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

Authors
  • Narayanan, Rishikesh
  • Johnston, Daniel
Type
Published Article
Journal
Journal of Neurophysiology
Publisher
American Physiological Society
Publication Date
Aug 01, 2010
Volume
104
Issue
2
Pages
1020–1033
Identifiers
DOI: 10.1152/jn.01129.2009
PMID: 20554832
Source
Medline
License
Unknown

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.

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