Homeostatic scaling of neuronal excitability by synaptic modulation of somatic hyperpolarization-activated Ih channels.
The hyperpolarization-activated cation current (Ih) plays an important role in determining membrane potential and firing characteristics of neurons and therefore is a potential target for regulation of intrinsic excitability. Here we show that an increase in AMPA-receptor-dependent synaptic activity induced by alpha-latrotoxin or glutamate application as well as direct depolarization results in an increase in Ih recorded from cell-attached patches in hippocampal CA1 pyramidal neurons. This mechanism requires Ca2+ influx but not increased levels of cAMP. Artificially increasing Ih by using a dynamic clamp during whole-cell current clamp recordings results in reduced firing rates in response to depolarizing current injections. We conclude that modulation of somatic Ih represents a previously uncharacterized mechanism of homeostatic plasticity, allowing a neuron to control its excitability in response to changes in synaptic activity on a relatively short-term time scale.
van Welie
Ingrid
I
Section of Neurobiology, Swammerdam Institute for Life Sciences, University of Amsterdam, P.O. Box 94084, NL-1090 GB, Amsterdam, The Netherlands. welie@science.uva.nl
van Hooft
Johannes A
JA
Wadman
Wytse J
WJ
D000818:Animals; D018698:Glutamic Acid / Q000502:physiology; D006706:Homeostasis; D007473:Ion Channels / Q000502:physiology*; D008297:Male; D009474:Neurons / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D018091:Receptors, AMPA / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D007473:Ion Channels; D018091:Receptors, AMPA; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid