Muscarinic-induced modulation of potassium conductances is unchanged in mouse hippocampal pyramidal cells that lack functional M1 receptors.

Rouse ST, Hamilton SE, Potter LT, Nathanson NM, Conn PJ
Neurosci Lett. 2000 278 (1-2): 61-4

PMID: 10643801 · DOI:10.1016/s0304-3940(99)00914-3

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.

MeSH Terms (19)

Action Potentials Animals Atropine Carbachol Elapid Venoms Hippocampus Ion Channel Gating Ion Transport Mice Mice, Knockout Muscarinic Agonists Muscarinic Antagonists Patch-Clamp Techniques Pirenzepine Potassium Potassium Channels Pyramidal Cells Receptor, Muscarinic M1 Receptors, Muscarinic

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