title: The h current is a candidate mechanism for regulating the sliding modification threshold in a BCM-like synaptic learning rule.
abstract: Hebbian synaptic plasticity acts as a positive feedback mechanism and can destabilize a neuronal network unless concomitant homeostatic processes that counterbalance this instability are activated. Within a Bienenstock-Cooper-Munro (BCM)-like plasticity framework, such compensation is achieved through a modification threshold that slides in an activity-dependent fashion. Although the BCM-like plasticity framework has been a useful formulation to understand synaptic plasticity and metaplasticity, a mechanism for the activity-dependent regulation of this modification threshold has remained an open question. In this simulation study based on CA1 pyramidal cells, we use a modification of the calcium-dependent hypothesis proposed elsewhere and show that a change in the hyperpolarization-activated, nonspecific-cation h current is capable of shifting the modification threshold. Based on the direction of such a shift in relation to changes in the h current, and supported by previous experimental results, we argue that the h current fits the requirements for an activity-dependent regulator of this modification threshold. Additionally, using the same framework, we show that multiple voltage- and ligand-gated ion channels present in a neuronal compartment can regulate the modification threshold through complex interactions among themselves. Our results underscore the heavy mutual interdependence of synaptic and intrinsic properties/plasticity in regulating learning and homeostasis in single neurons and their networks under both physiological and pathological brain states.
authors.affiliation: Center for Learning and Memory, The University of Texas, Austin, Texas 78712-0805, USA.
authors.forename: Rishikesh
authors.initials: R
authors.lastname: Narayanan
authors.forename: Daniel
authors.initials: D
authors.lastname: Johnston
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D025461:Feedback, Physiological; D006624:Hippocampus / Q000166:cytology; D007473:Ion Channels / Q000502:physiology*; D008959:Models, Neurological; D009473:Neuronal Plasticity / Q000502:physiology*; D017966:Pyramidal Cells / Q000502:physiology*; D017470:Receptors, Glutamate / Q000502:physiology; D013569:Synapses / Q000502:physiology*
chemical_list: D007473:Ion Channels; D017470:Receptors, Glutamate; D002118:Calcium