Identification of Acetylcholine Receptors from the Central Nervous System of Insects

Biochemical studies of the central nervous system (CNS) of locusts (Breer and Knipper, 1984; Knipper and Breer, 1988) have provided evidence for a muscarinic negative feedback mechanism in which muscarinic antagonists and agonists, respectively, enhance and decrease the acetylcholine (ACh) output. More recently, this inhibitory action of presynaptic muscarinic acetylcholine receptors (mAChrs) has been demonstrated in cockroach (Hue et al. 1989; Le Corronc et al. 1991) and in tobacco hornworm (Trimmer and Weeks, 1989) using electrophysiological methods. However, in insects, most experiments have not been performed under physiological conditions but in the presence of acetylcholinesterase inhibitors or exogenous agonists. The aim of this study was to determine whether the release of ACh at a central synapse in the cockroach, Periplaneta americana, could be modulated by endogenous ACh acting on presynaptic muscarinic receptors.

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Acetylcholine receptors in the central nervous system of Drosophila melanogaster

Experimental Cell Research ◽

10.1016/0014-4827(78)90248-3 ◽

1978 ◽

Vol 111 (1) ◽

pp. 185-190 ◽

Cited By ~ 49

Author(s):

Eberhard Rudloff

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Drosophila Melanogaster ◽

Acetylcholine Receptors ◽

The Central Nervous System

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Alpha4beta2 Neuronal Nicotinic Acetylcholine Receptors in the Central Nervous System Are Inhibited by Isoflurane and Propofol, but alpha7-type Nicotinic Acetylcholine Receptors Are Unaffected

Anesthesiology ◽

10.1097/00000542-199704000-00016 ◽

1997 ◽

Vol 86 (4) ◽

pp. 859-865 ◽

Cited By ~ 167

Author(s):

Pamela Flood ◽

Jose Ramirez-Latorre ◽

Lorna Role

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Acetylcholine Receptor ◽

Nicotinic Acetylcholine Receptors ◽

Acetylcholine Receptors ◽

General Anesthetics ◽

Nicotinic Acetylcholine ◽

The Central Nervous System ◽

Beta 2 ◽

Alpha 7

Background The mechanisms of action of general anesthetics are not completely understood. Many general anesthetics are reported to potentiate gamma-aminobutyric acid (GABAA) and glycine receptors in the central nervous system (CNS) and to inhibit the muscle-type nicotinic acetylcholine receptor (nAChR). The effects of general anesthetics on another family of ligand-gated ion channel in the CNS, the nAChRs, have not been defined. Methods Two types of CNS acetylcholine receptor, the alpha 4 beta 2 receptor or the alpha 7 homomeric receptor, were expressed heterologously in Xenopus laevis oocytes. Using the standard two-microelectrode voltage-clamp technique, peak acetylcholinegated current was measured before and after coapplication of isoflurane or propofol. Results Coapplication of either isoflurane or propofol with acetylcholine resulted in potent, dose-dependent inhibition of the alpha 4 beta 2 receptor current with median inhibitory concentrations of 85 and 19 microM, respectively. The inhibition of the alpha 4 beta 2 receptor by both isoflurane and propofol appears to be competitive with respect to acetylcholine. The alpha 7 receptor current was not effected by either anesthetic. Conclusions The CNS-type nAChRs are differentially affected by isoflurane and propofol. The alpha 4 beta 2 receptor is affected by isoflurane more potently than the most sensitive GABAA or glycine receptor that has been reported, whereas the alpha 7 homomeric receptor is not affected by either anesthetic. Inhibition of specific subtypes of nAChRs in the CNS, along with potentiation of GABAA and glycine receptors, may contribute to the effects and side effects of general anesthetics.

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