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 (IP₃R)‐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 IP₃Rs 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.