Regulation of synaptic timing in the olfactory bulb by an A-type potassium current

• Published in: Nature neuroscience Vol. 2; no. 12; pp. 1106 - 1113
• Main Authors: Schoppa, N. E, Westbrook, G. L
• Format: Journal Article
• Language: English
• Published: United States 01-12-1999
• Subjects: 4-Aminopyridine - pharmacology; Action Potentials - drug effects; Action Potentials - physiology; Animals; Dendrites - drug effects; Dendrites - metabolism; Electric Stimulation; Excitatory Amino Acid Antagonists - pharmacology; Excitatory Postsynaptic Potentials - drug effects; Excitatory Postsynaptic Potentials - physiology; Feedback; gamma-Aminobutyric Acid - metabolism; Glutamic Acid - metabolism; In Vitro Techniques; Ion Channel Gating - drug effects; Kinetics; Olfactory Bulb - cytology; Olfactory Bulb - drug effects; Olfactory Bulb - metabolism; Potassium - metabolism; Potassium Channel Blockers; Potassium Channels - metabolism; Rats; Rats, Sprague-Dawley; Receptors, AMPA - antagonists & inhibitors; Receptors, AMPA - physiology; Receptors, N-Methyl-D-Aspartate - physiology; Sodium Channel Blockers; Sodium Channels - metabolism; Synapses - drug effects; Synapses - metabolism; Synaptic Transmission - drug effects; Synaptic Transmission - physiology
• ISSN: 1097-6256; 1546-1726
• DOI: 10.1038/16033

Although rapid synaptic transmission confers signal fidelity, the activity of some neuronal circuits depends on prolonged excitation or inhibition. Here we demonstrate that GABAergic granule cells in the rat olfactory bulb produce prolonged inhibition of mitral cells through a precise kinetic matching between transmitter-gated and voltage-gated channels in their dendritic membrane. A transient A-type potassium current (IA) specifically attenuated dendrodendritic inputs mediated by fast-acting AMPA receptors such that the excitation and subsequent inhibitory output of granule cells followed the prolonged kinetics of their NMDA receptors. Altering the weights of the AMPA and NMDA receptor-mediated inputs by modulating IA provides a mechanism to regulate the timing of inhibition according to the demands on the bulb network.