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Distinct coincidence detectors govern the corticostriatal spike timing‐dependent plasticity
Author(s) -
Fino Elodie,
Paille Vincent,
Cui Yihui,
MoreraHerreras Teresa,
Deniau JeanMichel,
Venance Laurent
Publication year - 2010
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.188466
Subject(s) - neuroscience , coincidence detection in neurobiology , hebbian theory , long term depression , synaptic plasticity , metabotropic receptor , medium spiny neuron , chemistry , basal ganglia , biology , nmda receptor , receptor , glutamate receptor , computer science , ampa receptor , coincidence , central nervous system , artificial intelligence , artificial neural network , medicine , biochemistry , alternative medicine , pathology
Corticostriatal projections constitute the main input to the basal ganglia, an ensemble of interconnected subcortical nuclei involved in procedural learning. Thus, long‐term plasticity at corticostriatal synapses would provide a basic mechanism for the function of basal ganglia in learning and memory. We had previously reported the existence of a corticostriatal anti‐Hebbian spike timing‐dependent plasticity (STDP) at synapses onto striatal output neurons, the medium‐sized spiny neurons. Here, we show that the blockade of GABAergic transmission reversed the time dependence of corticostriatal STDP. We explored the receptors and signalling mechanisms involved in the corticostriatal STDP. Although classical models for STDP propose NMDA receptors as the unique coincidence detector, the involvement of multiple coincidence detectors has also been demonstrated. Here, we show that corticostriatal STDP depends on distinct coincidence detectors. Specifically, long‐term potentiation is dependent on NMDA receptor activation, while long‐term depression requires distinct coincidence detectors: the phospholipase Cβ (PLCβ) and the inositol‐trisphosphate receptor (IP 3 R)‐gated calcium stores. Furthermore, we found that PLCβ activation is controlled by group‐I metabotropic glutamate receptors, type‐1 muscarinic receptors and voltage‐sensitive calcium channel activities. Activation of PLCβ and IP 3 Rs leads to robust retrograde endocannabinoid signalling mediated by 2‐arachidonoyl‐glycerol and cannabinoid CB1 receptors. Interestingly, the same coincidence detectors govern the corticostriatal anti‐Hebbian STDP and the Hebbian STDP reported at cortical synapses. Therefore, LTP and LTD induced by STDP at corticostriatal synapses are mediated by independent signalling mechanisms, each one being controlled by distinct coincidence detectors.