a(HBP:"beta-2-containing nAChR")

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Name

beta-2-containing nAChR

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HBP

Namespace Version

20181221

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https://raw.githubusercontent.com/pharmacome/terminology/bd0996a28201cad363557315043c6392e31abf58/export/hbp-names.belns

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

The concept that beta2-containing nAChRs are involved in the reinforcing effects of nicotine was supported by the findings that these mice lacked the high-affinity nicotine binding site, exhibited poor nicotine self-administration, and failed to develop behaviors related to reinforcement (378). The demonstration that these mice developed symptoms of the nicotine withdrawal syndrome similar to those observed in wild-type mice led to the conclusion that beta2-containing nAChRs do not contribute to the physical dependence on nicotine (57). PubMed:19126755

Later it was shown that Abeta is able to activate also beta2*-nAChRs (beta2 subunit-containing nAChRs) PubMed:25514383

Aged beta2 null mutant mice have a thinner cortex compared to agematched wild-type controls (Zoli et al., 1999). This work should be pursued further as it indicates a “neurotrophic” action of beta2 receptor activation by endogenous ACh (Zanardi et al., 2007) PubMed:25514383

In both hippocampal interneurons and oocytes they observed a block of beta2*-nAChRs, that could be prevented by the application of a positive allosteric modulator (PAM) specific for beta2 subunit containing receptors, desformylflustrabromine (dFBr) (Pandya and Yakel, 2011) PubMed:25514383

The concept that beta2-containing nAChRs are involved in the reinforcing effects of nicotine was supported by the findings that these mice lacked the high-affinity nicotine binding site, exhibited poor nicotine self-administration, and failed to develop behaviors related to reinforcement (378). The demonstration that these mice developed symptoms of the nicotine withdrawal syndrome similar to those observed in wild-type mice led to the conclusion that beta2-containing nAChRs do not contribute to the physical dependence on nicotine (57). PubMed:19126755

The concept that beta2-containing nAChRs are involved in the reinforcing effects of nicotine was supported by the findings that these mice lacked the high-affinity nicotine binding site, exhibited poor nicotine self-administration, and failed to develop behaviors related to reinforcement (378). The demonstration that these mice developed symptoms of the nicotine withdrawal syndrome similar to those observed in wild-type mice led to the conclusion that beta2-containing nAChRs do not contribute to the physical dependence on nicotine (57). PubMed:19126755