Dynamic control of presynaptic Ca(2+) inflow by fast-inactivating K(+) channels in hippocampal mossy fiber boutons

• Published in: Neuron (Cambridge, Mass.) Vol. 28; no. 3; p. 927
• Main Authors: Geiger, J R, Jonas, P
• Format: Journal Article
• Language: English
• Published: United States 01-12-2000
• Subjects: Action Potentials - drug effects; Action Potentials - physiology; Animals; Calcium - metabolism; Elapid Venoms - pharmacology; Electric Stimulation - methods; Excitatory Postsynaptic Potentials - drug effects; Excitatory Postsynaptic Potentials - physiology; Glutamic Acid - metabolism; In Vitro Techniques; Ion Channel Gating - drug effects; Ion Channel Gating - physiology; Mossy Fibers, Hippocampal - metabolism; Patch-Clamp Techniques; Potassium Channel Blockers; Potassium Channels - metabolism; Presynaptic Terminals - drug effects; Presynaptic Terminals - metabolism; Rats; Rats, Wistar; Reaction Time - physiology; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Tetraethylammonium - pharmacology; Tetrodotoxin - pharmacology
• ISSN: 0896-6273
• DOI: 10.1016/S0896-6273(00)00164-1

Analysis of presynaptic determinants of synaptic strength has been difficult at cortical synapses, mainly due to the lack of direct access to presynaptic elements. Here we report patch-clamp recordings from mossy fiber boutons (MFBs) in rat hippocampal slices. The presynaptic action potential is very short during low-frequency stimulation but is prolonged up to 3-fold during high-frequency stimulation. Voltage-gated K(+) channels in MFBs inactivate rapidly but recover from inactivation very slowly, suggesting that cumulative K(+) channel inactivation mediates activity-dependent spike broadening. Prolongation of the presynaptic voltage waveform leads to an increase in the number of Ca(2+) ions entering the terminal per action potential and to a consecutive potentiation of evoked excitatory postsynaptic currents at MFB-CA3 pyramidal cell synapses. Thus, inactivation of presynaptic K(+) channels contributes to the control of efficacy of a glutamatergic synapse in the cortex.