title: Bursts modify electrical synaptic strength.
abstract: Changes in synaptic strength resulting from neuronal activity have been described in great detail for chemical synapses, but the relationship between natural forms of activity and the strength of electrical synapses had previously not been investigated. The thalamic reticular nucleus (TRN), a brain area rich in gap junctional (electrical) synapses, regulates cortical attention, initiates sleep spindles, and participates in shifts between states of arousal. Plasticity of electrical synapses in the TRN may be a key mechanism underlying these processes. Recently, we demonstrated a novel activity-dependent form of long-term depression of electrical synapses in the TRN (Haas et al., 2011). Here we provide an overview of those findings and discuss them in broader context. Because gap junctional proteins are widely expressed in the mammalian brain, modification of synaptic strength is likely to be a widespread and powerful mechanism at electrical synapses throughout the brain.
authors: Center for Brain Science, Harvard University, 52 Oxford St. NWL 202, Cambridge, MA 02138, USA. julie.haas@gmail.com
authors: Julie S
authors: JS
authors: Haas
authors: Carole E
authors: CE
authors: Landisman
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001921:Brain / Q000502:physiology; D020013:Calcium Signaling / Q000502:physiology; D017630:Connexins / Q000502:physiology; D054351:Electrical Synapses / Q000502:physiology*; D055724:Electrophysiological Phenomena / Q000502:physiology*; D017629:Gap Junctions / Q000502:physiology; D006801:Humans; D009473:Neuronal Plasticity / Q000502:physiology; D012964:Sodium / Q000502:physiology; D013787:Thalamic Nuclei / Q000502:physiology; D000097004:Gap Junction delta-2 Protein
chemical_list: D017630:Connexins; D012964:Sodium; D000097004:Gap Junction delta-2 Protein