The contribution of ion channels in input-output plasticity

• Published in: Neurobiology of learning and memory Vol. 166; p. 107095
• Main Authors: Debanne, Dominique, Russier, Michaël
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2019; Elsevier
• Subjects: Activity-dependent plasticity; Ion channels; Learning; Life Sciences; LTD; LTP; Memory; Neurobiology; Neurons and Cognition; STDP; Learning; Activity-dependent plasticity; Memory; LTP; Ion channels; STDP; LTD
• ISSN: 1074-7427; 1095-9564; 1095-9564
• DOI: 10.1016/j.nlm.2019.107095

•Ion channels determine EPSP amplification, spike threshold and membrane potential.•Changes in intrinsic excitability occur in parallel to synaptic plasticity.•Hebbian and homeostatic plasticity of intrinsic excitability are linked together. Persistent changes that occur in brain circuits are classically thought to be mediated by long-term modifications in synaptic efficacy. Yet, many studies have shown that voltage-gated ion channels located at the input and output side of the neurons are also the subject to persistent modifications. These channels are thus responsible for intrinsic plasticity that is expressed in many different neuronal types including glutamatergic principal neurons and GABAergic interneurons. As for synaptic plasticity, activation of synaptic glutamate receptors initiate persistent modification in neuronal excitability. We review here how synaptic input can be efficiently altered by activity-dependent modulation of ion channels that control EPSP amplification, spike threshold or resting membrane potential. We discuss the nature of the learning rules shared by intrinsic and synaptic plasticity, the mechanisms of ion channel regulation and the impact of intrinsic plasticity on induction of synaptic modifications.