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Physostigmine and acetylcholine differentially activate nicotinic receptor subpopulations in Locusta migratoria neurons.
Brain Res. 1998 Apr 13; 789(2):263-73.BR

Abstract

The effects of acetylcholine (ACh) and physostigmine (PHY) on thoracic ganglion neurons of Locusta migratoria were investigated using whole-cell and cell-attached voltage clamp. ACh activated whole-cell currents with variable amplitudes, time course and ion channel block between cells, suggesting differential expression of nicotinic acetylcholine receptor (nAChR) subtypes. This was supported by selective block of the peak of the currents by the alpha7-specific alpha-conotoxin ImI. PHY at 100 microM evoked smaller whole-cell currents with variable amplitudes and marginal desensitization. The PHY/ACh amplitude ratio varied between cells, and was positively related to the time constant of decay of the ACh response. EC50 values for the peak amplitude of the ACh- and PHY-induced currents were 50 microM and 3 microM, respectively. Both agonists activated nAChR, indicated by equal voltage-dependence and reversal potentials and the same pharmacological properties of ACh and PHY responses. In addition, PHY and ACh induced ion channel block. Co-application and cross-desensitization experiments showed that ACh and PHY activate the same nAChR subpopulations. Both agonists activated nicotinic single channels with three conductance levels, which were equal for ACh and PHY, indicating activation of the same nAChR subtypes by both agonists. However, for all levels PHY displayed a lower open probability than ACh. Taken together, different whole-cell responses appear to originate from differential activation, desensitization and ion channel block by ACh and PHY of distinct nAChR populations.

Authors+Show Affiliations

Research Institute of Toxicology, Utrecht University, P.O. Box 80. 176, NL-3508 TD Utrecht, Netherlands. i.vandenbeukel@ritox.dgk.ruu.nlNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

9573380

Citation

van den Beukel, I, et al. "Physostigmine and Acetylcholine Differentially Activate Nicotinic Receptor Subpopulations in Locusta Migratoria Neurons." Brain Research, vol. 789, no. 2, 1998, pp. 263-73.
van den Beukel I, van Kleef RG, Zwart R, et al. Physostigmine and acetylcholine differentially activate nicotinic receptor subpopulations in Locusta migratoria neurons. Brain Res. 1998;789(2):263-73.
van den Beukel, I., van Kleef, R. G., Zwart, R., & Oortgiesen, M. (1998). Physostigmine and acetylcholine differentially activate nicotinic receptor subpopulations in Locusta migratoria neurons. Brain Research, 789(2), 263-73.
van den Beukel I, et al. Physostigmine and Acetylcholine Differentially Activate Nicotinic Receptor Subpopulations in Locusta Migratoria Neurons. Brain Res. 1998 Apr 13;789(2):263-73. PubMed PMID: 9573380.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Physostigmine and acetylcholine differentially activate nicotinic receptor subpopulations in Locusta migratoria neurons. AU - van den Beukel,I, AU - van Kleef,R G, AU - Zwart,R, AU - Oortgiesen,M, PY - 1998/5/30/pubmed PY - 1998/5/30/medline PY - 1998/5/30/entrez SP - 263 EP - 73 JF - Brain research JO - Brain Res VL - 789 IS - 2 N2 - The effects of acetylcholine (ACh) and physostigmine (PHY) on thoracic ganglion neurons of Locusta migratoria were investigated using whole-cell and cell-attached voltage clamp. ACh activated whole-cell currents with variable amplitudes, time course and ion channel block between cells, suggesting differential expression of nicotinic acetylcholine receptor (nAChR) subtypes. This was supported by selective block of the peak of the currents by the alpha7-specific alpha-conotoxin ImI. PHY at 100 microM evoked smaller whole-cell currents with variable amplitudes and marginal desensitization. The PHY/ACh amplitude ratio varied between cells, and was positively related to the time constant of decay of the ACh response. EC50 values for the peak amplitude of the ACh- and PHY-induced currents were 50 microM and 3 microM, respectively. Both agonists activated nAChR, indicated by equal voltage-dependence and reversal potentials and the same pharmacological properties of ACh and PHY responses. In addition, PHY and ACh induced ion channel block. Co-application and cross-desensitization experiments showed that ACh and PHY activate the same nAChR subpopulations. Both agonists activated nicotinic single channels with three conductance levels, which were equal for ACh and PHY, indicating activation of the same nAChR subtypes by both agonists. However, for all levels PHY displayed a lower open probability than ACh. Taken together, different whole-cell responses appear to originate from differential activation, desensitization and ion channel block by ACh and PHY of distinct nAChR populations. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/9573380/Physostigmine_and_acetylcholine_differentially_activate_nicotinic_receptor_subpopulations_in_Locusta_migratoria_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(98)00007-9 DB - PRIME DP - Unbound Medicine ER -