J Wu1, Y C Okada. 1. Department of Neurology and Neurosciences, University of New Mexico School of Medicine, Albuquerque 87131, USA.
Abstract
OBJECTIVES: Roles of a calcium-dependent potassium conductance of slow afterhyperpolarization (AHP) type (gK(AHP)) in generating magnetoencephalographic (MEG) signals were studied in hippocampal longitudinal CA3 slices of the guinea pig. METHODS: The roles of gK(AHP) were experimentally inferred from effects of its blocker, carbamylcholine-chloride (carbachol, CCh), on MEG signals. The MEG signals were compared with extracellular field potentials and intracellular potentials of the pyramidal cells in the slice. RESULTS: CCh profoundly affected MEG waveforms. CCh reduced the initial spike of the evoked MEG signals independently of stimulation of the cell layer and apical dendrites. The slow wave of the evoked MEG signals was reduced by the somatic stimulation, but was enhanced by the apical stimulation. Elevated extracellular calcium and bath-applied tetraethylammonium (TEA) enhanced the CCh effects. CCh also increased spontaneous MEG signals. These effects on MEG and field potentials could be interpreted on the basis of synaptic and intracellular effects of CCh. CONCLUSIONS: Our results indicate that abnormality in this subtle calcium-dependent potassium channel may profoundly influence MEG and EEG signals.
OBJECTIVES: Roles of a calcium-dependent potassium conductance of slow afterhyperpolarization (AHP) type (gK(AHP)) in generating magnetoencephalographic (MEG) signals were studied in hippocampal longitudinal CA3 slices of the guinea pig. METHODS: The roles of gK(AHP) were experimentally inferred from effects of its blocker, carbamylcholine-chloride (carbachol, CCh), on MEG signals. The MEG signals were compared with extracellular field potentials and intracellular potentials of the pyramidal cells in the slice. RESULTS: CCh profoundly affected MEG waveforms. CCh reduced the initial spike of the evoked MEG signals independently of stimulation of the cell layer and apical dendrites. The slow wave of the evoked MEG signals was reduced by the somatic stimulation, but was enhanced by the apical stimulation. Elevated extracellular calcium and bath-applied tetraethylammonium (TEA) enhanced the CCh effects. CCh also increased spontaneous MEG signals. These effects on MEG and field potentials could be interpreted on the basis of synaptic and intracellular effects of CCh. CONCLUSIONS: Our results indicate that abnormality in this subtle calcium-dependent potassium channel may profoundly influence MEG and EEG signals.