, reduce hypopharyngeal gland size, and lead to developmental impairments within the colony. We assume that potential hazards of neonicotinoids on pollinating bees occur neuronally causing behavioral impairments on adult individuals, and non-neuronally causing developmental disturbances as well as destroying gland functioning.


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