Intracellular Calcium Regulation by Burst Discharge Determines Bidirectional Long-Term Synaptic Plasticity at the Cerebellum Input Stage

Variations in intracellular calcium concentration ([Ca2+]i) provide a critical signal for synaptic plasticity. In accordance with Hebb's postulate (Hebb, 1949), an increase in postsynaptic [Ca2+]i can induce bidirectional changes in synaptic strength depending on activation of specific biochemi...

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Bibliographic Details
Published in:The Journal of neuroscience 2005-05, Vol.25 (19), p.4813-4822
Main Authors: Gall, David, Prestori, Francesca, Sola, Elisabetta, D'Errico, Anna, Roussel, Celine, Forti, Lia, Rossi, Paola, D'Angelo, Egidio
Format: Article
Language:English
Subjects:
Action Potentials - physiology
Action Potentials - radiation effects
Animals
Animals, Newborn
Area Under Curve
Calcium - metabolism
Cellular/Molecular
Cerebellum - cytology
Dose-Response Relationship, Radiation
Electric Stimulation - methods
Enzyme Inhibitors - pharmacology
Excitatory Amino Acid Antagonists - pharmacology
Excitatory Postsynaptic Potentials - drug effects
Excitatory Postsynaptic Potentials - physiology
Excitatory Postsynaptic Potentials - radiation effects
Extracellular Space - metabolism
Imaging, Three-Dimensional - methods
In Vitro Techniques
Magnesium - pharmacology
Neural Pathways - physiology
Neural Pathways - radiation effects
Neuronal Plasticity - drug effects
Neuronal Plasticity - physiology
Neuronal Plasticity - radiation effects
Neurons - drug effects
Neurons - physiology
Neurons - radiation effects
Patch-Clamp Techniques - methods
Potassium - pharmacology
Rats
Synapses - physiology
Synapses - radiation effects
Synaptic Transmission - physiology
Synaptic Transmission - radiation effects
Thapsigargin - pharmacology
Time Factors
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Summary:Variations in intracellular calcium concentration ([Ca2+]i) provide a critical signal for synaptic plasticity. In accordance with Hebb's postulate (Hebb, 1949), an increase in postsynaptic [Ca2+]i can induce bidirectional changes in synaptic strength depending on activation of specific biochemical pathways (Bienenstock et al., 1982; Lisman, 1989; Stanton and Sejnowski, 1989). Despite its strategic location for signal processing, spatiotemporal dynamics of [Ca2+]i changes and their relationship with synaptic plasticity at the cerebellar mossy fiber (mf)-granule cell (GrC) relay were unknown. In this paper, we report the plasticity/[Ca2+]i relationship for GrCs, which are typically activated by mf bursts (Chadderton et al., 2004). Mf bursts caused a remarkable [Ca2+]i increase in GrC dendritic terminals through the activation of NMDA receptors, metabotropic glutamate receptors (probably acting through IP3-sensitive stores), voltage-dependent calcium channels, and Ca2+-induced Ca2+ release. Although [Ca2+]i increased with the duration of mf bursts, long-term depression was found with a small [Ca2+]i increase (bursts 250 ms). LTP and [Ca2+]i saturated for bursts >500 ms and with theta-burst stimulation. Thus, bursting enabled a Ca2+-dependent bidirectional Bienenstock-Cooper-Munro-like learning mechanism providing the cellular basis for effective learning of burst patterns at the input stage of the cerebellum.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.0410-05.2005