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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.

Homeostatic scaling of neuronal excitability by synaptic modulation of somatic hyperpolarization-activated I h channels

Homeostatic scaling of neuronal excitability by synaptic modulation of somatic hyperpolarization-activated I _h channels