Immunocytochemical localization of nicotinic acetylcholine receptors in the terminal abdominal ganglion of the cockroach ( Periplaneta americana )

1989 ◽  
Vol 238 (1291) ◽  
pp. 189-192 ◽  

A polyclonal, monospecific antiserum raised against a nicotinic acetylcholine receptor protein affinity-purified from insect nervous tissue, was employed to demonstrate the localization of antigenic sites in the neuropile of the terminal (sixth) abdominal ganglion of the cockroach Periplaneta americana . In agreement with previously published autoradiographic mapping of specific [ 125 I] α -bungarotoxin binding sites, specific areas of the central neuropile of this ganglion were densely stained, but not the cereal afferent axons. No staining was detected corresponding to the dense, peripheral, partly non-specific binding of α -bungarotoxin seen in autoradiographs of the same tissue. Certain peripherally located neuronal cell bodies, including the cell body of giant interneuron 2, contained intracellularly located antigenic sites.

1997 ◽  
Vol 200 (21) ◽  
pp. 2685-2692 ◽  
Author(s):  
S Buckingham ◽  
B Lapied ◽  
H Corronc ◽  
F Sattelle

The neonicotinoid insecticide Imidacloprid acts at three pharmacologically distinct acetylcholine receptor (AChR) subtypes in the cockroach (Periplaneta americana) nervous system, but is ineffective on muscarinic receptors. Imidacloprid (3-100µmoll-1) induced dose-dependent depolarizations at cockroach cercal afferent/giant interneurone synapses. These responses were insensitive to 20µmoll-1 atropine but were completely blocked by the nicotinic antagonist mecamylamine (50µmoll-1). Similarly, Imidacloprid-induced depolarizations of cultured cockroach dorsal unpaired median (DUM) neurones dissociated from the same (terminal abdominal) ganglion were also completely blocked by 100µmoll-1 mecamylamine. However, two components of the response could be distinguished on the basis of their differential sensitivities to 0.1µmoll-1-bungarotoxin (-BTX), which selectively blocks AChRs with 'mixed' nicotinic/muscarinic pharmacology in this preparation. This indicates that Imidacloprid affects both AChRs sensitive to -BTX and -BTX-insensitive nicotinic acetylcholine receptors (nAChRs). Thus, in the cockroach, Imidacloprid activates -BTX-sensitive synaptic nAChRs in giant interneurones, -BTX-insensitive extrasynaptic nAChRs in DUM neurones, and a recently characterized DUM neurone 'mixed' AChR that is sensitive to both nicotinic and muscarinic ligands. Imidacloprid does not act on muscarinic acetylcholine receptors (mAChRs) present on DUM neurone cell bodies and at the cercal afferent/giant interneurone synapses. This study shows that Imidacloprid can act on pharmacologically diverse nAChR subtypes.


2006 ◽  
Vol 31 (4) ◽  
pp. 417-419 ◽  
Author(s):  
Izumi Ikeda ◽  
Tsuyoshi Utsunomiya ◽  
Miki Sadamitsu ◽  
Yoshihisa Ozoe ◽  
Kazuo Mochida

2020 ◽  
Vol 5 (1) ◽  
pp. 54-61
Author(s):  
Angganararas Lungidningtyas ◽  
Arli Aditya Parikesit

Ethanol and nicotine are two common substances that are often linked to complications in alcoholic smokers. The high number of the co-consumptions in alcoholic smokers suggested a possible interaction between ethanol and nicotine in the central nervous system and a potential similar mechanism of action. Both ethanol and nicotine are shown to bind with neuronal nicotinic acetylcholine receptors (nAChRs), a ligand gated cation channel specifically targeted by the endogenous acetylcholine. Ethanol has a much less specific binding capability to modulate the receptors, however, emerging reports indicates that ethanol can interact with nAChRs both directly and indirectly. This study focuses on the analysis of ethanol binding sites with nAChRs using molecular docking techniques obtained from the Protein Data Bank. The obtained data showed a possible binding site for ethanol in nAChRs, however, upon validation, result is not substantial. Nevertheless, the obtained data should be useful for future reference for the basis of ethanol interactions with the human nAChRs proteins.


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