Muscarinic-induced modulation of potassium conductances is unchanged in mouse hippocampal pyramidal cells that lack functional M 1 receptors
| Autor: | Neil M. Nathanson, P. Jeffrey Conn, Susan E. Hamilton, Susan T. Rouse, Lincoln T. Potter |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Atropine
Agonist medicine.medical_specialty Patch-Clamp Techniques Potassium Channels Carbachol medicine.drug_class Action Potentials Muscarinic Antagonists Muscarinic Agonists Hippocampus Mice Internal medicine Muscarinic acetylcholine receptor M current medicine Animals Patch clamp Receptor Acetylcholine receptor Elapid Venoms Mice Knockout Ion Transport Chemistry Pyramidal Cells General Neuroscience Receptor Muscarinic M1 Pirenzepine Muscarinic acetylcholine receptor M1 Receptors Muscarinic Endocrinology Potassium Biophysics Ion Channel Gating medicine.drug |
| Zdroj: | Neuroscience Letters. 278:61-64 |
| ISSN: | 0304-3940 |
| DOI: | 10.1016/s0304-3940(99)00914-3 |
| Popis: | Activation of muscarinic acetylcholine (ACh) receptors (mAChRs) increases excitability of pyramidal cells by inhibiting several K+ conductances, including the after-hyperpolarization current (Iahp), the M-current (Im), and a leak K+ conductance (Ileak). Based on pharmacological evidence and the abundant localization of M1 receptors in pyramidal cells, it has been assumed that the M1 receptor is responsible for mediating these effects. However, given the poor selectivity of the pharmacological agents used to characterize these mAChR responses, rigorous characterization of the receptor subtypes that mediate these actions has not been possible. Surprisingly, patch clamp recording from CA1 pyramidal cells in M1 knockout mice revealed no significant difference in the degree of inhibition of Iahp, Im, or Ileak by the mAChR agonist, carbachol (CCh), as compared with wildtype controls. In addition, the M1-toxin was not able to block CCh's inhibition of the Iahp, Im, or Ileak. These data demonstrate that the M1 receptor is not involved in increasing CA1 pyramidal cell excitability by mediating ACh effects on these K+ conductances. |
| Databáze: | OpenAIRE |
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