The h current is a candidate mechanism for regulating the sliding modification threshold in a BCM-like synaptic learning rule

J Neurophysiol. 2010 Aug;104(2):1020-33. doi: 10.1152/jn.01129.2009. Epub 2010 Jun 16.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism
  • Feedback, Physiological
  • Hippocampus / cytology
  • Ion Channels / physiology*
  • Models, Neurological
  • Neuronal Plasticity / physiology*
  • Pyramidal Cells / physiology*
  • Receptors, Glutamate / physiology
  • Synapses / physiology*


  • Ion Channels
  • Receptors, Glutamate
  • Calcium